Jane S. Davis, CRNP, DNP

The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.

Q: I have a 58-year-old female patient who is taking warfarin for atrial fibrillation and is complaining about blood in her urine. She is postmenopausal, so I think it is just the warfarin. Other than checking her international normalized ratio (INR), what else should I be doing?

In addition to checking an INR, it is important to investigate benign causes for the hematuria. Asymptomatic hematuria requires obtaining a thorough history, which includes common risk factors for urinary tract malignancy, physical exam, and laboratory evaluation. Initially, a noncontaminated urinalysis with culture and sensitivity should be obtained to rule out infection.

If a benign cause cannot be found in any patient undergoing anticoagulation therapy, the AUA (guideline 6)¹ recommends a urologic and nephrologic evaluation. Anticoagulation therapy would include all anticoagulant and antiplatelet agents, such as aspirin, Plavix (clopidogrel), Pletal (cilostazol), Coumadin (warfarin), heparin, or heparin derivatives, such as Lovenox (enoxaparin).

The urologic evaluation may include urology referral, cystoscopy for patients 35 or older, and multiphasic CT urography, performed with and without contrast. A nephrologic evaluation would initially include a urinalysis, calculated eGFR, creatinine, and BUN, and a nephrology referral when indicated. A thorough evaluation is indicated for all patients with hematuria who are on anticoagulant therapy to ensure that a urinary tract malignancy is not present.

AUA guidelines 10 through 13¹ address alternative tests for patients with kidney disease in whom contrast dye is contraindicated.

Kristy Washinger, MSN, CRNP, Nephrology Associates of Central Pennsylvania, Camp Hill, PA

References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012.  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.

Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.

The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.

Q: I have a 58-year-old female patient who is taking warfarin for atrial fibrillation and is complaining about blood in her urine. She is postmenopausal, so I think it is just the warfarin. Other than checking her international normalized ratio (INR), what else should I be doing?

In addition to checking an INR, it is important to investigate benign causes for the hematuria. Asymptomatic hematuria requires obtaining a thorough history, which includes common risk factors for urinary tract malignancy, physical exam, and laboratory evaluation. Initially, a noncontaminated urinalysis with culture and sensitivity should be obtained to rule out infection.

If a benign cause cannot be found in any patient undergoing anticoagulation therapy, the AUA (guideline 6)¹ recommends a urologic and nephrologic evaluation. Anticoagulation therapy would include all anticoagulant and antiplatelet agents, such as aspirin, Plavix (clopidogrel), Pletal (cilostazol), Coumadin (warfarin), heparin, or heparin derivatives, such as Lovenox (enoxaparin).

The urologic evaluation may include urology referral, cystoscopy for patients 35 or older, and multiphasic CT urography, performed with and without contrast. A nephrologic evaluation would initially include a urinalysis, calculated eGFR, creatinine, and BUN, and a nephrology referral when indicated. A thorough evaluation is indicated for all patients with hematuria who are on anticoagulant therapy to ensure that a urinary tract malignancy is not present.

AUA guidelines 10 through 13¹ address alternative tests for patients with kidney disease in whom contrast dye is contraindicated.

Kristy Washinger, MSN, CRNP, Nephrology Associates of Central Pennsylvania, Camp Hill, PA

References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012.  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.

Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.

The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.

Q: I have a 58-year-old female patient who is taking warfarin for atrial fibrillation and is complaining about blood in her urine. She is postmenopausal, so I think it is just the warfarin. Other than checking her international normalized ratio (INR), what else should I be doing?

In addition to checking an INR, it is important to investigate benign causes for the hematuria. Asymptomatic hematuria requires obtaining a thorough history, which includes common risk factors for urinary tract malignancy, physical exam, and laboratory evaluation. Initially, a noncontaminated urinalysis with culture and sensitivity should be obtained to rule out infection.

If a benign cause cannot be found in any patient undergoing anticoagulation therapy, the AUA (guideline 6)¹ recommends a urologic and nephrologic evaluation. Anticoagulation therapy would include all anticoagulant and antiplatelet agents, such as aspirin, Plavix (clopidogrel), Pletal (cilostazol), Coumadin (warfarin), heparin, or heparin derivatives, such as Lovenox (enoxaparin).

The urologic evaluation may include urology referral, cystoscopy for patients 35 or older, and multiphasic CT urography, performed with and without contrast. A nephrologic evaluation would initially include a urinalysis, calculated eGFR, creatinine, and BUN, and a nephrology referral when indicated. A thorough evaluation is indicated for all patients with hematuria who are on anticoagulant therapy to ensure that a urinary tract malignancy is not present.

AUA guidelines 10 through 13¹ address alternative tests for patients with kidney disease in whom contrast dye is contraindicated.

Kristy Washinger, MSN, CRNP, Nephrology Associates of Central Pennsylvania, Camp Hill, PA

References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012.  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.

Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.

The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.

Q: I am studying for my boards and am deep into the renal/urology section. I graduated so long ago that IVPs were the evaluation of choice. What is the “expert opinion” now on managing the patient with hematuria? Do we go straight to cystoscopy or use a different test?

First-line evaluation for asymptomatic microscopic hematuria now requires CT urography instead of IV pyelography (IVP) or cystoscopy (see AUA guideline 10).¹ The CT should be done with and without IV contrast and be multiphasic in nature. Specific high-resolution evaluation of the urothelium of the upper urinary tracts during the excretory phase must be included. This is the most sensitive and specific radiologic examination to adequately evaluate for a renal mass in the parenchyma as well as for abnormalities in the upper tracts simultaneously.¹

Using contrast dye in a patient with decreased renal function is always problematic. Precautions to be taken include withholding ACE inhibitors and angiotensin receptor blockers before and after the procedure and hydrating the patient before, during, and after administration of contrast dye.

Sarah Sparks, NP, St. Luke’s Clinic–Nephrology, St. Luke’s Health System, Boise, ID

References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012.  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.

Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.

The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.

Q: I am studying for my boards and am deep into the renal/urology section. I graduated so long ago that IVPs were the evaluation of choice. What is the “expert opinion” now on managing the patient with hematuria? Do we go straight to cystoscopy or use a different test?

First-line evaluation for asymptomatic microscopic hematuria now requires CT urography instead of IV pyelography (IVP) or cystoscopy (see AUA guideline 10).¹ The CT should be done with and without IV contrast and be multiphasic in nature. Specific high-resolution evaluation of the urothelium of the upper urinary tracts during the excretory phase must be included. This is the most sensitive and specific radiologic examination to adequately evaluate for a renal mass in the parenchyma as well as for abnormalities in the upper tracts simultaneously.¹

Using contrast dye in a patient with decreased renal function is always problematic. Precautions to be taken include withholding ACE inhibitors and angiotensin receptor blockers before and after the procedure and hydrating the patient before, during, and after administration of contrast dye.

Sarah Sparks, NP, St. Luke’s Clinic–Nephrology, St. Luke’s Health System, Boise, ID

References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012.  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.

Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.

The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.

Q: I am studying for my boards and am deep into the renal/urology section. I graduated so long ago that IVPs were the evaluation of choice. What is the “expert opinion” now on managing the patient with hematuria? Do we go straight to cystoscopy or use a different test?

First-line evaluation for asymptomatic microscopic hematuria now requires CT urography instead of IV pyelography (IVP) or cystoscopy (see AUA guideline 10).¹ The CT should be done with and without IV contrast and be multiphasic in nature. Specific high-resolution evaluation of the urothelium of the upper urinary tracts during the excretory phase must be included. This is the most sensitive and specific radiologic examination to adequately evaluate for a renal mass in the parenchyma as well as for abnormalities in the upper tracts simultaneously.¹

Using contrast dye in a patient with decreased renal function is always problematic. Precautions to be taken include withholding ACE inhibitors and angiotensin receptor blockers before and after the procedure and hydrating the patient before, during, and after administration of contrast dye.

Sarah Sparks, NP, St. Luke’s Clinic–Nephrology, St. Luke’s Health System, Boise, ID

References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012.  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.

Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.

The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.

Q: A 39-year-old woman came to my office for an annual physical, and there was blood in the urine when I sent her urine out for microscopy. She is having abnormal menses, so she could not be sure this was not contamination (and neither could I). I repeated the urine and it was positive for blood on micro. What do I do now? Where do I refer her?

There are numerous causes of microhematuria, and the answer can often be found by considering the possible differential diagnoses. The causes of hematuria include urinary tract infection (UTI), bladder or kidney stones, kidney disease, use of certain medications, strenuous exercise, and trauma.² Health care professionals should follow a process to make logical assessments and decisions in the care of this 39-year-old woman with microhematuria.

What to do first? The first step is to obtain a complete history, including any associated symptoms, medication history, last menstrual period, family history, previous medical history, recent trauma, strenuous exercise, and easy bruising or bleeding. In this case, since the urinalysis was repeated and remained positive for hematuria, the next step is to consider a renal function panel and complete blood count (CBC).

A renal function panel (sodium, potassium, chloride, carbon dioxide, anion gap, glucose, urea reduction ratio, creatinine, albumin, calcium, and phosphorous) will help to rule out existing renal function dysfunction.

The CBC will help to rule out any blood loss or presence of systemic involvement. Also, look at other results noted on the urinalysis, such as protein, nitrates, and leukocytes. Looking for protein will help the clinician determine whether fever, diabetes, chronic kidney disease, or hypertension may be the cause. Nitrates will appear as a result of UTI, and leukocytes may suggest a UTI or possible contamination. Dysmorphic red blood cells (RBCs with irregular shapes) found on the microscopic exam of the urine indicate a glomerular etiology, in which case the patient should be referred to nephrology for possible renal biopsy. If the red blood cells are nonglomerular (ie, the glomerulus is not the source of the bleeding) and there is no other obvious cause, then the patient should be referred to urology.

When is it time to refer? If microhematuria is persistent, the patient will need to be referred to a urologist for further evaluation. According to AUA guidelines 7, 8, and 16 through 19,¹ cystoscopy should be considered for patients 35 or older with asymptomatic hematuria. For younger patients, a cystoscopy may be considered at the discretion of the provider. Although blue light cystoscopy has FDA approval, in the opinion of the AUA, the risks of the technique outweigh its benefits. Blue light cystoscopy is reported to improve identification of bladder tumors.³

For patients with a history of persistent asymptomatic hematuria, no further urinalyses are needed after two consecutive yearly tests with negative results. Those with a negative urologic workup should have urinalyses performed annually. If a patient has persistent or recurrent asymptomatic microhematuria with an initially negative urologic workup, then patients should be considered for reevaluation by urology every 3 to 5 years.¹

In conclusion, the best approach to microhematuria is to obtain a thorough history, check the necessary labs, and if microhematuria persists, make the necessary referral to the appropriate specialist, ensuring that the patient receives the best possible care.

Tia Austin Hayes, FNP-C, JMM Renal Clinic/Outpatient Dialysis, University of Mississippi Department of Nephrology; Donna Anderson, PA-C, CAQ, Nephrology Specialists of Oklahoma, Tulsa

References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012.  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.

Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.

The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.

Q: A 39-year-old woman came to my office for an annual physical, and there was blood in the urine when I sent her urine out for microscopy. She is having abnormal menses, so she could not be sure this was not contamination (and neither could I). I repeated the urine and it was positive for blood on micro. What do I do now? Where do I refer her?

There are numerous causes of microhematuria, and the answer can often be found by considering the possible differential diagnoses. The causes of hematuria include urinary tract infection (UTI), bladder or kidney stones, kidney disease, use of certain medications, strenuous exercise, and trauma.² Health care professionals should follow a process to make logical assessments and decisions in the care of this 39-year-old woman with microhematuria.

What to do first? The first step is to obtain a complete history, including any associated symptoms, medication history, last menstrual period, family history, previous medical history, recent trauma, strenuous exercise, and easy bruising or bleeding. In this case, since the urinalysis was repeated and remained positive for hematuria, the next step is to consider a renal function panel and complete blood count (CBC).

A renal function panel (sodium, potassium, chloride, carbon dioxide, anion gap, glucose, urea reduction ratio, creatinine, albumin, calcium, and phosphorous) will help to rule out existing renal function dysfunction.

The CBC will help to rule out any blood loss or presence of systemic involvement. Also, look at other results noted on the urinalysis, such as protein, nitrates, and leukocytes. Looking for protein will help the clinician determine whether fever, diabetes, chronic kidney disease, or hypertension may be the cause. Nitrates will appear as a result of UTI, and leukocytes may suggest a UTI or possible contamination. Dysmorphic red blood cells (RBCs with irregular shapes) found on the microscopic exam of the urine indicate a glomerular etiology, in which case the patient should be referred to nephrology for possible renal biopsy. If the red blood cells are nonglomerular (ie, the glomerulus is not the source of the bleeding) and there is no other obvious cause, then the patient should be referred to urology.

When is it time to refer? If microhematuria is persistent, the patient will need to be referred to a urologist for further evaluation. According to AUA guidelines 7, 8, and 16 through 19,¹ cystoscopy should be considered for patients 35 or older with asymptomatic hematuria. For younger patients, a cystoscopy may be considered at the discretion of the provider. Although blue light cystoscopy has FDA approval, in the opinion of the AUA, the risks of the technique outweigh its benefits. Blue light cystoscopy is reported to improve identification of bladder tumors.³

For patients with a history of persistent asymptomatic hematuria, no further urinalyses are needed after two consecutive yearly tests with negative results. Those with a negative urologic workup should have urinalyses performed annually. If a patient has persistent or recurrent asymptomatic microhematuria with an initially negative urologic workup, then patients should be considered for reevaluation by urology every 3 to 5 years.¹

In conclusion, the best approach to microhematuria is to obtain a thorough history, check the necessary labs, and if microhematuria persists, make the necessary referral to the appropriate specialist, ensuring that the patient receives the best possible care.

Tia Austin Hayes, FNP-C, JMM Renal Clinic/Outpatient Dialysis, University of Mississippi Department of Nephrology; Donna Anderson, PA-C, CAQ, Nephrology Specialists of Oklahoma, Tulsa

References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012.  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.

Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.

The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.

Q: A 39-year-old woman came to my office for an annual physical, and there was blood in the urine when I sent her urine out for microscopy. She is having abnormal menses, so she could not be sure this was not contamination (and neither could I). I repeated the urine and it was positive for blood on micro. What do I do now? Where do I refer her?

There are numerous causes of microhematuria, and the answer can often be found by considering the possible differential diagnoses. The causes of hematuria include urinary tract infection (UTI), bladder or kidney stones, kidney disease, use of certain medications, strenuous exercise, and trauma.² Health care professionals should follow a process to make logical assessments and decisions in the care of this 39-year-old woman with microhematuria.

What to do first? The first step is to obtain a complete history, including any associated symptoms, medication history, last menstrual period, family history, previous medical history, recent trauma, strenuous exercise, and easy bruising or bleeding. In this case, since the urinalysis was repeated and remained positive for hematuria, the next step is to consider a renal function panel and complete blood count (CBC).

A renal function panel (sodium, potassium, chloride, carbon dioxide, anion gap, glucose, urea reduction ratio, creatinine, albumin, calcium, and phosphorous) will help to rule out existing renal function dysfunction.

The CBC will help to rule out any blood loss or presence of systemic involvement. Also, look at other results noted on the urinalysis, such as protein, nitrates, and leukocytes. Looking for protein will help the clinician determine whether fever, diabetes, chronic kidney disease, or hypertension may be the cause. Nitrates will appear as a result of UTI, and leukocytes may suggest a UTI or possible contamination. Dysmorphic red blood cells (RBCs with irregular shapes) found on the microscopic exam of the urine indicate a glomerular etiology, in which case the patient should be referred to nephrology for possible renal biopsy. If the red blood cells are nonglomerular (ie, the glomerulus is not the source of the bleeding) and there is no other obvious cause, then the patient should be referred to urology.

When is it time to refer? If microhematuria is persistent, the patient will need to be referred to a urologist for further evaluation. According to AUA guidelines 7, 8, and 16 through 19,¹ cystoscopy should be considered for patients 35 or older with asymptomatic hematuria. For younger patients, a cystoscopy may be considered at the discretion of the provider. Although blue light cystoscopy has FDA approval, in the opinion of the AUA, the risks of the technique outweigh its benefits. Blue light cystoscopy is reported to improve identification of bladder tumors.³

For patients with a history of persistent asymptomatic hematuria, no further urinalyses are needed after two consecutive yearly tests with negative results. Those with a negative urologic workup should have urinalyses performed annually. If a patient has persistent or recurrent asymptomatic microhematuria with an initially negative urologic workup, then patients should be considered for reevaluation by urology every 3 to 5 years.¹

In conclusion, the best approach to microhematuria is to obtain a thorough history, check the necessary labs, and if microhematuria persists, make the necessary referral to the appropriate specialist, ensuring that the patient receives the best possible care.

Tia Austin Hayes, FNP-C, JMM Renal Clinic/Outpatient Dialysis, University of Mississippi Department of Nephrology; Donna Anderson, PA-C, CAQ, Nephrology Specialists of Oklahoma, Tulsa

References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012.  http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.

Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.

Q:  How much of a bump in serum creatinine (SCr) can I expect after I start a patient on an ACE inhibitor or an angiotensin II receptor blocker (ARB)? How often should I check the patient’s SCr?

ACE inhibitors and ARBs inhibit the angiotensin-induced vasoconstriction of the efferent arterioles of the glomerular microcirculation. Inhibition of the renin-angiotensin-aldosterone system (RAAS) by these medications reduces both intraglomerular filtration pressure and proteinuria, delaying the progression of kidney disease.⁶ In response to RAAS inhibition, the GFR is slightly decreased and SCr is increased, reflecting the beneficial effects of the ACE inhibitor or the ARB on renal hemodynamics.^7,8 SCr may rise 10% to 30% from baseline within the first two weeks and generally stabilizes within two to four weeks.⁸

Patients with normal renal function initiated on an ACE inhibitor or an ARB experience a rise in SCr of about 0.2 mg/dL over a two- to three-week period, returning to baseline during week 4. Patients with abnormal renal function will have an increase in SCr of approximately 0.5 mg/dL over a four-week period.⁹ A progressive increase in SCr as great as 2.0 mg/dL may be seen in patients with bilateral renal artery stenosis, extensive atherosclerotic cardiovascular disease, or dehydration. In these instances, treatment with the ACE inhibitor or the ARB should be discontinued.⁹ 

Close monitoring is recommended in patients with chronic kidney disease Stage 3 through Stage 5 who are started on an ACE inhibitor or an ARB. SCr and K should be evaluated before and four weeks after initiating or titrating therapy.⁹ If SCr has increased by less than 0.5 mg/dL from a baseline measurement of 2.5 mg/dL or less; or if the rise in SCr is 1.0 mg/dL or less when the baseline SCr exceeds 2.5 mg/dL and K is 5.5 mEq/L or less, continue to titrate the agents, rechecking blood pressure (BP) and levels of SCr and K every four weeks until BP is at goal.⁸ Once SCr, K, and BP are stable, they should be rechecked annually.⁹

The adverse effects of ACE inhibitor/ARB use include angioedema and hyperkalemia, while only ACE inhibitors cause patients to cough. 

Afix Kehinde, PharmD, College of Pharmacy, University of Illinois at Chicago; Cheryl L. Gilmartin, PharmD, Clinical Assistant Professor, Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago; Clinical Pharmacist, Ambulatory Pharmacy Services, University of Illinois Hospital & Health Sciences System, Chicago

REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q:  How much of a bump in serum creatinine (SCr) can I expect after I start a patient on an ACE inhibitor or an angiotensin II receptor blocker (ARB)? How often should I check the patient’s SCr?

ACE inhibitors and ARBs inhibit the angiotensin-induced vasoconstriction of the efferent arterioles of the glomerular microcirculation. Inhibition of the renin-angiotensin-aldosterone system (RAAS) by these medications reduces both intraglomerular filtration pressure and proteinuria, delaying the progression of kidney disease.⁶ In response to RAAS inhibition, the GFR is slightly decreased and SCr is increased, reflecting the beneficial effects of the ACE inhibitor or the ARB on renal hemodynamics.^7,8 SCr may rise 10% to 30% from baseline within the first two weeks and generally stabilizes within two to four weeks.⁸

Patients with normal renal function initiated on an ACE inhibitor or an ARB experience a rise in SCr of about 0.2 mg/dL over a two- to three-week period, returning to baseline during week 4. Patients with abnormal renal function will have an increase in SCr of approximately 0.5 mg/dL over a four-week period.⁹ A progressive increase in SCr as great as 2.0 mg/dL may be seen in patients with bilateral renal artery stenosis, extensive atherosclerotic cardiovascular disease, or dehydration. In these instances, treatment with the ACE inhibitor or the ARB should be discontinued.⁹ 

Close monitoring is recommended in patients with chronic kidney disease Stage 3 through Stage 5 who are started on an ACE inhibitor or an ARB. SCr and K should be evaluated before and four weeks after initiating or titrating therapy.⁹ If SCr has increased by less than 0.5 mg/dL from a baseline measurement of 2.5 mg/dL or less; or if the rise in SCr is 1.0 mg/dL or less when the baseline SCr exceeds 2.5 mg/dL and K is 5.5 mEq/L or less, continue to titrate the agents, rechecking blood pressure (BP) and levels of SCr and K every four weeks until BP is at goal.⁸ Once SCr, K, and BP are stable, they should be rechecked annually.⁹

The adverse effects of ACE inhibitor/ARB use include angioedema and hyperkalemia, while only ACE inhibitors cause patients to cough. 

Afix Kehinde, PharmD, College of Pharmacy, University of Illinois at Chicago; Cheryl L. Gilmartin, PharmD, Clinical Assistant Professor, Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago; Clinical Pharmacist, Ambulatory Pharmacy Services, University of Illinois Hospital & Health Sciences System, Chicago

REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q:  How much of a bump in serum creatinine (SCr) can I expect after I start a patient on an ACE inhibitor or an angiotensin II receptor blocker (ARB)? How often should I check the patient’s SCr?

ACE inhibitors and ARBs inhibit the angiotensin-induced vasoconstriction of the efferent arterioles of the glomerular microcirculation. Inhibition of the renin-angiotensin-aldosterone system (RAAS) by these medications reduces both intraglomerular filtration pressure and proteinuria, delaying the progression of kidney disease.⁶ In response to RAAS inhibition, the GFR is slightly decreased and SCr is increased, reflecting the beneficial effects of the ACE inhibitor or the ARB on renal hemodynamics.^7,8 SCr may rise 10% to 30% from baseline within the first two weeks and generally stabilizes within two to four weeks.⁸

Patients with normal renal function initiated on an ACE inhibitor or an ARB experience a rise in SCr of about 0.2 mg/dL over a two- to three-week period, returning to baseline during week 4. Patients with abnormal renal function will have an increase in SCr of approximately 0.5 mg/dL over a four-week period.⁹ A progressive increase in SCr as great as 2.0 mg/dL may be seen in patients with bilateral renal artery stenosis, extensive atherosclerotic cardiovascular disease, or dehydration. In these instances, treatment with the ACE inhibitor or the ARB should be discontinued.⁹ 

Close monitoring is recommended in patients with chronic kidney disease Stage 3 through Stage 5 who are started on an ACE inhibitor or an ARB. SCr and K should be evaluated before and four weeks after initiating or titrating therapy.⁹ If SCr has increased by less than 0.5 mg/dL from a baseline measurement of 2.5 mg/dL or less; or if the rise in SCr is 1.0 mg/dL or less when the baseline SCr exceeds 2.5 mg/dL and K is 5.5 mEq/L or less, continue to titrate the agents, rechecking blood pressure (BP) and levels of SCr and K every four weeks until BP is at goal.⁸ Once SCr, K, and BP are stable, they should be rechecked annually.⁹

The adverse effects of ACE inhibitor/ARB use include angioedema and hyperkalemia, while only ACE inhibitors cause patients to cough. 

Afix Kehinde, PharmD, College of Pharmacy, University of Illinois at Chicago; Cheryl L. Gilmartin, PharmD, Clinical Assistant Professor, Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago; Clinical Pharmacist, Ambulatory Pharmacy Services, University of Illinois Hospital & Health Sciences System, Chicago

REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q: Is there any science behind the use of acetylcysteine/fluid prep for cardiac catheterizations, or is that just “voodoo” medicine?

Contrast-induced nephropathy (CIN) is the third most common cause of hospital-acquired acute kidney injury. In recent years, the use of iodinated radiocontrast medium has increased significantly, due to increased use of both percutaneous coronary interventions and CT scanning. The radiocontrast medium causes vasoconstriction, which leads to a reduction in renal blood flow, with a resulting decrease in GFR. Preexisting impaired kidney function results in increased risk due to slower clearance of the contrast materials, and the resulting prolonged exposure increases the risk for further renal injury.¹⁰

A GFR below 60 mL/min/1.73m², volume depletion, and diabetes all increase the risk for CIN. Among patients who experience an acute kidney injury due to contrast medium, the risk for adverse outcomes increases, including early or late cardiovascular events, prolonged hospitalizations, and death. As no FDA-approved treatment yet exists for CIN, the best medicine is to try to prevent it.¹¹

Several interventions can reduce the patient’s risk for CIN. These include IV hydration, acetylcysteine/fluid prep, selection of the safest possible type and volume of radiocontrast medium, and avoidance of nephrotoxic medications immediately before the patient’s exposure to contrast medium.

In multiple randomized clinical trials, the efficacy of IV hydration in reducing the risk for CIN has been examined. Most notably, the REMEDIAL trial¹² demonstrated that IV hydration with sodium bicarbonate was superior to 0.9% hydration with normal saline. However, the largest trial to date did not show any benefit in using sodium bicarbonate, compared with normal saline.¹³ There is no consensus regarding the optimal hydration solution or timing, rate, or total volume of fluid administered, although the current literature does show that IV hydration in some form appears to decrease the risk for CIN.¹¹

The recently released Kidney Disease Improving Global Outcomes (K/DIGO) Clinical Practice Guidelines for Acute Kidney Injury¹⁴ recommend IV volume expansion with normal saline or sodium bicarbonate solution. No particular regimen is recommended.

Acetylcysteine is an antioxidant with vasodilatory properties. A number of clinical trials and meta-analyses have been conducted to examine its efficacy. For instance, Kelly et al¹⁵ have suggested the benefit of acetylcysteine in the prevention of CIN, but several studies included in their meta-analysis were criticized for being of low quality. While the findings among these studies vary, none of the research teams reported any negative outcomes from the use of acetylcysteine. Although there is no definitive proof of its benefit, acetylcysteine is well tolerated, economical, and easily accessible; the general consensus is to use it.¹¹ The K/DIGO Clinical Practice Guidelines for Acute Kidney Injury¹⁴ recommend using acetylcysteine in conjunction with isotonic solution in patients at increased risk for acute kidney injury.¹⁵

Other interventions include careful consideration of the type of radiocontrast agent to be used. Use of a low-osmolality agent such as iohexol (Omnipaque™ 350) or an iso-osmolar agent such as iodixanol (Visipaque™ 320) incurs much lower risk than do older, higher-osmolarity agents.¹⁶ In addition, although there are no scientific data to support this, withholding all potentially nephrotoxic medications (eg, ACE inhibitors, ARBs, NSAIDs, aminoglycosides, high-dose loop diuretics) prior to exposure to contrast medium is a prudent measure to reduce a patient’s risk profile.¹⁰

In summary, there are considerable conflicting data from multiple clinical studies regarding the use of acetylcysteine or IV hydration to minimize the risk for CIN. In fact, new guidelines are due to be published soon that may take a more definitive stand. Nevertheless, categorization as “voodoo” medicine seems inappropriate when an intervention appears to offer positive impact on patient care.
Kimberley Brinkman, MS, CNN, GNP-BC, Nephrology, Hypertension, and

Internal Medicine, Lawrence, MA

REFERENCES

1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q: Is there any science behind the use of acetylcysteine/fluid prep for cardiac catheterizations, or is that just “voodoo” medicine?

Contrast-induced nephropathy (CIN) is the third most common cause of hospital-acquired acute kidney injury. In recent years, the use of iodinated radiocontrast medium has increased significantly, due to increased use of both percutaneous coronary interventions and CT scanning. The radiocontrast medium causes vasoconstriction, which leads to a reduction in renal blood flow, with a resulting decrease in GFR. Preexisting impaired kidney function results in increased risk due to slower clearance of the contrast materials, and the resulting prolonged exposure increases the risk for further renal injury.¹⁰

A GFR below 60 mL/min/1.73m², volume depletion, and diabetes all increase the risk for CIN. Among patients who experience an acute kidney injury due to contrast medium, the risk for adverse outcomes increases, including early or late cardiovascular events, prolonged hospitalizations, and death. As no FDA-approved treatment yet exists for CIN, the best medicine is to try to prevent it.¹¹

Several interventions can reduce the patient’s risk for CIN. These include IV hydration, acetylcysteine/fluid prep, selection of the safest possible type and volume of radiocontrast medium, and avoidance of nephrotoxic medications immediately before the patient’s exposure to contrast medium.

In multiple randomized clinical trials, the efficacy of IV hydration in reducing the risk for CIN has been examined. Most notably, the REMEDIAL trial¹² demonstrated that IV hydration with sodium bicarbonate was superior to 0.9% hydration with normal saline. However, the largest trial to date did not show any benefit in using sodium bicarbonate, compared with normal saline.¹³ There is no consensus regarding the optimal hydration solution or timing, rate, or total volume of fluid administered, although the current literature does show that IV hydration in some form appears to decrease the risk for CIN.¹¹

The recently released Kidney Disease Improving Global Outcomes (K/DIGO) Clinical Practice Guidelines for Acute Kidney Injury¹⁴ recommend IV volume expansion with normal saline or sodium bicarbonate solution. No particular regimen is recommended.

Acetylcysteine is an antioxidant with vasodilatory properties. A number of clinical trials and meta-analyses have been conducted to examine its efficacy. For instance, Kelly et al¹⁵ have suggested the benefit of acetylcysteine in the prevention of CIN, but several studies included in their meta-analysis were criticized for being of low quality. While the findings among these studies vary, none of the research teams reported any negative outcomes from the use of acetylcysteine. Although there is no definitive proof of its benefit, acetylcysteine is well tolerated, economical, and easily accessible; the general consensus is to use it.¹¹ The K/DIGO Clinical Practice Guidelines for Acute Kidney Injury¹⁴ recommend using acetylcysteine in conjunction with isotonic solution in patients at increased risk for acute kidney injury.¹⁵

Other interventions include careful consideration of the type of radiocontrast agent to be used. Use of a low-osmolality agent such as iohexol (Omnipaque™ 350) or an iso-osmolar agent such as iodixanol (Visipaque™ 320) incurs much lower risk than do older, higher-osmolarity agents.¹⁶ In addition, although there are no scientific data to support this, withholding all potentially nephrotoxic medications (eg, ACE inhibitors, ARBs, NSAIDs, aminoglycosides, high-dose loop diuretics) prior to exposure to contrast medium is a prudent measure to reduce a patient’s risk profile.¹⁰

In summary, there are considerable conflicting data from multiple clinical studies regarding the use of acetylcysteine or IV hydration to minimize the risk for CIN. In fact, new guidelines are due to be published soon that may take a more definitive stand. Nevertheless, categorization as “voodoo” medicine seems inappropriate when an intervention appears to offer positive impact on patient care.
Kimberley Brinkman, MS, CNN, GNP-BC, Nephrology, Hypertension, and

Internal Medicine, Lawrence, MA

REFERENCES

1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q: Is there any science behind the use of acetylcysteine/fluid prep for cardiac catheterizations, or is that just “voodoo” medicine?

Contrast-induced nephropathy (CIN) is the third most common cause of hospital-acquired acute kidney injury. In recent years, the use of iodinated radiocontrast medium has increased significantly, due to increased use of both percutaneous coronary interventions and CT scanning. The radiocontrast medium causes vasoconstriction, which leads to a reduction in renal blood flow, with a resulting decrease in GFR. Preexisting impaired kidney function results in increased risk due to slower clearance of the contrast materials, and the resulting prolonged exposure increases the risk for further renal injury.¹⁰

A GFR below 60 mL/min/1.73m², volume depletion, and diabetes all increase the risk for CIN. Among patients who experience an acute kidney injury due to contrast medium, the risk for adverse outcomes increases, including early or late cardiovascular events, prolonged hospitalizations, and death. As no FDA-approved treatment yet exists for CIN, the best medicine is to try to prevent it.¹¹

Several interventions can reduce the patient’s risk for CIN. These include IV hydration, acetylcysteine/fluid prep, selection of the safest possible type and volume of radiocontrast medium, and avoidance of nephrotoxic medications immediately before the patient’s exposure to contrast medium.

In multiple randomized clinical trials, the efficacy of IV hydration in reducing the risk for CIN has been examined. Most notably, the REMEDIAL trial¹² demonstrated that IV hydration with sodium bicarbonate was superior to 0.9% hydration with normal saline. However, the largest trial to date did not show any benefit in using sodium bicarbonate, compared with normal saline.¹³ There is no consensus regarding the optimal hydration solution or timing, rate, or total volume of fluid administered, although the current literature does show that IV hydration in some form appears to decrease the risk for CIN.¹¹

The recently released Kidney Disease Improving Global Outcomes (K/DIGO) Clinical Practice Guidelines for Acute Kidney Injury¹⁴ recommend IV volume expansion with normal saline or sodium bicarbonate solution. No particular regimen is recommended.

Acetylcysteine is an antioxidant with vasodilatory properties. A number of clinical trials and meta-analyses have been conducted to examine its efficacy. For instance, Kelly et al¹⁵ have suggested the benefit of acetylcysteine in the prevention of CIN, but several studies included in their meta-analysis were criticized for being of low quality. While the findings among these studies vary, none of the research teams reported any negative outcomes from the use of acetylcysteine. Although there is no definitive proof of its benefit, acetylcysteine is well tolerated, economical, and easily accessible; the general consensus is to use it.¹¹ The K/DIGO Clinical Practice Guidelines for Acute Kidney Injury¹⁴ recommend using acetylcysteine in conjunction with isotonic solution in patients at increased risk for acute kidney injury.¹⁵

Other interventions include careful consideration of the type of radiocontrast agent to be used. Use of a low-osmolality agent such as iohexol (Omnipaque™ 350) or an iso-osmolar agent such as iodixanol (Visipaque™ 320) incurs much lower risk than do older, higher-osmolarity agents.¹⁶ In addition, although there are no scientific data to support this, withholding all potentially nephrotoxic medications (eg, ACE inhibitors, ARBs, NSAIDs, aminoglycosides, high-dose loop diuretics) prior to exposure to contrast medium is a prudent measure to reduce a patient’s risk profile.¹⁰

In summary, there are considerable conflicting data from multiple clinical studies regarding the use of acetylcysteine or IV hydration to minimize the risk for CIN. In fact, new guidelines are due to be published soon that may take a more definitive stand. Nevertheless, categorization as “voodoo” medicine seems inappropriate when an intervention appears to offer positive impact on patient care.
Kimberley Brinkman, MS, CNN, GNP-BC, Nephrology, Hypertension, and

Internal Medicine, Lawrence, MA

REFERENCES

1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q: I know that I have to tell my patients to be careful with dietary potassium when they are taking spironolactone and ACE inhibitors or angiotensin II receptor blockers (ARBs). However, what foods are bad? What is an acceptable K+ level for patients with chronic kidney disease (CKD)? 

Potassium (K) is a mineral that aids in the regulation of osmotic pressure and acid–base balance. It is essential for normal excitability of muscle tissue, in particular the cardiac muscle, and it plays a role in the conduction of nerve impulses. A safe serum potassium level for a patient with CKD is 4.0 to 5.0 mmol/L. A serum level between 5.0 and 5.5 mmol/L is considered a caution zone, requiring potassium restriction and laboratory monitoring¹ (note: values and ranges vary according to lab). Prescription and OTC medications, herbs, herbals, and dietary intake affect serum potassium. 

Medications such as ACE inhibitors and ARBs can cause hyperkalemia by blocking aldosterone production. The Kidney Disease Outcomes Quality Initiative (K/DOQI)² defines hyperkalemia resulting from ACE inhibitor/ARB use as an increase of serum potassium exceeding 5.0 mmol/L. Therapeutic options to reduce serum potassium include:

•Lowering the dose of the ACE inhibitor or ARB by 50%

•Stopping or reducing other medications that can cause hyperkalemia

•Starting or increasing the dosage of a loop diuretic; or

•Reinforcing dietary restriction.²

Alkali replacement or the use of Kayexalate® (sodium polystyrene sulfonate) may also be used to treat persistent or significant increases in serum potassium.

Diets high in potassium may lead to hyperkalemia in patients with CKD, particularly in patients with a glomerular filtration rate (GFR) below 60 mL/min/1.73 m². K/DOQI² recommends 4 g/d of potassium for patients with CKD Stage 1 or Stage 2 and 2 to 4 g/d for patients with CKD Stage 3 or Stage 4. In the latter group, daily recommendations for potassium intake should be based on the individual patient’s serum potassium level.³

Foods containing more than 200 mg of potassium per serving are considered high-potassium foods. Fruits in this designation include avocado, bananas, cantaloupe, honeydew, kiwi, orange, mango, nectarines, bananas, and prunes. High-potassium vegetables include artichokes, dried beans (including baked beans, refried beans, and black beans), broccoli, carrots, canned mushrooms, potatoes (white or sweet), pumpkin, spinach, and tomatoes. Other foods that are high in potassium include bran products, chocolate, milk, molasses, nuts, seeds, peanut butter, salt substitutes, and yogurt.¹

Leaching is a helpful way to “pull out” some of the potassium in high-potassium vegetables.^4,5 For potatoes, sweet potatoes, or carrots, cut the peeled vegetable into 1/8-inch-thick slices, rinse in warm water, and soak in water 10 times the volume of the vegetables’ volume for a minimum of two hours. Rinse under warm water again, then cook the vegetable in water five times the volume of the vegetables’.
Kristy Washinger, MSN, CRNP, Nephrology Associates of Central Pennsylvania, Camp Hill, PA

REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q: I know that I have to tell my patients to be careful with dietary potassium when they are taking spironolactone and ACE inhibitors or angiotensin II receptor blockers (ARBs). However, what foods are bad? What is an acceptable K+ level for patients with chronic kidney disease (CKD)? 

Potassium (K) is a mineral that aids in the regulation of osmotic pressure and acid–base balance. It is essential for normal excitability of muscle tissue, in particular the cardiac muscle, and it plays a role in the conduction of nerve impulses. A safe serum potassium level for a patient with CKD is 4.0 to 5.0 mmol/L. A serum level between 5.0 and 5.5 mmol/L is considered a caution zone, requiring potassium restriction and laboratory monitoring¹ (note: values and ranges vary according to lab). Prescription and OTC medications, herbs, herbals, and dietary intake affect serum potassium. 

Medications such as ACE inhibitors and ARBs can cause hyperkalemia by blocking aldosterone production. The Kidney Disease Outcomes Quality Initiative (K/DOQI)² defines hyperkalemia resulting from ACE inhibitor/ARB use as an increase of serum potassium exceeding 5.0 mmol/L. Therapeutic options to reduce serum potassium include:

•Lowering the dose of the ACE inhibitor or ARB by 50%

•Stopping or reducing other medications that can cause hyperkalemia

•Starting or increasing the dosage of a loop diuretic; or

•Reinforcing dietary restriction.²

Alkali replacement or the use of Kayexalate® (sodium polystyrene sulfonate) may also be used to treat persistent or significant increases in serum potassium.

Diets high in potassium may lead to hyperkalemia in patients with CKD, particularly in patients with a glomerular filtration rate (GFR) below 60 mL/min/1.73 m². K/DOQI² recommends 4 g/d of potassium for patients with CKD Stage 1 or Stage 2 and 2 to 4 g/d for patients with CKD Stage 3 or Stage 4. In the latter group, daily recommendations for potassium intake should be based on the individual patient’s serum potassium level.³

Foods containing more than 200 mg of potassium per serving are considered high-potassium foods. Fruits in this designation include avocado, bananas, cantaloupe, honeydew, kiwi, orange, mango, nectarines, bananas, and prunes. High-potassium vegetables include artichokes, dried beans (including baked beans, refried beans, and black beans), broccoli, carrots, canned mushrooms, potatoes (white or sweet), pumpkin, spinach, and tomatoes. Other foods that are high in potassium include bran products, chocolate, milk, molasses, nuts, seeds, peanut butter, salt substitutes, and yogurt.¹

Leaching is a helpful way to “pull out” some of the potassium in high-potassium vegetables.^4,5 For potatoes, sweet potatoes, or carrots, cut the peeled vegetable into 1/8-inch-thick slices, rinse in warm water, and soak in water 10 times the volume of the vegetables’ volume for a minimum of two hours. Rinse under warm water again, then cook the vegetable in water five times the volume of the vegetables’.
Kristy Washinger, MSN, CRNP, Nephrology Associates of Central Pennsylvania, Camp Hill, PA

REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q: I know that I have to tell my patients to be careful with dietary potassium when they are taking spironolactone and ACE inhibitors or angiotensin II receptor blockers (ARBs). However, what foods are bad? What is an acceptable K+ level for patients with chronic kidney disease (CKD)? 

Potassium (K) is a mineral that aids in the regulation of osmotic pressure and acid–base balance. It is essential for normal excitability of muscle tissue, in particular the cardiac muscle, and it plays a role in the conduction of nerve impulses. A safe serum potassium level for a patient with CKD is 4.0 to 5.0 mmol/L. A serum level between 5.0 and 5.5 mmol/L is considered a caution zone, requiring potassium restriction and laboratory monitoring¹ (note: values and ranges vary according to lab). Prescription and OTC medications, herbs, herbals, and dietary intake affect serum potassium. 

Medications such as ACE inhibitors and ARBs can cause hyperkalemia by blocking aldosterone production. The Kidney Disease Outcomes Quality Initiative (K/DOQI)² defines hyperkalemia resulting from ACE inhibitor/ARB use as an increase of serum potassium exceeding 5.0 mmol/L. Therapeutic options to reduce serum potassium include:

•Lowering the dose of the ACE inhibitor or ARB by 50%

•Stopping or reducing other medications that can cause hyperkalemia

•Starting or increasing the dosage of a loop diuretic; or

•Reinforcing dietary restriction.²

Alkali replacement or the use of Kayexalate® (sodium polystyrene sulfonate) may also be used to treat persistent or significant increases in serum potassium.

Diets high in potassium may lead to hyperkalemia in patients with CKD, particularly in patients with a glomerular filtration rate (GFR) below 60 mL/min/1.73 m². K/DOQI² recommends 4 g/d of potassium for patients with CKD Stage 1 or Stage 2 and 2 to 4 g/d for patients with CKD Stage 3 or Stage 4. In the latter group, daily recommendations for potassium intake should be based on the individual patient’s serum potassium level.³

Foods containing more than 200 mg of potassium per serving are considered high-potassium foods. Fruits in this designation include avocado, bananas, cantaloupe, honeydew, kiwi, orange, mango, nectarines, bananas, and prunes. High-potassium vegetables include artichokes, dried beans (including baked beans, refried beans, and black beans), broccoli, carrots, canned mushrooms, potatoes (white or sweet), pumpkin, spinach, and tomatoes. Other foods that are high in potassium include bran products, chocolate, milk, molasses, nuts, seeds, peanut butter, salt substitutes, and yogurt.¹

Leaching is a helpful way to “pull out” some of the potassium in high-potassium vegetables.^4,5 For potatoes, sweet potatoes, or carrots, cut the peeled vegetable into 1/8-inch-thick slices, rinse in warm water, and soak in water 10 times the volume of the vegetables’ volume for a minimum of two hours. Rinse under warm water again, then cook the vegetable in water five times the volume of the vegetables’.
Kristy Washinger, MSN, CRNP, Nephrology Associates of Central Pennsylvania, Camp Hill, PA

REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q: I have many diabetic patients who do not monitor their blood sugars or watch their diet. I try to encourage them to manage their diabetes better to decrease their risk for kidney disease, blindness, or amputation. But they want to know what are their chances of ending up on dialysis. What percentage of patients develop kidney failure? What can I say to encourage my patients to take better care of themselves? 

Diabetes is an epidemic in the United States and worldwide. It is the leading cause of chronic kidney disease and kidney failure.¹ Diabetes is the primary diagnosis for about 44% of US patients who start dialysis, and hypertension for about 28%.²

Chronic kidney disease (CKD) can be viewed as a spectrum, ranging from mild (glomerular filtration rate [GFR] ≥ 60 mL/min/1.73 m²) to severe (GFR < 15 mL/min/1.73 m², also referred to as end-stage renal disease [ESRD]).

A diabetic patient’s likelihood of developing diabetic nephropathy (DN) varies by race and geographic location. For patients with type 2 diabetes (T2DM), the rate is 5% to 10% for white patients and 10% to 20% for African-Americans.³ Hispanic patients develop DN at 1.5 times the rate among non-Hispanic whites.¹ In the Pima Indians, who live primarily in Arizona, the incidence of DN approaches 60%. For patients with type 1 diabetes, the incidence of DN is 30% to 40%.¹

While not all patients progress to ESRD, they are at increased risk for renal and cardiovascular complications, compared with nondiabetic patients.¹ In general, about one in three patients with diabetes will develop significant nephropathy during the five to 10 years following diagnosis. For many years, microalbuminuria has been considered a predictor of renal disease progression.⁴

Previously, it was thought that patients with T2DM were more likely to die of cardiovascular complications than to progress to ESRD and require renal replacement therapy (RRT). However, researchers recently showed that patients with T2DM, DN, and proteinuria were more likely to progress to ESRD than to die of other complications.⁵

Given the alarming increase in the incidence of diabetes and diabetic kidney disease, a tool to predict the likelihood of an individual patient’s risk for kidney failure would be extremely helpful. As there are no widely accepted predictive instruments for CKD progression, providers must make ad hoc decisions about patients. This practice can result in treatment delays for patients whose disease does progress or unnecessary treatments for patients unlikely to experience kidney failure.⁶

In 2011, Tangri et al⁷ published a predictive model for patients with stages 3 to 5 CKD. The model relies on demographic data and clinical laboratory markers of CKD severity to accurately predict risk for future kidney failure. The study is available at http://jama.ama-assn.org/content/305/15/1553.long,⁷ and a smartphone app can be accessed at www.qxmd.com/Kidney-Failure-Risk-Equation.

To improve patient compliance, however, I would suggest the following steps:

• Ask yourself, “Does my patient perceive there is a problem?” Assess the patient’s readiness to modify behavior.⁸
• Target no more than one behavior change at each visit.
• Find at least one reason to praise the patient at each visit (eg, remembering to bring his/her glucose log, keeping the scheduled appointment, initiating an exercise program, cutting down on cigarettes).
• Use diabetes educators to reinforce teaching.
• Suggest that your patient join the ADA. The more interested and informed patients become about this chronic illness, the more likely they are to become active participants in their own long-term care. 

Wanda Y. Willis, MSN, FNP-C, CNN, Renal nurse practitioner
Washington Nephrology Associates, LLC
Takoma Park, Maryland

See next page for references... 

REFERENCES

1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.

2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.

3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.

4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.

5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.

6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.

7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.

8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.

9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.

10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.

11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.

12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.

13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.

Q: I have many diabetic patients who do not monitor their blood sugars or watch their diet. I try to encourage them to manage their diabetes better to decrease their risk for kidney disease, blindness, or amputation. But they want to know what are their chances of ending up on dialysis. What percentage of patients develop kidney failure? What can I say to encourage my patients to take better care of themselves? 

Diabetes is an epidemic in the United States and worldwide. It is the leading cause of chronic kidney disease and kidney failure.¹ Diabetes is the primary diagnosis for about 44% of US patients who start dialysis, and hypertension for about 28%.²

Chronic kidney disease (CKD) can be viewed as a spectrum, ranging from mild (glomerular filtration rate [GFR] ≥ 60 mL/min/1.73 m²) to severe (GFR < 15 mL/min/1.73 m², also referred to as end-stage renal disease [ESRD]).

A diabetic patient’s likelihood of developing diabetic nephropathy (DN) varies by race and geographic location. For patients with type 2 diabetes (T2DM), the rate is 5% to 10% for white patients and 10% to 20% for African-Americans.³ Hispanic patients develop DN at 1.5 times the rate among non-Hispanic whites.¹ In the Pima Indians, who live primarily in Arizona, the incidence of DN approaches 60%. For patients with type 1 diabetes, the incidence of DN is 30% to 40%.¹

While not all patients progress to ESRD, they are at increased risk for renal and cardiovascular complications, compared with nondiabetic patients.¹ In general, about one in three patients with diabetes will develop significant nephropathy during the five to 10 years following diagnosis. For many years, microalbuminuria has been considered a predictor of renal disease progression.⁴

Previously, it was thought that patients with T2DM were more likely to die of cardiovascular complications than to progress to ESRD and require renal replacement therapy (RRT). However, researchers recently showed that patients with T2DM, DN, and proteinuria were more likely to progress to ESRD than to die of other complications.⁵

Given the alarming increase in the incidence of diabetes and diabetic kidney disease, a tool to predict the likelihood of an individual patient’s risk for kidney failure would be extremely helpful. As there are no widely accepted predictive instruments for CKD progression, providers must make ad hoc decisions about patients. This practice can result in treatment delays for patients whose disease does progress or unnecessary treatments for patients unlikely to experience kidney failure.⁶

In 2011, Tangri et al⁷ published a predictive model for patients with stages 3 to 5 CKD. The model relies on demographic data and clinical laboratory markers of CKD severity to accurately predict risk for future kidney failure. The study is available at http://jama.ama-assn.org/content/305/15/1553.long,⁷ and a smartphone app can be accessed at www.qxmd.com/Kidney-Failure-Risk-Equation.

To improve patient compliance, however, I would suggest the following steps:

• Ask yourself, “Does my patient perceive there is a problem?” Assess the patient’s readiness to modify behavior.⁸
• Target no more than one behavior change at each visit.
• Find at least one reason to praise the patient at each visit (eg, remembering to bring his/her glucose log, keeping the scheduled appointment, initiating an exercise program, cutting down on cigarettes).
• Use diabetes educators to reinforce teaching.
• Suggest that your patient join the ADA. The more interested and informed patients become about this chronic illness, the more likely they are to become active participants in their own long-term care. 

Wanda Y. Willis, MSN, FNP-C, CNN, Renal nurse practitioner
Washington Nephrology Associates, LLC
Takoma Park, Maryland

See next page for references... 

REFERENCES

1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.

2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.

3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.

4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.

5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.

6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.

7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.

8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.

9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.

10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.

11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.

12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.

13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.

Q: I have many diabetic patients who do not monitor their blood sugars or watch their diet. I try to encourage them to manage their diabetes better to decrease their risk for kidney disease, blindness, or amputation. But they want to know what are their chances of ending up on dialysis. What percentage of patients develop kidney failure? What can I say to encourage my patients to take better care of themselves? 

Diabetes is an epidemic in the United States and worldwide. It is the leading cause of chronic kidney disease and kidney failure.¹ Diabetes is the primary diagnosis for about 44% of US patients who start dialysis, and hypertension for about 28%.²

Chronic kidney disease (CKD) can be viewed as a spectrum, ranging from mild (glomerular filtration rate [GFR] ≥ 60 mL/min/1.73 m²) to severe (GFR < 15 mL/min/1.73 m², also referred to as end-stage renal disease [ESRD]).

A diabetic patient’s likelihood of developing diabetic nephropathy (DN) varies by race and geographic location. For patients with type 2 diabetes (T2DM), the rate is 5% to 10% for white patients and 10% to 20% for African-Americans.³ Hispanic patients develop DN at 1.5 times the rate among non-Hispanic whites.¹ In the Pima Indians, who live primarily in Arizona, the incidence of DN approaches 60%. For patients with type 1 diabetes, the incidence of DN is 30% to 40%.¹

While not all patients progress to ESRD, they are at increased risk for renal and cardiovascular complications, compared with nondiabetic patients.¹ In general, about one in three patients with diabetes will develop significant nephropathy during the five to 10 years following diagnosis. For many years, microalbuminuria has been considered a predictor of renal disease progression.⁴

Previously, it was thought that patients with T2DM were more likely to die of cardiovascular complications than to progress to ESRD and require renal replacement therapy (RRT). However, researchers recently showed that patients with T2DM, DN, and proteinuria were more likely to progress to ESRD than to die of other complications.⁵

Given the alarming increase in the incidence of diabetes and diabetic kidney disease, a tool to predict the likelihood of an individual patient’s risk for kidney failure would be extremely helpful. As there are no widely accepted predictive instruments for CKD progression, providers must make ad hoc decisions about patients. This practice can result in treatment delays for patients whose disease does progress or unnecessary treatments for patients unlikely to experience kidney failure.⁶

In 2011, Tangri et al⁷ published a predictive model for patients with stages 3 to 5 CKD. The model relies on demographic data and clinical laboratory markers of CKD severity to accurately predict risk for future kidney failure. The study is available at http://jama.ama-assn.org/content/305/15/1553.long,⁷ and a smartphone app can be accessed at www.qxmd.com/Kidney-Failure-Risk-Equation.

To improve patient compliance, however, I would suggest the following steps:

• Ask yourself, “Does my patient perceive there is a problem?” Assess the patient’s readiness to modify behavior.⁸
• Target no more than one behavior change at each visit.
• Find at least one reason to praise the patient at each visit (eg, remembering to bring his/her glucose log, keeping the scheduled appointment, initiating an exercise program, cutting down on cigarettes).
• Use diabetes educators to reinforce teaching.
• Suggest that your patient join the ADA. The more interested and informed patients become about this chronic illness, the more likely they are to become active participants in their own long-term care. 

Wanda Y. Willis, MSN, FNP-C, CNN, Renal nurse practitioner
Washington Nephrology Associates, LLC
Takoma Park, Maryland

See next page for references... 

REFERENCES

1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.

2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.

3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.

4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.

5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.

6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.

7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.

8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.

9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.

10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.

11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.

12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.

13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.

Q: I have a dialysis patient whose cholesterol numbers were getting quite high. I gave him a prescription for a lipid-lowering medication. He brought the prescription back, saying the nephrology AP told him it would make no difference since he was a dialysis patient. Is this true? 

This is an excellent question that has been researched and debated over the past 10 years. Cardiovascular disease is the leading cause of death in patients with CKD and those in the dialysis population. So intuitively, it makes sense in these patients to control cholesterol—one of the main risk factors for cardiovascular disease. However, the research that has been done to date contradicts that hypothesis in dialysis patients.⁹

With a 2002 observational study, Iseki et al¹⁰ became the first researchers to document that cholesterol levels are inversely related to mortality in patients undergoing dialysis. However, this study team did not adjust for inflammation or infection—which, in addition to malnutrition, reduce HDL and LDL levels (and increase mortality).¹⁰

The goal of the Deutsche Diabetes and Dialysis (4D) trial,¹¹ funded by a pharmaceutical company and involving 1,255 subjects, was to demonstrate the benefits of atorvastatin use in diabetic patients on dialysis. Although the agent was shown to improve patients’ lipid parameters, no statistically significant effect was found on the primary endpoints: all-cause mortality and cardiovascular and cerebrovascular events. In fact, the incidence of fatal stroke was significantly higher in the atorvastatin-treated patients, compared with those taking placebo.¹¹

In the Evaluation of the Use of Rosuvastatin in Subjects on Regular Hemodialysis (AURORA) study,¹² in which 2,776 patients were enrolled, the primary endpoint was time to major cardiovascular events (including fatal and nonfatal MI and stroke). No statistically significant changes were reported in mortality or primary or secondary endpoints in either treatment arm. However, the AURORA study did demonstrate an increased risk for fatal hemorrhagic stroke in the treatment arm.¹²

Most recently, in the seven-year-long Study of Heart and Renal Protection (SHARP),¹³ researchers investigated the benefits of cholesterol-lowering therapy, enrolling 9,270 patients with CKD and 3,023 patients undergoing dialysis. In the treatment arm of the CKD group (ie, those receiving simvastatin plus ezetimibe), a 17% reduction was reported in major atherosclerotic events. In the dialysis patients randomized to receive treatment, however, no significant reduction was found in mortality rates or cardiovascular events, compared with patients taking placebo.¹³

Thus, no cardioprotective benefit has yet been reported for statin use in patients receiving dialysis. In fact, these agents may increase patients’ risk for stroke. They surely increase the pill burden and treatment costs for dialysis patients. As for patients with CKD, a number of studies (including the SHARP study¹³) have demonstrated a benefit in statin use for primary prevention of cardiovascular events.

Susan Busch, MSN, CNP, Cleveland Clinic; Family NP Program
Kent State University, Ohio

For see next page for references... 

REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.

2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.

3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.

4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.

5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.

6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.

7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.

8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.

9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.

10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.

11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.

12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.

13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.

Q: I have a dialysis patient whose cholesterol numbers were getting quite high. I gave him a prescription for a lipid-lowering medication. He brought the prescription back, saying the nephrology AP told him it would make no difference since he was a dialysis patient. Is this true? 

This is an excellent question that has been researched and debated over the past 10 years. Cardiovascular disease is the leading cause of death in patients with CKD and those in the dialysis population. So intuitively, it makes sense in these patients to control cholesterol—one of the main risk factors for cardiovascular disease. However, the research that has been done to date contradicts that hypothesis in dialysis patients.⁹

With a 2002 observational study, Iseki et al¹⁰ became the first researchers to document that cholesterol levels are inversely related to mortality in patients undergoing dialysis. However, this study team did not adjust for inflammation or infection—which, in addition to malnutrition, reduce HDL and LDL levels (and increase mortality).¹⁰

The goal of the Deutsche Diabetes and Dialysis (4D) trial,¹¹ funded by a pharmaceutical company and involving 1,255 subjects, was to demonstrate the benefits of atorvastatin use in diabetic patients on dialysis. Although the agent was shown to improve patients’ lipid parameters, no statistically significant effect was found on the primary endpoints: all-cause mortality and cardiovascular and cerebrovascular events. In fact, the incidence of fatal stroke was significantly higher in the atorvastatin-treated patients, compared with those taking placebo.¹¹

In the Evaluation of the Use of Rosuvastatin in Subjects on Regular Hemodialysis (AURORA) study,¹² in which 2,776 patients were enrolled, the primary endpoint was time to major cardiovascular events (including fatal and nonfatal MI and stroke). No statistically significant changes were reported in mortality or primary or secondary endpoints in either treatment arm. However, the AURORA study did demonstrate an increased risk for fatal hemorrhagic stroke in the treatment arm.¹²

Most recently, in the seven-year-long Study of Heart and Renal Protection (SHARP),¹³ researchers investigated the benefits of cholesterol-lowering therapy, enrolling 9,270 patients with CKD and 3,023 patients undergoing dialysis. In the treatment arm of the CKD group (ie, those receiving simvastatin plus ezetimibe), a 17% reduction was reported in major atherosclerotic events. In the dialysis patients randomized to receive treatment, however, no significant reduction was found in mortality rates or cardiovascular events, compared with patients taking placebo.¹³

Thus, no cardioprotective benefit has yet been reported for statin use in patients receiving dialysis. In fact, these agents may increase patients’ risk for stroke. They surely increase the pill burden and treatment costs for dialysis patients. As for patients with CKD, a number of studies (including the SHARP study¹³) have demonstrated a benefit in statin use for primary prevention of cardiovascular events.

Susan Busch, MSN, CNP, Cleveland Clinic; Family NP Program
Kent State University, Ohio

For see next page for references... 

REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.

2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.

3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.

4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.

5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.

6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.

7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.

8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.

9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.

10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.

11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.

12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.

13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.

Q: I have a dialysis patient whose cholesterol numbers were getting quite high. I gave him a prescription for a lipid-lowering medication. He brought the prescription back, saying the nephrology AP told him it would make no difference since he was a dialysis patient. Is this true? 

This is an excellent question that has been researched and debated over the past 10 years. Cardiovascular disease is the leading cause of death in patients with CKD and those in the dialysis population. So intuitively, it makes sense in these patients to control cholesterol—one of the main risk factors for cardiovascular disease. However, the research that has been done to date contradicts that hypothesis in dialysis patients.⁹

With a 2002 observational study, Iseki et al¹⁰ became the first researchers to document that cholesterol levels are inversely related to mortality in patients undergoing dialysis. However, this study team did not adjust for inflammation or infection—which, in addition to malnutrition, reduce HDL and LDL levels (and increase mortality).¹⁰

The goal of the Deutsche Diabetes and Dialysis (4D) trial,¹¹ funded by a pharmaceutical company and involving 1,255 subjects, was to demonstrate the benefits of atorvastatin use in diabetic patients on dialysis. Although the agent was shown to improve patients’ lipid parameters, no statistically significant effect was found on the primary endpoints: all-cause mortality and cardiovascular and cerebrovascular events. In fact, the incidence of fatal stroke was significantly higher in the atorvastatin-treated patients, compared with those taking placebo.¹¹

In the Evaluation of the Use of Rosuvastatin in Subjects on Regular Hemodialysis (AURORA) study,¹² in which 2,776 patients were enrolled, the primary endpoint was time to major cardiovascular events (including fatal and nonfatal MI and stroke). No statistically significant changes were reported in mortality or primary or secondary endpoints in either treatment arm. However, the AURORA study did demonstrate an increased risk for fatal hemorrhagic stroke in the treatment arm.¹²

Most recently, in the seven-year-long Study of Heart and Renal Protection (SHARP),¹³ researchers investigated the benefits of cholesterol-lowering therapy, enrolling 9,270 patients with CKD and 3,023 patients undergoing dialysis. In the treatment arm of the CKD group (ie, those receiving simvastatin plus ezetimibe), a 17% reduction was reported in major atherosclerotic events. In the dialysis patients randomized to receive treatment, however, no significant reduction was found in mortality rates or cardiovascular events, compared with patients taking placebo.¹³

Thus, no cardioprotective benefit has yet been reported for statin use in patients receiving dialysis. In fact, these agents may increase patients’ risk for stroke. They surely increase the pill burden and treatment costs for dialysis patients. As for patients with CKD, a number of studies (including the SHARP study¹³) have demonstrated a benefit in statin use for primary prevention of cardiovascular events.

Susan Busch, MSN, CNP, Cleveland Clinic; Family NP Program
Kent State University, Ohio

For see next page for references... 

REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.

2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.

3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.

4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.

5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.

6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.

7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.

8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.

9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.

10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.

11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.

12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.

13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.

Chronic kidney disease (CKD) is the silent epidemic. It often follows hypertension, diabetes, and obesity. Patients with CKD are not seen exclusively in a nephrology practice. Often, they are not referred to a nephrologist until their glomerular filtration rate (GFR) is less than 60 mL/min/1.73m².

CKD affects 11.5% of the US population ages 20 and older,¹ which translates to some 23 million people. According to the National Institute of Diabetes and Digestive and Kidney Diseases, more than 382,000 people were receiving dialysis in 2008,¹ and this number is expected to more than double by 2020. It is essential for the practitioner in any specialty to be aware of their patients’ renal status and any adjustments that may entail.

Q: In diabetic patients with incipient nephropathy (microalbuminuria, but GFR > 90 mL/min, more specifically), do evidence-based recommendations exist that suggest renal dosing parameters be followed in order to protect against progressive nephropathy? This, of course, would constitute a secondary prevention strategy, since (as most clinicians know) glycemic and blood pressure control are the most important primary steps toward prevention.

A patient with microalbuminuria and preserved renal function, according to the estimated GFR (eGFR), would be classified as having CKD stage 2. Currently, no medication dosing guidelines are available for patients at this stage of CKD; however, as providers, we should be aware that the presence of microalbuminuria has important clinical implications.

Microalbuminuria is associated with increased risk for cardiovascular disease and progression of CKD.⁴ Accordingly, medication selection should be targeted at avoiding renal insult, limiting progression of nephropathy through the use of ACE inhibitors or angiotensin receptor blockers (ARBs), and promptly addressing and modifying the risk factors for cardiovascular disease.

Blood pressure (BP), glycemic control, and lipids should all be managed aggressively. The JNC7 (Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure)⁵ and the K/DOQI (Kidney Disease Outcomes Quality Initiative) guidelines⁶ recommend a target BP below 130/80 mm Hg for CKD patients with proteinuria of less than 1 g/24 h; and below 120/80 mm Hg for patients with proteinuria greater than 1 g/24 h. Unpublished guidelines from “Kidney Disease: Improving Global Outcomes” (see www.kdigo.org) are encouraging practitioners to give nonhypertensive diabetic patients with proteinuria an ACE inhibitor or an ARB.

Nephrotoxins, such as NSAIDs and aminoglycosides, should be avoided. Contrast dye and nephrotoxic chemotherapeutic agents should be used with caution and only if clinically justified. If they are used, renal precautions should be taken, including preprocedure and postprocedure hydration.⁷

Whenever possible, an ACE inhibitor or an ARB should be initiated early, as the greatest benefit in slowing the progression of nephrosclerosis is realized when these medications are initiated before irreversible scarring has occurred.^5,6 Initiating one of these agents is preferable while the serum creatinine level is below 1.2 mg/dL.⁸ Creatinine and potassium should be checked within two weeks of initiating or increasing ACE inhibitor or ARB dosing.

As CKD progresses, patients are at risk for acidemia and hyperkalemia. Typically, these concerns are greater in CKD stages 4 to 5 but can be seen as early as CKD stage 3. Metformin should be prescribed with caution in patients with CKD stage 2 and changed to an alternate antihyperglycemic agent for men whose serum creatinine exceeds 1.5 mg/dL and for women with serum creatinine greater than 1.4 mg/dL.⁸

Clinically, it is recommended that metformin be avoided in patients whose eGFR is below 60 to 70 mL/min.⁹ The eGFR is a better indicator of CKD stage than serum creatinine; using serum creatinine alone to calculate the CKD stage could lead to a very wrong result. For example, a thin, elderly white woman can have a very low eGFR but a serum creatinine of 1.4 mg/dL or less (which is essentially normal).

Diabetic patients in particular are susceptible to hyperkalemia, so spironolactone, potassium, and sulfamethoxazole should be prescribed with caution. Potassium levels should be monitored in patients receiving b-blockers, ACE inhibitors, or ARBs.

Renal medication dosing guidelines, as noted in the FDA information in each drug’s package insert, generally offer recommendations for adjustment in CKD stage 4 or 5, which correspond to an eGFR of < 30 mL/min or < 15 mL/min, respectively. FDA renal dosing guidelines are often based on serum creatinine, but eGFR can vary widely for a particular serum creatinine level, depending upon patient variables such as age, weight, race, and gender (as in the example above).

In summary, although no specific published guidelines exist for patients with CKD stage 2, the presence of microalbuminuria is an important clinical indicator that should inform the provider’s approach to patient management.
Alexis Chettiar, ACNP, East Bay Nephrology Medical Group, Oakland, CA

References
1. National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC). http://kidney.niddk.nih.gov. Accessed November 18, 2011.

2. Thorp ML, Morris CD, Bagby SP. A crossover study of gabapentin in treatment of restless legs syndrome among hemodialysis patients. Am J Kidney Dis. 2001;38(1):104-108.

3. Blommel ML, Blommel AL. Pregabalin: an antiepileptic agent useful for neuropathic pain. Am J Health-System Pharm. 2007;64(14):1475-1482.

4. Gerstein HC, Mann JF, Yi Q, et al. Albuminuria and risk of cardiovascular events, death, and heart failure in diabetic and nondiabetic individuals. JAMA. 2001;286(4):421-426.

5. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289(19):2560-2572.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004; 43(5 suppl 1):S1-290.

7. National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI™). www.kidney.org/professionals/kdoqi. Accessed November 18, 2011.

8. Post TW, Rose BD. Overview of management of chronic kidney disease in adults. www.uptodate.com/contents/overview-of-the-management-of-chronic-kidney-disease-in-adults/contributors. Accessed November 18, 2011.

9. DeFronzo RA. Pharmacologic therapy for type 2 diabetes mellitus. Ann Intern Med. 1999;131(4):281-303.

Chronic kidney disease (CKD) is the silent epidemic. It often follows hypertension, diabetes, and obesity. Patients with CKD are not seen exclusively in a nephrology practice. Often, they are not referred to a nephrologist until their glomerular filtration rate (GFR) is less than 60 mL/min/1.73m².

CKD affects 11.5% of the US population ages 20 and older,¹ which translates to some 23 million people. According to the National Institute of Diabetes and Digestive and Kidney Diseases, more than 382,000 people were receiving dialysis in 2008,¹ and this number is expected to more than double by 2020. It is essential for the practitioner in any specialty to be aware of their patients’ renal status and any adjustments that may entail.

Q: In diabetic patients with incipient nephropathy (microalbuminuria, but GFR > 90 mL/min, more specifically), do evidence-based recommendations exist that suggest renal dosing parameters be followed in order to protect against progressive nephropathy? This, of course, would constitute a secondary prevention strategy, since (as most clinicians know) glycemic and blood pressure control are the most important primary steps toward prevention.

A patient with microalbuminuria and preserved renal function, according to the estimated GFR (eGFR), would be classified as having CKD stage 2. Currently, no medication dosing guidelines are available for patients at this stage of CKD; however, as providers, we should be aware that the presence of microalbuminuria has important clinical implications.

Microalbuminuria is associated with increased risk for cardiovascular disease and progression of CKD.⁴ Accordingly, medication selection should be targeted at avoiding renal insult, limiting progression of nephropathy through the use of ACE inhibitors or angiotensin receptor blockers (ARBs), and promptly addressing and modifying the risk factors for cardiovascular disease.

Blood pressure (BP), glycemic control, and lipids should all be managed aggressively. The JNC7 (Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure)⁵ and the K/DOQI (Kidney Disease Outcomes Quality Initiative) guidelines⁶ recommend a target BP below 130/80 mm Hg for CKD patients with proteinuria of less than 1 g/24 h; and below 120/80 mm Hg for patients with proteinuria greater than 1 g/24 h. Unpublished guidelines from “Kidney Disease: Improving Global Outcomes” (see www.kdigo.org) are encouraging practitioners to give nonhypertensive diabetic patients with proteinuria an ACE inhibitor or an ARB.

Nephrotoxins, such as NSAIDs and aminoglycosides, should be avoided. Contrast dye and nephrotoxic chemotherapeutic agents should be used with caution and only if clinically justified. If they are used, renal precautions should be taken, including preprocedure and postprocedure hydration.⁷

Whenever possible, an ACE inhibitor or an ARB should be initiated early, as the greatest benefit in slowing the progression of nephrosclerosis is realized when these medications are initiated before irreversible scarring has occurred.^5,6 Initiating one of these agents is preferable while the serum creatinine level is below 1.2 mg/dL.⁸ Creatinine and potassium should be checked within two weeks of initiating or increasing ACE inhibitor or ARB dosing.

As CKD progresses, patients are at risk for acidemia and hyperkalemia. Typically, these concerns are greater in CKD stages 4 to 5 but can be seen as early as CKD stage 3. Metformin should be prescribed with caution in patients with CKD stage 2 and changed to an alternate antihyperglycemic agent for men whose serum creatinine exceeds 1.5 mg/dL and for women with serum creatinine greater than 1.4 mg/dL.⁸

Clinically, it is recommended that metformin be avoided in patients whose eGFR is below 60 to 70 mL/min.⁹ The eGFR is a better indicator of CKD stage than serum creatinine; using serum creatinine alone to calculate the CKD stage could lead to a very wrong result. For example, a thin, elderly white woman can have a very low eGFR but a serum creatinine of 1.4 mg/dL or less (which is essentially normal).

Diabetic patients in particular are susceptible to hyperkalemia, so spironolactone, potassium, and sulfamethoxazole should be prescribed with caution. Potassium levels should be monitored in patients receiving b-blockers, ACE inhibitors, or ARBs.

Renal medication dosing guidelines, as noted in the FDA information in each drug’s package insert, generally offer recommendations for adjustment in CKD stage 4 or 5, which correspond to an eGFR of < 30 mL/min or < 15 mL/min, respectively. FDA renal dosing guidelines are often based on serum creatinine, but eGFR can vary widely for a particular serum creatinine level, depending upon patient variables such as age, weight, race, and gender (as in the example above).

In summary, although no specific published guidelines exist for patients with CKD stage 2, the presence of microalbuminuria is an important clinical indicator that should inform the provider’s approach to patient management.
Alexis Chettiar, ACNP, East Bay Nephrology Medical Group, Oakland, CA

References
1. National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC). http://kidney.niddk.nih.gov. Accessed November 18, 2011.

2. Thorp ML, Morris CD, Bagby SP. A crossover study of gabapentin in treatment of restless legs syndrome among hemodialysis patients. Am J Kidney Dis. 2001;38(1):104-108.

3. Blommel ML, Blommel AL. Pregabalin: an antiepileptic agent useful for neuropathic pain. Am J Health-System Pharm. 2007;64(14):1475-1482.

4. Gerstein HC, Mann JF, Yi Q, et al. Albuminuria and risk of cardiovascular events, death, and heart failure in diabetic and nondiabetic individuals. JAMA. 2001;286(4):421-426.

5. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289(19):2560-2572.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004; 43(5 suppl 1):S1-290.

7. National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI™). www.kidney.org/professionals/kdoqi. Accessed November 18, 2011.

8. Post TW, Rose BD. Overview of management of chronic kidney disease in adults. www.uptodate.com/contents/overview-of-the-management-of-chronic-kidney-disease-in-adults/contributors. Accessed November 18, 2011.

9. DeFronzo RA. Pharmacologic therapy for type 2 diabetes mellitus. Ann Intern Med. 1999;131(4):281-303.

Chronic kidney disease (CKD) is the silent epidemic. It often follows hypertension, diabetes, and obesity. Patients with CKD are not seen exclusively in a nephrology practice. Often, they are not referred to a nephrologist until their glomerular filtration rate (GFR) is less than 60 mL/min/1.73m².

CKD affects 11.5% of the US population ages 20 and older,¹ which translates to some 23 million people. According to the National Institute of Diabetes and Digestive and Kidney Diseases, more than 382,000 people were receiving dialysis in 2008,¹ and this number is expected to more than double by 2020. It is essential for the practitioner in any specialty to be aware of their patients’ renal status and any adjustments that may entail.

Q: In diabetic patients with incipient nephropathy (microalbuminuria, but GFR > 90 mL/min, more specifically), do evidence-based recommendations exist that suggest renal dosing parameters be followed in order to protect against progressive nephropathy? This, of course, would constitute a secondary prevention strategy, since (as most clinicians know) glycemic and blood pressure control are the most important primary steps toward prevention.

A patient with microalbuminuria and preserved renal function, according to the estimated GFR (eGFR), would be classified as having CKD stage 2. Currently, no medication dosing guidelines are available for patients at this stage of CKD; however, as providers, we should be aware that the presence of microalbuminuria has important clinical implications.

Microalbuminuria is associated with increased risk for cardiovascular disease and progression of CKD.⁴ Accordingly, medication selection should be targeted at avoiding renal insult, limiting progression of nephropathy through the use of ACE inhibitors or angiotensin receptor blockers (ARBs), and promptly addressing and modifying the risk factors for cardiovascular disease.

Blood pressure (BP), glycemic control, and lipids should all be managed aggressively. The JNC7 (Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure)⁵ and the K/DOQI (Kidney Disease Outcomes Quality Initiative) guidelines⁶ recommend a target BP below 130/80 mm Hg for CKD patients with proteinuria of less than 1 g/24 h; and below 120/80 mm Hg for patients with proteinuria greater than 1 g/24 h. Unpublished guidelines from “Kidney Disease: Improving Global Outcomes” (see www.kdigo.org) are encouraging practitioners to give nonhypertensive diabetic patients with proteinuria an ACE inhibitor or an ARB.

Nephrotoxins, such as NSAIDs and aminoglycosides, should be avoided. Contrast dye and nephrotoxic chemotherapeutic agents should be used with caution and only if clinically justified. If they are used, renal precautions should be taken, including preprocedure and postprocedure hydration.⁷

Whenever possible, an ACE inhibitor or an ARB should be initiated early, as the greatest benefit in slowing the progression of nephrosclerosis is realized when these medications are initiated before irreversible scarring has occurred.^5,6 Initiating one of these agents is preferable while the serum creatinine level is below 1.2 mg/dL.⁸ Creatinine and potassium should be checked within two weeks of initiating or increasing ACE inhibitor or ARB dosing.

As CKD progresses, patients are at risk for acidemia and hyperkalemia. Typically, these concerns are greater in CKD stages 4 to 5 but can be seen as early as CKD stage 3. Metformin should be prescribed with caution in patients with CKD stage 2 and changed to an alternate antihyperglycemic agent for men whose serum creatinine exceeds 1.5 mg/dL and for women with serum creatinine greater than 1.4 mg/dL.⁸

Clinically, it is recommended that metformin be avoided in patients whose eGFR is below 60 to 70 mL/min.⁹ The eGFR is a better indicator of CKD stage than serum creatinine; using serum creatinine alone to calculate the CKD stage could lead to a very wrong result. For example, a thin, elderly white woman can have a very low eGFR but a serum creatinine of 1.4 mg/dL or less (which is essentially normal).

Diabetic patients in particular are susceptible to hyperkalemia, so spironolactone, potassium, and sulfamethoxazole should be prescribed with caution. Potassium levels should be monitored in patients receiving b-blockers, ACE inhibitors, or ARBs.

Renal medication dosing guidelines, as noted in the FDA information in each drug’s package insert, generally offer recommendations for adjustment in CKD stage 4 or 5, which correspond to an eGFR of < 30 mL/min or < 15 mL/min, respectively. FDA renal dosing guidelines are often based on serum creatinine, but eGFR can vary widely for a particular serum creatinine level, depending upon patient variables such as age, weight, race, and gender (as in the example above).

In summary, although no specific published guidelines exist for patients with CKD stage 2, the presence of microalbuminuria is an important clinical indicator that should inform the provider’s approach to patient management.
Alexis Chettiar, ACNP, East Bay Nephrology Medical Group, Oakland, CA

References
1. National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC). http://kidney.niddk.nih.gov. Accessed November 18, 2011.

2. Thorp ML, Morris CD, Bagby SP. A crossover study of gabapentin in treatment of restless legs syndrome among hemodialysis patients. Am J Kidney Dis. 2001;38(1):104-108.

3. Blommel ML, Blommel AL. Pregabalin: an antiepileptic agent useful for neuropathic pain. Am J Health-System Pharm. 2007;64(14):1475-1482.

4. Gerstein HC, Mann JF, Yi Q, et al. Albuminuria and risk of cardiovascular events, death, and heart failure in diabetic and nondiabetic individuals. JAMA. 2001;286(4):421-426.

5. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289(19):2560-2572.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004; 43(5 suppl 1):S1-290.

7. National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI™). www.kidney.org/professionals/kdoqi. Accessed November 18, 2011.

8. Post TW, Rose BD. Overview of management of chronic kidney disease in adults. www.uptodate.com/contents/overview-of-the-management-of-chronic-kidney-disease-in-adults/contributors. Accessed November 18, 2011.

9. DeFronzo RA. Pharmacologic therapy for type 2 diabetes mellitus. Ann Intern Med. 1999;131(4):281-303.

Chronic kidney disease (CKD) is the silent epidemic. It often follows hypertension, diabetes, and obesity. Patients with CKD are not seen exclusively in a nephrology practice. Often, they are not referred to a nephrologist until their glomerular filtration rate (GFR) is less than 60 mL/min/1.73m².

CKD affects 11.5% of the US population ages 20 and older,¹ which translates to some 23 million people. According to the National Institute of Diabetes and Digestive and Kidney Diseases, more than 382,000 people were receiving dialysis in 2008,¹ and this number is expected to more than double by 2020. It is essential for the practitioner in any specialty to be aware of their patients’ renal status and any adjustments that may entail.

Q: In my primary care office, I saw a dialysis patient with peripheral neuropathy caused by her diabetes. I treated her with gabapentin 300 mg qd with an increase of 100 mg each week until her symptoms resolved. I received a note from the nephrology group that the dose I ordered was way too high, and they adjusted it down to 100 mg/d. Is that right? Would it have been better for me to prescribe pregabalin? I was trying to use an inexpensive medication because this patient has to take so many. 

Gabapentin has been used for years in the dialysis unit to treat patients with diabetes-related peripheral neuropathy.² It is one of the most commonly prescribed drugs for this population of patients due to its effectiveness and low adverse-effect profile. However, because gabapentin is cleared solely by renal excretion, it is recommended that patients on dialysis receive 200 to 300 mg after each four-hour hemodialysis session. This dose should be reached with gradual titration to avoid adverse effects, which include dizziness, ataxia, sedation, euphoria, ankle edema, and weight gain.

The risk for altered consciousness and myoclonus associated with gabapentin is increased in the dialysis population. When these adverse effects occur, the drug should be stopped. Doses above the recommended 200 to 300 mg per dialysis session have not been shown to provide any added analgesic effect and may increase adverse effects, putting patients at greater risk for falls, in addition to other side effects. Gabapentin has a much longer half-life in patients on dialysis, compared with those who have normal kidney function. These patients will benefit from a minimal dosing schedule as well as the prolonged pain control with gaba­pentin.

The efficacy of pregabalin (Lyrica^®) in the management of painful diabetic neuropathy has been established in several controlled clinical trials.³ Because it has not been in use as long as gabapentin, its safety profile has not yet been established. Pregabalin has better gastrointestinal absorption than gabapentin and offers more rapid pain relief; it can be administered twice daily. Pregabalin is cleared rapidly by dialysis and has a short half-life; therefore, an extra dose is required after each dialysis session. Pregabalin dosing must also be adjusted for creatinine clearance.*

Pregabalin is a Schedule V controlled substance because of its potential for abuse. It cannot be prescribed by advanced practitioners in all states.
Dawn McCombs, CRNP, Nephrology Associates, PC, Birmingham, AL

* Several sources are available on the Internet to determine creatinine clearance or stage of kidney disease if your lab does not calculate it for you.

References
1. National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC). http://kidney.niddk.nih.gov. Accessed November 18, 2011.

2. Thorp ML, Morris CD, Bagby SP. A crossover study of gabapentin in treatment of restless legs syndrome among hemodialysis patients. Am J Kidney Dis. 2001;38(1):104-108.

3. Blommel ML, Blommel AL. Pregabalin: an antiepileptic agent useful for neuropathic pain. Am J Health-System Pharm. 2007;64(14):1475-1482.

4. Gerstein HC, Mann JF, Yi Q, et al. Albuminuria and risk of cardiovascular events, death, and heart failure in diabetic and nondiabetic individuals. JAMA. 2001;286(4):421-426.

5. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289(19):2560-2572.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004; 43(5 suppl 1):S1-290.

7. National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI™). www.kidney.org/professionals/kdoqi. Accessed November 18, 2011.

8. Post TW, Rose BD. Overview of management of chronic kidney disease in adults. www.uptodate.com/contents/overview-of-the-management-of-chronic-kidney-disease-in-adults/contributors. Accessed November 18, 2011.

9. DeFronzo RA. Pharmacologic therapy for type 2 diabetes mellitus. Ann Intern Med. 1999;131(4):281-303.

Chronic kidney disease (CKD) is the silent epidemic. It often follows hypertension, diabetes, and obesity. Patients with CKD are not seen exclusively in a nephrology practice. Often, they are not referred to a nephrologist until their glomerular filtration rate (GFR) is less than 60 mL/min/1.73m².

CKD affects 11.5% of the US population ages 20 and older,¹ which translates to some 23 million people. According to the National Institute of Diabetes and Digestive and Kidney Diseases, more than 382,000 people were receiving dialysis in 2008,¹ and this number is expected to more than double by 2020. It is essential for the practitioner in any specialty to be aware of their patients’ renal status and any adjustments that may entail.

Q: In my primary care office, I saw a dialysis patient with peripheral neuropathy caused by her diabetes. I treated her with gabapentin 300 mg qd with an increase of 100 mg each week until her symptoms resolved. I received a note from the nephrology group that the dose I ordered was way too high, and they adjusted it down to 100 mg/d. Is that right? Would it have been better for me to prescribe pregabalin? I was trying to use an inexpensive medication because this patient has to take so many. 

Gabapentin has been used for years in the dialysis unit to treat patients with diabetes-related peripheral neuropathy.² It is one of the most commonly prescribed drugs for this population of patients due to its effectiveness and low adverse-effect profile. However, because gabapentin is cleared solely by renal excretion, it is recommended that patients on dialysis receive 200 to 300 mg after each four-hour hemodialysis session. This dose should be reached with gradual titration to avoid adverse effects, which include dizziness, ataxia, sedation, euphoria, ankle edema, and weight gain.

The risk for altered consciousness and myoclonus associated with gabapentin is increased in the dialysis population. When these adverse effects occur, the drug should be stopped. Doses above the recommended 200 to 300 mg per dialysis session have not been shown to provide any added analgesic effect and may increase adverse effects, putting patients at greater risk for falls, in addition to other side effects. Gabapentin has a much longer half-life in patients on dialysis, compared with those who have normal kidney function. These patients will benefit from a minimal dosing schedule as well as the prolonged pain control with gaba­pentin.

The efficacy of pregabalin (Lyrica^®) in the management of painful diabetic neuropathy has been established in several controlled clinical trials.³ Because it has not been in use as long as gabapentin, its safety profile has not yet been established. Pregabalin has better gastrointestinal absorption than gabapentin and offers more rapid pain relief; it can be administered twice daily. Pregabalin is cleared rapidly by dialysis and has a short half-life; therefore, an extra dose is required after each dialysis session. Pregabalin dosing must also be adjusted for creatinine clearance.*

Pregabalin is a Schedule V controlled substance because of its potential for abuse. It cannot be prescribed by advanced practitioners in all states.
Dawn McCombs, CRNP, Nephrology Associates, PC, Birmingham, AL

* Several sources are available on the Internet to determine creatinine clearance or stage of kidney disease if your lab does not calculate it for you.

References
1. National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC). http://kidney.niddk.nih.gov. Accessed November 18, 2011.

2. Thorp ML, Morris CD, Bagby SP. A crossover study of gabapentin in treatment of restless legs syndrome among hemodialysis patients. Am J Kidney Dis. 2001;38(1):104-108.

3. Blommel ML, Blommel AL. Pregabalin: an antiepileptic agent useful for neuropathic pain. Am J Health-System Pharm. 2007;64(14):1475-1482.

4. Gerstein HC, Mann JF, Yi Q, et al. Albuminuria and risk of cardiovascular events, death, and heart failure in diabetic and nondiabetic individuals. JAMA. 2001;286(4):421-426.

5. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289(19):2560-2572.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004; 43(5 suppl 1):S1-290.

7. National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI™). www.kidney.org/professionals/kdoqi. Accessed November 18, 2011.

8. Post TW, Rose BD. Overview of management of chronic kidney disease in adults. www.uptodate.com/contents/overview-of-the-management-of-chronic-kidney-disease-in-adults/contributors. Accessed November 18, 2011.

9. DeFronzo RA. Pharmacologic therapy for type 2 diabetes mellitus. Ann Intern Med. 1999;131(4):281-303.

Chronic kidney disease (CKD) is the silent epidemic. It often follows hypertension, diabetes, and obesity. Patients with CKD are not seen exclusively in a nephrology practice. Often, they are not referred to a nephrologist until their glomerular filtration rate (GFR) is less than 60 mL/min/1.73m².

CKD affects 11.5% of the US population ages 20 and older,¹ which translates to some 23 million people. According to the National Institute of Diabetes and Digestive and Kidney Diseases, more than 382,000 people were receiving dialysis in 2008,¹ and this number is expected to more than double by 2020. It is essential for the practitioner in any specialty to be aware of their patients’ renal status and any adjustments that may entail.

Q: In my primary care office, I saw a dialysis patient with peripheral neuropathy caused by her diabetes. I treated her with gabapentin 300 mg qd with an increase of 100 mg each week until her symptoms resolved. I received a note from the nephrology group that the dose I ordered was way too high, and they adjusted it down to 100 mg/d. Is that right? Would it have been better for me to prescribe pregabalin? I was trying to use an inexpensive medication because this patient has to take so many. 

Gabapentin has been used for years in the dialysis unit to treat patients with diabetes-related peripheral neuropathy.² It is one of the most commonly prescribed drugs for this population of patients due to its effectiveness and low adverse-effect profile. However, because gabapentin is cleared solely by renal excretion, it is recommended that patients on dialysis receive 200 to 300 mg after each four-hour hemodialysis session. This dose should be reached with gradual titration to avoid adverse effects, which include dizziness, ataxia, sedation, euphoria, ankle edema, and weight gain.

The risk for altered consciousness and myoclonus associated with gabapentin is increased in the dialysis population. When these adverse effects occur, the drug should be stopped. Doses above the recommended 200 to 300 mg per dialysis session have not been shown to provide any added analgesic effect and may increase adverse effects, putting patients at greater risk for falls, in addition to other side effects. Gabapentin has a much longer half-life in patients on dialysis, compared with those who have normal kidney function. These patients will benefit from a minimal dosing schedule as well as the prolonged pain control with gaba­pentin.

The efficacy of pregabalin (Lyrica^®) in the management of painful diabetic neuropathy has been established in several controlled clinical trials.³ Because it has not been in use as long as gabapentin, its safety profile has not yet been established. Pregabalin has better gastrointestinal absorption than gabapentin and offers more rapid pain relief; it can be administered twice daily. Pregabalin is cleared rapidly by dialysis and has a short half-life; therefore, an extra dose is required after each dialysis session. Pregabalin dosing must also be adjusted for creatinine clearance.*

Pregabalin is a Schedule V controlled substance because of its potential for abuse. It cannot be prescribed by advanced practitioners in all states.
Dawn McCombs, CRNP, Nephrology Associates, PC, Birmingham, AL

* Several sources are available on the Internet to determine creatinine clearance or stage of kidney disease if your lab does not calculate it for you.

References
1. National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC). http://kidney.niddk.nih.gov. Accessed November 18, 2011.

2. Thorp ML, Morris CD, Bagby SP. A crossover study of gabapentin in treatment of restless legs syndrome among hemodialysis patients. Am J Kidney Dis. 2001;38(1):104-108.

3. Blommel ML, Blommel AL. Pregabalin: an antiepileptic agent useful for neuropathic pain. Am J Health-System Pharm. 2007;64(14):1475-1482.

4. Gerstein HC, Mann JF, Yi Q, et al. Albuminuria and risk of cardiovascular events, death, and heart failure in diabetic and nondiabetic individuals. JAMA. 2001;286(4):421-426.

5. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289(19):2560-2572.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004; 43(5 suppl 1):S1-290.

7. National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI™). www.kidney.org/professionals/kdoqi. Accessed November 18, 2011.

8. Post TW, Rose BD. Overview of management of chronic kidney disease in adults. www.uptodate.com/contents/overview-of-the-management-of-chronic-kidney-disease-in-adults/contributors. Accessed November 18, 2011.

9. DeFronzo RA. Pharmacologic therapy for type 2 diabetes mellitus. Ann Intern Med. 1999;131(4):281-303.