Q&A

Fifteen years ago, Mr. L, age 40, was given a diagnosis of schizophrenia, which has been treated with haloperidol, 10 mg/d. Approximately 1 year ago, he began experiencing consistent lip smacking, a sign of tardive dyskinesia. Vitamin E was added to the treatment regimen, after which the tardive dyskinesia symptoms resolved.

A few months later, however, those symptoms returned and became worse. In addition to lip smacking, Mr. L now also describes involuntary bilateral twitching and muscle spasms in both legs.

Haloperidol and vitamin E are discontinued and Mr. L is switched to olanzapine, 20 mg/d. Although olanzapine is effective for Mr. L's symptoms of schizophrenia, tardive dyskinesia persists, and he gains 60 pounds and develops diabetes. Olanzapine is discontinued and he begins a trial of risperidone, 4 mg/d.

While on risperidone, blood sugar control, measured by hemoglobin A1c, and insulin resistance improve, but Mr. L continues to have symptoms of tardive dyskinesia. Vitamin E is added again, but is ineffective. The treatment team switches Mr. L to clozapine but symptoms of tardive dyskinesia do not improve.

Extrapyramidal side effects are common with first-generation antipsychotics (FGA) such as haloperidol. Types of antipsychotic-induced movement disorders include dystonias, akathisias, pseudoparkinsonism, and tardive dyskinesia. Of these, tardive dyskinesia is the most concerning because it often is difficult to treat and may be irreversible.

Tardive dyskinesia involves abnormal, involuntary movements, usually involving the face and, sometimes, the limbs. Common symptoms include lip smacking, tongue protrusions, and puffing the cheeks¹; severe tardive dyskinesia may affect the larynx and diaphragm, which can be life-threatening. The incidence of tardive dyskinesia is approximately 5% after the first year of FGA treatment and 1% with second-generation antipsychotics (SGAs).² The risk increases with higher doses and longer duration of treatment, with a prevalence of 20% to 25% with long-term FGA use.³

Treatment strategies
There are no FDA-approved drugs for tardive dyskinesia (Table).^4-6 The best strategy is to prevent tardive dyskinesia with judicious use of an antipsychotic. If a patient taking a FGA develops tardive dyskinesia, the first-line treatment is to switch to a SGA. Risperidone, olanzapine, quetiapine, and clozapine have a low risk of tardive dyskinesia. Newer agents, such as lurasidone, asenapine, iloperidone, and aripiprazole, might have a lower risk of tardive dyskinesia, possibly because of differences in dopamine blockage between these agents and FGAs. Clozapine is least likely to cause tardive dyskinesia, but it often is used as a last resort because of the risk of agranulocytosis and the need for frequent tests to measurewhite blood cells.^1,4

Fifteen years ago, Mr. L, age 40, was given a diagnosis of schizophrenia, which has been treated with haloperidol, 10 mg/d. Approximately 1 year ago, he began experiencing consistent lip smacking, a sign of tardive dyskinesia. Vitamin E was added to the treatment regimen, after which the tardive dyskinesia symptoms resolved.

A few months later, however, those symptoms returned and became worse. In addition to lip smacking, Mr. L now also describes involuntary bilateral twitching and muscle spasms in both legs.

Haloperidol and vitamin E are discontinued and Mr. L is switched to olanzapine, 20 mg/d. Although olanzapine is effective for Mr. L's symptoms of schizophrenia, tardive dyskinesia persists, and he gains 60 pounds and develops diabetes. Olanzapine is discontinued and he begins a trial of risperidone, 4 mg/d.

While on risperidone, blood sugar control, measured by hemoglobin A1c, and insulin resistance improve, but Mr. L continues to have symptoms of tardive dyskinesia. Vitamin E is added again, but is ineffective. The treatment team switches Mr. L to clozapine but symptoms of tardive dyskinesia do not improve.

Extrapyramidal side effects are common with first-generation antipsychotics (FGA) such as haloperidol. Types of antipsychotic-induced movement disorders include dystonias, akathisias, pseudoparkinsonism, and tardive dyskinesia. Of these, tardive dyskinesia is the most concerning because it often is difficult to treat and may be irreversible.

Tardive dyskinesia involves abnormal, involuntary movements, usually involving the face and, sometimes, the limbs. Common symptoms include lip smacking, tongue protrusions, and puffing the cheeks¹; severe tardive dyskinesia may affect the larynx and diaphragm, which can be life-threatening. The incidence of tardive dyskinesia is approximately 5% after the first year of FGA treatment and 1% with second-generation antipsychotics (SGAs).² The risk increases with higher doses and longer duration of treatment, with a prevalence of 20% to 25% with long-term FGA use.³

Treatment strategies
There are no FDA-approved drugs for tardive dyskinesia (Table).^4-6 The best strategy is to prevent tardive dyskinesia with judicious use of an antipsychotic. If a patient taking a FGA develops tardive dyskinesia, the first-line treatment is to switch to a SGA. Risperidone, olanzapine, quetiapine, and clozapine have a low risk of tardive dyskinesia. Newer agents, such as lurasidone, asenapine, iloperidone, and aripiprazole, might have a lower risk of tardive dyskinesia, possibly because of differences in dopamine blockage between these agents and FGAs. Clozapine is least likely to cause tardive dyskinesia, but it often is used as a last resort because of the risk of agranulocytosis and the need for frequent tests to measurewhite blood cells.^1,4

Fifteen years ago, Mr. L, age 40, was given a diagnosis of schizophrenia, which has been treated with haloperidol, 10 mg/d. Approximately 1 year ago, he began experiencing consistent lip smacking, a sign of tardive dyskinesia. Vitamin E was added to the treatment regimen, after which the tardive dyskinesia symptoms resolved.

A few months later, however, those symptoms returned and became worse. In addition to lip smacking, Mr. L now also describes involuntary bilateral twitching and muscle spasms in both legs.

Haloperidol and vitamin E are discontinued and Mr. L is switched to olanzapine, 20 mg/d. Although olanzapine is effective for Mr. L's symptoms of schizophrenia, tardive dyskinesia persists, and he gains 60 pounds and develops diabetes. Olanzapine is discontinued and he begins a trial of risperidone, 4 mg/d.

While on risperidone, blood sugar control, measured by hemoglobin A1c, and insulin resistance improve, but Mr. L continues to have symptoms of tardive dyskinesia. Vitamin E is added again, but is ineffective. The treatment team switches Mr. L to clozapine but symptoms of tardive dyskinesia do not improve.

Extrapyramidal side effects are common with first-generation antipsychotics (FGA) such as haloperidol. Types of antipsychotic-induced movement disorders include dystonias, akathisias, pseudoparkinsonism, and tardive dyskinesia. Of these, tardive dyskinesia is the most concerning because it often is difficult to treat and may be irreversible.

Tardive dyskinesia involves abnormal, involuntary movements, usually involving the face and, sometimes, the limbs. Common symptoms include lip smacking, tongue protrusions, and puffing the cheeks¹; severe tardive dyskinesia may affect the larynx and diaphragm, which can be life-threatening. The incidence of tardive dyskinesia is approximately 5% after the first year of FGA treatment and 1% with second-generation antipsychotics (SGAs).² The risk increases with higher doses and longer duration of treatment, with a prevalence of 20% to 25% with long-term FGA use.³

Treatment strategies
There are no FDA-approved drugs for tardive dyskinesia (Table).^4-6 The best strategy is to prevent tardive dyskinesia with judicious use of an antipsychotic. If a patient taking a FGA develops tardive dyskinesia, the first-line treatment is to switch to a SGA. Risperidone, olanzapine, quetiapine, and clozapine have a low risk of tardive dyskinesia. Newer agents, such as lurasidone, asenapine, iloperidone, and aripiprazole, might have a lower risk of tardive dyskinesia, possibly because of differences in dopamine blockage between these agents and FGAs. Clozapine is least likely to cause tardive dyskinesia, but it often is used as a last resort because of the risk of agranulocytosis and the need for frequent tests to measurewhite blood cells.^1,4

Q) A 53-year-old dialysis patient in my clinic says her nephrologist told her she did not need a DXA scan because it was not valid for kidney patients. Why not?

Osteoporosis is a condition of reduced bone mass, causing decreased bone strength and leading to increased risk for fractures. The World Health Organization definition of osteoporosis is based on bone mineral density (BMD). While there is some overlap between idiopathic osteoporosis and chronic kidney disease–mineral bone disorder (CKD-MBD), both conditions have different pathophysiologic backgrounds and require different treatments.¹

There is not an accurate correlation between BMD as measured by DXA and the type of CKD-associated bone disease.² Patients with CKD typically have lower bone density than the general population, making the interpretation of DXA (dual x-ray absorptiometry) scans more complicated. This is due to focal areas of osteosclerosis, the presence of extraskeletal calcifications, and the variable presence of osteomalacia.

The gold standard for assessment and diagnosis of bone disease in CKD patients is the iliac crest bone biopsy. However, it is not frequently performed due to the painful and invasive nature of the procedure and the limitations in access to centers where it is performed and to experienced pathologists.

KDIGO (Kidney Disease Improving Global Outcomes) guidelines³ recommend that in patients with CKD stages 3 to 5D (see chart for explanation), measurements of serum parathyroid hormone or bone-specific alkaline phosphatase be used to evaluate bone disease, because markedly high or low values ­predict underlying bone turnover. 

Shelly Levinstein, MSN, CRNP

Nephrology Associates of York
York, PA

REFERENCES

1. Toussaint N, Elder G, Kerr P.  Bisphosphonates in chronic kidney disease; balancing potential benefits and adverse effects on bone and soft tissue. Clin J Am Soc Nephrol. 2009;4:221-233.

2. Tanenbaum N, Quarles LD. Bone disorders in chronic kidney disease. In: Greenberg A, Cheung AK, eds. Primer on Kidney Diseases. 5th ed. Philadelphia, PA: Elsevier Saunders; 2009:487-498.

3. Moe S, Drueke T, Cunningham J, et al; Kidney Disease: Improving Global Outcomes (KDIGO). Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2006;69:1945-1953.

4. Gilbert S, Weiner DE. National Kidney ­Foundation’s Primer on Kidney Diseases. 6th ed. Philadelphia, PA: Elsevier Saunders; 2013:330.

Q) A 53-year-old dialysis patient in my clinic says her nephrologist told her she did not need a DXA scan because it was not valid for kidney patients. Why not?

Osteoporosis is a condition of reduced bone mass, causing decreased bone strength and leading to increased risk for fractures. The World Health Organization definition of osteoporosis is based on bone mineral density (BMD). While there is some overlap between idiopathic osteoporosis and chronic kidney disease–mineral bone disorder (CKD-MBD), both conditions have different pathophysiologic backgrounds and require different treatments.¹

There is not an accurate correlation between BMD as measured by DXA and the type of CKD-associated bone disease.² Patients with CKD typically have lower bone density than the general population, making the interpretation of DXA (dual x-ray absorptiometry) scans more complicated. This is due to focal areas of osteosclerosis, the presence of extraskeletal calcifications, and the variable presence of osteomalacia.

The gold standard for assessment and diagnosis of bone disease in CKD patients is the iliac crest bone biopsy. However, it is not frequently performed due to the painful and invasive nature of the procedure and the limitations in access to centers where it is performed and to experienced pathologists.

KDIGO (Kidney Disease Improving Global Outcomes) guidelines³ recommend that in patients with CKD stages 3 to 5D (see chart for explanation), measurements of serum parathyroid hormone or bone-specific alkaline phosphatase be used to evaluate bone disease, because markedly high or low values ­predict underlying bone turnover. 

Shelly Levinstein, MSN, CRNP

Nephrology Associates of York
York, PA

REFERENCES

1. Toussaint N, Elder G, Kerr P.  Bisphosphonates in chronic kidney disease; balancing potential benefits and adverse effects on bone and soft tissue. Clin J Am Soc Nephrol. 2009;4:221-233.

2. Tanenbaum N, Quarles LD. Bone disorders in chronic kidney disease. In: Greenberg A, Cheung AK, eds. Primer on Kidney Diseases. 5th ed. Philadelphia, PA: Elsevier Saunders; 2009:487-498.

3. Moe S, Drueke T, Cunningham J, et al; Kidney Disease: Improving Global Outcomes (KDIGO). Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2006;69:1945-1953.

4. Gilbert S, Weiner DE. National Kidney ­Foundation’s Primer on Kidney Diseases. 6th ed. Philadelphia, PA: Elsevier Saunders; 2013:330.

Q) A 53-year-old dialysis patient in my clinic says her nephrologist told her she did not need a DXA scan because it was not valid for kidney patients. Why not?

Osteoporosis is a condition of reduced bone mass, causing decreased bone strength and leading to increased risk for fractures. The World Health Organization definition of osteoporosis is based on bone mineral density (BMD). While there is some overlap between idiopathic osteoporosis and chronic kidney disease–mineral bone disorder (CKD-MBD), both conditions have different pathophysiologic backgrounds and require different treatments.¹

There is not an accurate correlation between BMD as measured by DXA and the type of CKD-associated bone disease.² Patients with CKD typically have lower bone density than the general population, making the interpretation of DXA (dual x-ray absorptiometry) scans more complicated. This is due to focal areas of osteosclerosis, the presence of extraskeletal calcifications, and the variable presence of osteomalacia.

The gold standard for assessment and diagnosis of bone disease in CKD patients is the iliac crest bone biopsy. However, it is not frequently performed due to the painful and invasive nature of the procedure and the limitations in access to centers where it is performed and to experienced pathologists.

KDIGO (Kidney Disease Improving Global Outcomes) guidelines³ recommend that in patients with CKD stages 3 to 5D (see chart for explanation), measurements of serum parathyroid hormone or bone-specific alkaline phosphatase be used to evaluate bone disease, because markedly high or low values ­predict underlying bone turnover. 

Shelly Levinstein, MSN, CRNP

Nephrology Associates of York
York, PA

REFERENCES

1. Toussaint N, Elder G, Kerr P.  Bisphosphonates in chronic kidney disease; balancing potential benefits and adverse effects on bone and soft tissue. Clin J Am Soc Nephrol. 2009;4:221-233.

2. Tanenbaum N, Quarles LD. Bone disorders in chronic kidney disease. In: Greenberg A, Cheung AK, eds. Primer on Kidney Diseases. 5th ed. Philadelphia, PA: Elsevier Saunders; 2009:487-498.

3. Moe S, Drueke T, Cunningham J, et al; Kidney Disease: Improving Global Outcomes (KDIGO). Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2006;69:1945-1953.

4. Gilbert S, Weiner DE. National Kidney ­Foundation’s Primer on Kidney Diseases. 6th ed. Philadelphia, PA: Elsevier Saunders; 2013:330.

Q) Since bone loss is common in patients with kidney disease, how should it be treated?

In elderly CKD patients, it is recognized that osteoporosis and CKD-MBD may co-exist—which only makes the bone-loss issue more problematic. Therefore, diagnosis and management are crucial to effective treatment.

Although osteoporosis is recognized and treated in CKD stages 1 to 3a, the interpretation of BMD levels in the osteoporotic range is controversial in advanced kidney disease (GFR < 35).¹ There are limited data for treatment of patients with CKD-MBD.

Studies of bisphosphonate use in postmenopausal women and in patients with glucocorticoid-induced osteoporosis have generally excluded those with renal impairment. For these patients, treatment of low BMD using standard therapies for osteoporosis is not without potential for harm, due to the possibility of worsening low bone turnover, osteomalacia, mixed uremic osteodystrophy, and exacerbated hyperparathyroidism.

The choice of pharmaceutical treatment should be based on whether you are treating CKD-MBD or osteoporosis. A large percentage of CKD patients have adynamic bone disease with low bone resorption. In patients with low bone resorption, treatment entails choosing a drug that stimulates bone formation and not those that inhibit bone resorption. The benefit of bisphosphonate therapy is seen in patients with high bone resorption.⁴

In CKD stages 1 to 3, one must evaluate laboratory features of low BMD, including serum levels of calcium, phosphate, parathyroid hormone, alkaline phosphatase, and vitamin D. If all are found to be normal, bisphosphonate use in CKD stages 1 to 3 is usually safe.¹ 

A bone biopsy is recommended for patients with advanced CKD stages 4 to 5/5D, with ther­apy individualized per disease process.¹

Shelly Levinstein, MSN, CRNP

Nephrology Associates of York
York, PA

REFERENCES

1. Toussaint N, Elder G, Kerr P.  Bisphosphonates in chronic kidney disease; balancing potential benefits and adverse effects on bone and soft tissue. Clin J Am Soc Nephrol. 2009;4:221-233.

2. Tanenbaum N, Quarles LD. Bone disorders in chronic kidney disease. In: Greenberg A, Cheung AK, eds. Primer on Kidney Diseases. 5th ed. Philadelphia, PA: Elsevier Saunders; 2009:487-498.

3. Moe S, Drueke T, Cunningham J, et al; Kidney Disease: Improving Global Outcomes (KDIGO). Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2006;69:1945-1953.

4. Gilbert S, Weiner DE. National Kidney ­Foundation’s Primer on Kidney Diseases. 6th ed. Philadelphia, PA: Elsevier Saunders; 2013:330.

Q) Since bone loss is common in patients with kidney disease, how should it be treated?

In elderly CKD patients, it is recognized that osteoporosis and CKD-MBD may co-exist—which only makes the bone-loss issue more problematic. Therefore, diagnosis and management are crucial to effective treatment.

Although osteoporosis is recognized and treated in CKD stages 1 to 3a, the interpretation of BMD levels in the osteoporotic range is controversial in advanced kidney disease (GFR < 35).¹ There are limited data for treatment of patients with CKD-MBD.

Studies of bisphosphonate use in postmenopausal women and in patients with glucocorticoid-induced osteoporosis have generally excluded those with renal impairment. For these patients, treatment of low BMD using standard therapies for osteoporosis is not without potential for harm, due to the possibility of worsening low bone turnover, osteomalacia, mixed uremic osteodystrophy, and exacerbated hyperparathyroidism.

The choice of pharmaceutical treatment should be based on whether you are treating CKD-MBD or osteoporosis. A large percentage of CKD patients have adynamic bone disease with low bone resorption. In patients with low bone resorption, treatment entails choosing a drug that stimulates bone formation and not those that inhibit bone resorption. The benefit of bisphosphonate therapy is seen in patients with high bone resorption.⁴

In CKD stages 1 to 3, one must evaluate laboratory features of low BMD, including serum levels of calcium, phosphate, parathyroid hormone, alkaline phosphatase, and vitamin D. If all are found to be normal, bisphosphonate use in CKD stages 1 to 3 is usually safe.¹ 

A bone biopsy is recommended for patients with advanced CKD stages 4 to 5/5D, with ther­apy individualized per disease process.¹

Shelly Levinstein, MSN, CRNP

Nephrology Associates of York
York, PA

REFERENCES

1. Toussaint N, Elder G, Kerr P.  Bisphosphonates in chronic kidney disease; balancing potential benefits and adverse effects on bone and soft tissue. Clin J Am Soc Nephrol. 2009;4:221-233.

2. Tanenbaum N, Quarles LD. Bone disorders in chronic kidney disease. In: Greenberg A, Cheung AK, eds. Primer on Kidney Diseases. 5th ed. Philadelphia, PA: Elsevier Saunders; 2009:487-498.

3. Moe S, Drueke T, Cunningham J, et al; Kidney Disease: Improving Global Outcomes (KDIGO). Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2006;69:1945-1953.

4. Gilbert S, Weiner DE. National Kidney ­Foundation’s Primer on Kidney Diseases. 6th ed. Philadelphia, PA: Elsevier Saunders; 2013:330.

Q) Since bone loss is common in patients with kidney disease, how should it be treated?

In elderly CKD patients, it is recognized that osteoporosis and CKD-MBD may co-exist—which only makes the bone-loss issue more problematic. Therefore, diagnosis and management are crucial to effective treatment.

Although osteoporosis is recognized and treated in CKD stages 1 to 3a, the interpretation of BMD levels in the osteoporotic range is controversial in advanced kidney disease (GFR < 35).¹ There are limited data for treatment of patients with CKD-MBD.

Studies of bisphosphonate use in postmenopausal women and in patients with glucocorticoid-induced osteoporosis have generally excluded those with renal impairment. For these patients, treatment of low BMD using standard therapies for osteoporosis is not without potential for harm, due to the possibility of worsening low bone turnover, osteomalacia, mixed uremic osteodystrophy, and exacerbated hyperparathyroidism.

The choice of pharmaceutical treatment should be based on whether you are treating CKD-MBD or osteoporosis. A large percentage of CKD patients have adynamic bone disease with low bone resorption. In patients with low bone resorption, treatment entails choosing a drug that stimulates bone formation and not those that inhibit bone resorption. The benefit of bisphosphonate therapy is seen in patients with high bone resorption.⁴

In CKD stages 1 to 3, one must evaluate laboratory features of low BMD, including serum levels of calcium, phosphate, parathyroid hormone, alkaline phosphatase, and vitamin D. If all are found to be normal, bisphosphonate use in CKD stages 1 to 3 is usually safe.¹ 

A bone biopsy is recommended for patients with advanced CKD stages 4 to 5/5D, with ther­apy individualized per disease process.¹

Shelly Levinstein, MSN, CRNP

Nephrology Associates of York
York, PA

REFERENCES

1. Toussaint N, Elder G, Kerr P.  Bisphosphonates in chronic kidney disease; balancing potential benefits and adverse effects on bone and soft tissue. Clin J Am Soc Nephrol. 2009;4:221-233.

2. Tanenbaum N, Quarles LD. Bone disorders in chronic kidney disease. In: Greenberg A, Cheung AK, eds. Primer on Kidney Diseases. 5th ed. Philadelphia, PA: Elsevier Saunders; 2009:487-498.

3. Moe S, Drueke T, Cunningham J, et al; Kidney Disease: Improving Global Outcomes (KDIGO). Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2006;69:1945-1953.

4. Gilbert S, Weiner DE. National Kidney ­Foundation’s Primer on Kidney Diseases. 6th ed. Philadelphia, PA: Elsevier Saunders; 2013:330.

Q) I am new to practice and working in urgent care. I was discussing the diagnosis of kidney stones with my supervising physician. He said he does an intravenous pyelogram (IVP) to diagnose stones. He is a little “old school,” and I’m not sure he is right. What is “state of the art” in the work-up and acute treatment for kidney stones?

An IVP involves taking a series of x-rays following the injection of dye into a patient’s vein. As the dye moves through the bloodstream, the anatomy of the urinary system can be better visualized and the stone location identified, as the dye tends to accumulate at areas of obstruction. The downside to this test is that contrast can cause allergic reactions in some patients and can only be used in those with normal renal function. Also, a radiologist is required to be present during the procedure, and the test can take a long time to complete if a severe blockage is present.⁴

Today, noncontrast CT is considered the gold standard for imaging renal calculi because it is fast, safe (no worries for those with contrast allergy or renal impairment), and nearly 100% accurate.⁵

There are multiple options for treating kidney stones, though some are more invasive than others. For stones 2 cm or less identified in the upper or middle calyx and renal pelvis, extracorporeal shock wave lithotripsy (ESWL) is the treatment of choice.^5,6 The goal of ESWL is to break the stone into small particles that can then be expelled through the urinary system. Adjunct measures, including mechanical percussion, diuresis, and inversion therapy, are often used following lithotripsy to facilitate passage of stone fragments. Medications such as calcium blockers and α-receptor blockers are also used to improve outcomes after lithotripsy. In the past, obese patients had less success with lithotripsy; however, technological advances have improved outcomes in depths up to 17 cm from skin to stone.⁶

For stones in the lower pole of the kidney (and depending on the size of the stone), ESWL, percutaneous nephrolitholapaxy, retrograde flexible ureteronephroscopy, and partial nephrectomy are options for treatment.^3,7 Using an intravenous urogram, measurements and angles are calculated to help determine which procedure would be best for a particular patient.⁷ In simple terms, narrow angles and longer tube distances make it more difficult for stone particles to exit the urinary system. Therefore, if these problems are identified, an invasive approach may be needed to remove a stone. Other important considerations include stone size, patient symptoms, evidence of infection, or obstruction.⁷

ESWL is an attractive option for stone removal because it is noninvasive, has a reasonable safety profile, and is less costly than other, more invasive measures. However, advances in endoscopic instrument design are reducing complications previously associated with more invasive approaches, while improving long-term stone-free outcome rates. There may be increased utilization of procedures such as percutaneous nephrolitholapaxy and retrograde flexible ureteronephroscopy in the future.

Kristina Unterseher, CNN-NP
PeaceHealth
St. John Medical Group
Longview, WA

REFERENCES

1. Fink HA, Wilt TJ, Eidman KE, et al. Medical management to prevent recurrent nephrolithiasis in adults: a systematic review for an American College of Physicians Clinical Guideline. Ann Intern Med. 2013;158(7):535-543.

2. Hiatt RA, Ettinger B, Caan B, et al. Randomized controlled trial of a low animal protein, high fiber diet in the prevention of recurrent calcium oxalate kidney stones. Am J Epidemiol. 1996;144(1):25-33.

3. Moe OW. Kidney stones: pathophysiology and medical management. Lancet. 2006; 367(9507):333-344.

4. American College of Radiology and Radiological Society of North America. Intravenous pyelogram (2013). www.radiologyinfo.org/en/info.cfm?pg=ivp. Accessed December 16, 2013.

5. Boyce CJ, Pickhardt PJ, Lawrence EM, et al. Prevalence of urolithiasis in asymptomatic adults: objective determination using low dose noncontrast computerized tomography. J Urol. 2010;183(3):1017-1021.

6. Christian C, Thorsten B.  The preferred treatment for upper tract stones is extracorporeal shock wave lithotripsy (ESWL) or ureteroscopic: pro ESWL. Urology. 2009;74(2):259-262.

7. Bourdoumis A, Papatsoris AG, Chrisofos M, Deliveliotis C. Lower pole stone management. Med Surg Urol. 2012. www.omicsonline.org/lower-pole-stone-management%20-2168-9857.S4-004.php?aid=7058?abstract _id=7058. Accessed December 16, 2013.

Q) I am new to practice and working in urgent care. I was discussing the diagnosis of kidney stones with my supervising physician. He said he does an intravenous pyelogram (IVP) to diagnose stones. He is a little “old school,” and I’m not sure he is right. What is “state of the art” in the work-up and acute treatment for kidney stones?

An IVP involves taking a series of x-rays following the injection of dye into a patient’s vein. As the dye moves through the bloodstream, the anatomy of the urinary system can be better visualized and the stone location identified, as the dye tends to accumulate at areas of obstruction. The downside to this test is that contrast can cause allergic reactions in some patients and can only be used in those with normal renal function. Also, a radiologist is required to be present during the procedure, and the test can take a long time to complete if a severe blockage is present.⁴

Today, noncontrast CT is considered the gold standard for imaging renal calculi because it is fast, safe (no worries for those with contrast allergy or renal impairment), and nearly 100% accurate.⁵

There are multiple options for treating kidney stones, though some are more invasive than others. For stones 2 cm or less identified in the upper or middle calyx and renal pelvis, extracorporeal shock wave lithotripsy (ESWL) is the treatment of choice.^5,6 The goal of ESWL is to break the stone into small particles that can then be expelled through the urinary system. Adjunct measures, including mechanical percussion, diuresis, and inversion therapy, are often used following lithotripsy to facilitate passage of stone fragments. Medications such as calcium blockers and α-receptor blockers are also used to improve outcomes after lithotripsy. In the past, obese patients had less success with lithotripsy; however, technological advances have improved outcomes in depths up to 17 cm from skin to stone.⁶

For stones in the lower pole of the kidney (and depending on the size of the stone), ESWL, percutaneous nephrolitholapaxy, retrograde flexible ureteronephroscopy, and partial nephrectomy are options for treatment.^3,7 Using an intravenous urogram, measurements and angles are calculated to help determine which procedure would be best for a particular patient.⁷ In simple terms, narrow angles and longer tube distances make it more difficult for stone particles to exit the urinary system. Therefore, if these problems are identified, an invasive approach may be needed to remove a stone. Other important considerations include stone size, patient symptoms, evidence of infection, or obstruction.⁷

ESWL is an attractive option for stone removal because it is noninvasive, has a reasonable safety profile, and is less costly than other, more invasive measures. However, advances in endoscopic instrument design are reducing complications previously associated with more invasive approaches, while improving long-term stone-free outcome rates. There may be increased utilization of procedures such as percutaneous nephrolitholapaxy and retrograde flexible ureteronephroscopy in the future.

Kristina Unterseher, CNN-NP
PeaceHealth
St. John Medical Group
Longview, WA

REFERENCES

1. Fink HA, Wilt TJ, Eidman KE, et al. Medical management to prevent recurrent nephrolithiasis in adults: a systematic review for an American College of Physicians Clinical Guideline. Ann Intern Med. 2013;158(7):535-543.

2. Hiatt RA, Ettinger B, Caan B, et al. Randomized controlled trial of a low animal protein, high fiber diet in the prevention of recurrent calcium oxalate kidney stones. Am J Epidemiol. 1996;144(1):25-33.

3. Moe OW. Kidney stones: pathophysiology and medical management. Lancet. 2006; 367(9507):333-344.

4. American College of Radiology and Radiological Society of North America. Intravenous pyelogram (2013). www.radiologyinfo.org/en/info.cfm?pg=ivp. Accessed December 16, 2013.

5. Boyce CJ, Pickhardt PJ, Lawrence EM, et al. Prevalence of urolithiasis in asymptomatic adults: objective determination using low dose noncontrast computerized tomography. J Urol. 2010;183(3):1017-1021.

6. Christian C, Thorsten B.  The preferred treatment for upper tract stones is extracorporeal shock wave lithotripsy (ESWL) or ureteroscopic: pro ESWL. Urology. 2009;74(2):259-262.

7. Bourdoumis A, Papatsoris AG, Chrisofos M, Deliveliotis C. Lower pole stone management. Med Surg Urol. 2012. www.omicsonline.org/lower-pole-stone-management%20-2168-9857.S4-004.php?aid=7058?abstract _id=7058. Accessed December 16, 2013.

Q) I am new to practice and working in urgent care. I was discussing the diagnosis of kidney stones with my supervising physician. He said he does an intravenous pyelogram (IVP) to diagnose stones. He is a little “old school,” and I’m not sure he is right. What is “state of the art” in the work-up and acute treatment for kidney stones?

An IVP involves taking a series of x-rays following the injection of dye into a patient’s vein. As the dye moves through the bloodstream, the anatomy of the urinary system can be better visualized and the stone location identified, as the dye tends to accumulate at areas of obstruction. The downside to this test is that contrast can cause allergic reactions in some patients and can only be used in those with normal renal function. Also, a radiologist is required to be present during the procedure, and the test can take a long time to complete if a severe blockage is present.⁴

Today, noncontrast CT is considered the gold standard for imaging renal calculi because it is fast, safe (no worries for those with contrast allergy or renal impairment), and nearly 100% accurate.⁵

There are multiple options for treating kidney stones, though some are more invasive than others. For stones 2 cm or less identified in the upper or middle calyx and renal pelvis, extracorporeal shock wave lithotripsy (ESWL) is the treatment of choice.^5,6 The goal of ESWL is to break the stone into small particles that can then be expelled through the urinary system. Adjunct measures, including mechanical percussion, diuresis, and inversion therapy, are often used following lithotripsy to facilitate passage of stone fragments. Medications such as calcium blockers and α-receptor blockers are also used to improve outcomes after lithotripsy. In the past, obese patients had less success with lithotripsy; however, technological advances have improved outcomes in depths up to 17 cm from skin to stone.⁶

For stones in the lower pole of the kidney (and depending on the size of the stone), ESWL, percutaneous nephrolitholapaxy, retrograde flexible ureteronephroscopy, and partial nephrectomy are options for treatment.^3,7 Using an intravenous urogram, measurements and angles are calculated to help determine which procedure would be best for a particular patient.⁷ In simple terms, narrow angles and longer tube distances make it more difficult for stone particles to exit the urinary system. Therefore, if these problems are identified, an invasive approach may be needed to remove a stone. Other important considerations include stone size, patient symptoms, evidence of infection, or obstruction.⁷

ESWL is an attractive option for stone removal because it is noninvasive, has a reasonable safety profile, and is less costly than other, more invasive measures. However, advances in endoscopic instrument design are reducing complications previously associated with more invasive approaches, while improving long-term stone-free outcome rates. There may be increased utilization of procedures such as percutaneous nephrolitholapaxy and retrograde flexible ureteronephroscopy in the future.

Kristina Unterseher, CNN-NP
PeaceHealth
St. John Medical Group
Longview, WA

REFERENCES

1. Fink HA, Wilt TJ, Eidman KE, et al. Medical management to prevent recurrent nephrolithiasis in adults: a systematic review for an American College of Physicians Clinical Guideline. Ann Intern Med. 2013;158(7):535-543.

2. Hiatt RA, Ettinger B, Caan B, et al. Randomized controlled trial of a low animal protein, high fiber diet in the prevention of recurrent calcium oxalate kidney stones. Am J Epidemiol. 1996;144(1):25-33.

3. Moe OW. Kidney stones: pathophysiology and medical management. Lancet. 2006; 367(9507):333-344.

4. American College of Radiology and Radiological Society of North America. Intravenous pyelogram (2013). www.radiologyinfo.org/en/info.cfm?pg=ivp. Accessed December 16, 2013.

5. Boyce CJ, Pickhardt PJ, Lawrence EM, et al. Prevalence of urolithiasis in asymptomatic adults: objective determination using low dose noncontrast computerized tomography. J Urol. 2010;183(3):1017-1021.

6. Christian C, Thorsten B.  The preferred treatment for upper tract stones is extracorporeal shock wave lithotripsy (ESWL) or ureteroscopic: pro ESWL. Urology. 2009;74(2):259-262.

7. Bourdoumis A, Papatsoris AG, Chrisofos M, Deliveliotis C. Lower pole stone management. Med Surg Urol. 2012. www.omicsonline.org/lower-pole-stone-management%20-2168-9857.S4-004.php?aid=7058?abstract _id=7058. Accessed December 16, 2013.

Q) A patient recently came in after an episode of kidney stones. He said he had never experienced such pain before (and this is a former Army Ranger!) and asked if there was anything he could do to keep it from happening again. I told him what I had learned in school (lots of fluids, no organ meats), but is there anything new?

Your patient has some reason for concern. For people who have had a symptomatic kidney stone, the likelihood of developing another within five years is 35% to 50% if no preventive action is taken.¹ Certain factors—including family history, younger age at onset, and predisposing medical conditions (eg, hyperparathyroidism, diabetes, obesity, gout)—increase risk for recurrence.^2,3

In the past, patients were often advised to restrict their dietary calcium intake to prevent calcium oxalate and/or calcium phosphate stones. However, more recent research has proven the opposite to be true: People with lower dietary calcium intake can be at greater risk for kidney stones.^1-3 Therefore, encourage patients to consume about 800 to 1,200 mg/d of dietary calcium. Oral supplementation does not seem to yield the same protective benefits as dietary calcium. This may be related to absorption.¹

Diets high in oxalates (eg, chocolate, nuts, spinach) can increase risk for stone formation, particularly in patients who have bowel diseases that cause inflammation or a history of a bowel resection.² Animal protein in the diet can cause hypercalcinuria and increased uric acid levels, which is particularly problematic for individuals with gout or inflammatory arthritis. High-sodium diets can cause higher urinary calcium oxalate levels, while diets high in phosphorus (particularly dark cola soft drinks) can increase risk for stone formation. Advise your patient to avoid foods high in oxalates, animal proteins, sodium, and phosphorus.²

Dehydration, either due to exercise or poor fluid intake, can result in concentrated urine, which facilitates stone formation. While opinions differ on the benefits of certain dietary restrictions, most research supports the idea that generous fluid intake is the most successful intervention in preventing recurrence of stone formation (regardless of underlying cause). Diluting the urine decreases the concentration of solutes responsible for stone formation.^1-3

If the conservative measures of dietary restriction and adequate hydration fail, medications may be beneficial, depending on stone type or underlying metabolic condition. Thiazide diuretics can help lower urinary calcium by enhancing reabsorption of calcium from the distal convoluted tubule and sodium excretion; however, they should be used cautiously due to the risk for adverse effects such as dizziness and lightheadedness.^1,3 Allopurinol can lower uric acid levels, decreasing recurrence of both uric acid and calcium oxalate stones. Hypocitraturia is prevalent in 20% to 60% of persons with stones; prescribing potassium citrate can inhibit crystal growth of calcium phosphate and calcium oxalate in urine.²

To help patients prevent stone recurrence, perform a comprehensive assessment of their dietary and lifestyle habits and medical history to identify possible contributing factors. Educate patients on adequate dietary calcium intake, generous water intake to keep urine dilute, and avoidance of dietary triggers. 

Nephrolithiasis should be considered a manifestation of another underlying problem. If a patient presents with a kidney stone, attempt to identify the cause—not only to try to prevent recurrence, but also to identify a previously unrecognized disease process.

Kristina Unterseher, CNN-NP
PeaceHealth
St. John Medical Group
Longview, WA

REFERENCES

1. Fink HA, Wilt TJ, Eidman KE, et al. Medical management to prevent recurrent nephrolithiasis in adults: a systematic review for an American College of Physicians Clinical Guideline. Ann Intern Med. 2013;158(7):535-543.

2. Hiatt RA, Ettinger B, Caan B, et al. Randomized controlled trial of a low animal protein, high fiber diet in the prevention of recurrent calcium oxalate kidney stones. Am J Epidemiol. 1996;144(1):25-33.

3. Moe OW. Kidney stones: pathophysiology and medical management. Lancet. 2006; 367(9507):333-344.

4. American College of Radiology and Radiological Society of North America. Intravenous pyelogram (2013). www.radiologyinfo.org/en/info.cfm?pg=ivp. Accessed December 16, 2013.

5. Boyce CJ, Pickhardt PJ, Lawrence EM, et al. Prevalence of urolithiasis in asymptomatic adults: objective determination using low dose noncontrast computerized tomography. J Urol. 2010;183(3):1017-1021.

6. Christian C, Thorsten B.  The preferred treatment for upper tract stones is extracorporeal shock wave lithotripsy (ESWL) or ureteroscopic: pro ESWL. Urology. 2009;74(2):259-262.

7. Bourdoumis A, Papatsoris AG, Chrisofos M, Deliveliotis C. Lower pole stone management. Med Surg Urol. 2012. www.omicsonline.org/lower-pole-stone-management%20-2168-9857.S4-004.php?aid=7058?abstract _id=7058. Accessed December 16, 2013.

Q) A patient recently came in after an episode of kidney stones. He said he had never experienced such pain before (and this is a former Army Ranger!) and asked if there was anything he could do to keep it from happening again. I told him what I had learned in school (lots of fluids, no organ meats), but is there anything new?

Your patient has some reason for concern. For people who have had a symptomatic kidney stone, the likelihood of developing another within five years is 35% to 50% if no preventive action is taken.¹ Certain factors—including family history, younger age at onset, and predisposing medical conditions (eg, hyperparathyroidism, diabetes, obesity, gout)—increase risk for recurrence.^2,3

In the past, patients were often advised to restrict their dietary calcium intake to prevent calcium oxalate and/or calcium phosphate stones. However, more recent research has proven the opposite to be true: People with lower dietary calcium intake can be at greater risk for kidney stones.^1-3 Therefore, encourage patients to consume about 800 to 1,200 mg/d of dietary calcium. Oral supplementation does not seem to yield the same protective benefits as dietary calcium. This may be related to absorption.¹

Diets high in oxalates (eg, chocolate, nuts, spinach) can increase risk for stone formation, particularly in patients who have bowel diseases that cause inflammation or a history of a bowel resection.² Animal protein in the diet can cause hypercalcinuria and increased uric acid levels, which is particularly problematic for individuals with gout or inflammatory arthritis. High-sodium diets can cause higher urinary calcium oxalate levels, while diets high in phosphorus (particularly dark cola soft drinks) can increase risk for stone formation. Advise your patient to avoid foods high in oxalates, animal proteins, sodium, and phosphorus.²

Dehydration, either due to exercise or poor fluid intake, can result in concentrated urine, which facilitates stone formation. While opinions differ on the benefits of certain dietary restrictions, most research supports the idea that generous fluid intake is the most successful intervention in preventing recurrence of stone formation (regardless of underlying cause). Diluting the urine decreases the concentration of solutes responsible for stone formation.^1-3

If the conservative measures of dietary restriction and adequate hydration fail, medications may be beneficial, depending on stone type or underlying metabolic condition. Thiazide diuretics can help lower urinary calcium by enhancing reabsorption of calcium from the distal convoluted tubule and sodium excretion; however, they should be used cautiously due to the risk for adverse effects such as dizziness and lightheadedness.^1,3 Allopurinol can lower uric acid levels, decreasing recurrence of both uric acid and calcium oxalate stones. Hypocitraturia is prevalent in 20% to 60% of persons with stones; prescribing potassium citrate can inhibit crystal growth of calcium phosphate and calcium oxalate in urine.²

To help patients prevent stone recurrence, perform a comprehensive assessment of their dietary and lifestyle habits and medical history to identify possible contributing factors. Educate patients on adequate dietary calcium intake, generous water intake to keep urine dilute, and avoidance of dietary triggers. 

Nephrolithiasis should be considered a manifestation of another underlying problem. If a patient presents with a kidney stone, attempt to identify the cause—not only to try to prevent recurrence, but also to identify a previously unrecognized disease process.

Kristina Unterseher, CNN-NP
PeaceHealth
St. John Medical Group
Longview, WA

REFERENCES

1. Fink HA, Wilt TJ, Eidman KE, et al. Medical management to prevent recurrent nephrolithiasis in adults: a systematic review for an American College of Physicians Clinical Guideline. Ann Intern Med. 2013;158(7):535-543.

2. Hiatt RA, Ettinger B, Caan B, et al. Randomized controlled trial of a low animal protein, high fiber diet in the prevention of recurrent calcium oxalate kidney stones. Am J Epidemiol. 1996;144(1):25-33.

3. Moe OW. Kidney stones: pathophysiology and medical management. Lancet. 2006; 367(9507):333-344.

4. American College of Radiology and Radiological Society of North America. Intravenous pyelogram (2013). www.radiologyinfo.org/en/info.cfm?pg=ivp. Accessed December 16, 2013.

5. Boyce CJ, Pickhardt PJ, Lawrence EM, et al. Prevalence of urolithiasis in asymptomatic adults: objective determination using low dose noncontrast computerized tomography. J Urol. 2010;183(3):1017-1021.

6. Christian C, Thorsten B.  The preferred treatment for upper tract stones is extracorporeal shock wave lithotripsy (ESWL) or ureteroscopic: pro ESWL. Urology. 2009;74(2):259-262.

7. Bourdoumis A, Papatsoris AG, Chrisofos M, Deliveliotis C. Lower pole stone management. Med Surg Urol. 2012. www.omicsonline.org/lower-pole-stone-management%20-2168-9857.S4-004.php?aid=7058?abstract _id=7058. Accessed December 16, 2013.

Q) A patient recently came in after an episode of kidney stones. He said he had never experienced such pain before (and this is a former Army Ranger!) and asked if there was anything he could do to keep it from happening again. I told him what I had learned in school (lots of fluids, no organ meats), but is there anything new?

Your patient has some reason for concern. For people who have had a symptomatic kidney stone, the likelihood of developing another within five years is 35% to 50% if no preventive action is taken.¹ Certain factors—including family history, younger age at onset, and predisposing medical conditions (eg, hyperparathyroidism, diabetes, obesity, gout)—increase risk for recurrence.^2,3

In the past, patients were often advised to restrict their dietary calcium intake to prevent calcium oxalate and/or calcium phosphate stones. However, more recent research has proven the opposite to be true: People with lower dietary calcium intake can be at greater risk for kidney stones.^1-3 Therefore, encourage patients to consume about 800 to 1,200 mg/d of dietary calcium. Oral supplementation does not seem to yield the same protective benefits as dietary calcium. This may be related to absorption.¹

Diets high in oxalates (eg, chocolate, nuts, spinach) can increase risk for stone formation, particularly in patients who have bowel diseases that cause inflammation or a history of a bowel resection.² Animal protein in the diet can cause hypercalcinuria and increased uric acid levels, which is particularly problematic for individuals with gout or inflammatory arthritis. High-sodium diets can cause higher urinary calcium oxalate levels, while diets high in phosphorus (particularly dark cola soft drinks) can increase risk for stone formation. Advise your patient to avoid foods high in oxalates, animal proteins, sodium, and phosphorus.²

Dehydration, either due to exercise or poor fluid intake, can result in concentrated urine, which facilitates stone formation. While opinions differ on the benefits of certain dietary restrictions, most research supports the idea that generous fluid intake is the most successful intervention in preventing recurrence of stone formation (regardless of underlying cause). Diluting the urine decreases the concentration of solutes responsible for stone formation.^1-3

If the conservative measures of dietary restriction and adequate hydration fail, medications may be beneficial, depending on stone type or underlying metabolic condition. Thiazide diuretics can help lower urinary calcium by enhancing reabsorption of calcium from the distal convoluted tubule and sodium excretion; however, they should be used cautiously due to the risk for adverse effects such as dizziness and lightheadedness.^1,3 Allopurinol can lower uric acid levels, decreasing recurrence of both uric acid and calcium oxalate stones. Hypocitraturia is prevalent in 20% to 60% of persons with stones; prescribing potassium citrate can inhibit crystal growth of calcium phosphate and calcium oxalate in urine.²

To help patients prevent stone recurrence, perform a comprehensive assessment of their dietary and lifestyle habits and medical history to identify possible contributing factors. Educate patients on adequate dietary calcium intake, generous water intake to keep urine dilute, and avoidance of dietary triggers. 

Nephrolithiasis should be considered a manifestation of another underlying problem. If a patient presents with a kidney stone, attempt to identify the cause—not only to try to prevent recurrence, but also to identify a previously unrecognized disease process.

Kristina Unterseher, CNN-NP
PeaceHealth
St. John Medical Group
Longview, WA

REFERENCES

1. Fink HA, Wilt TJ, Eidman KE, et al. Medical management to prevent recurrent nephrolithiasis in adults: a systematic review for an American College of Physicians Clinical Guideline. Ann Intern Med. 2013;158(7):535-543.

2. Hiatt RA, Ettinger B, Caan B, et al. Randomized controlled trial of a low animal protein, high fiber diet in the prevention of recurrent calcium oxalate kidney stones. Am J Epidemiol. 1996;144(1):25-33.

3. Moe OW. Kidney stones: pathophysiology and medical management. Lancet. 2006; 367(9507):333-344.

4. American College of Radiology and Radiological Society of North America. Intravenous pyelogram (2013). www.radiologyinfo.org/en/info.cfm?pg=ivp. Accessed December 16, 2013.

5. Boyce CJ, Pickhardt PJ, Lawrence EM, et al. Prevalence of urolithiasis in asymptomatic adults: objective determination using low dose noncontrast computerized tomography. J Urol. 2010;183(3):1017-1021.

6. Christian C, Thorsten B.  The preferred treatment for upper tract stones is extracorporeal shock wave lithotripsy (ESWL) or ureteroscopic: pro ESWL. Urology. 2009;74(2):259-262.

7. Bourdoumis A, Papatsoris AG, Chrisofos M, Deliveliotis C. Lower pole stone management. Med Surg Urol. 2012. www.omicsonline.org/lower-pole-stone-management%20-2168-9857.S4-004.php?aid=7058?abstract _id=7058. Accessed December 16, 2013.

Q If a pregnant woman has mild hypertension  (eg, 140/90 mm Hg) but no albuminuria, is she at higher risk for kidney disease as she ages?

Gestational hypertension and preeclampsia are two types of hypertension that occur during pregnancy. Both occur after 20 weeks’ gestation and include a blood pressure reading greater than 140/90 mm Hg and no maternal history of hypertension. Proteinuria does not occur in gestational hypertension as it does in preeclampsia (proteinuria ≥ 300 mg in a 24-h urine collection).

One study evaluated more than 26,000 Taiwanese women with hypertension during pregnancy and compared them to more than 200,000 women without hypertension during pregnancy. It was found that hypertension during pregnancy increased the risk for chronic kidney disease (CKD) and end-stage renal disease (ESRD) later in life. Preeclampsia and ­eclampsia were even more likely to increase the risk for ESRD, ­compared with gestational hypertension.¹

Preeclampsia occurs after 20 weeks’ gestation and includes elevated blood pressure (≥ 140 mm Hg systolic or ≥ 90 mm Hg diastolic) and proteinuria (≥ 0.3 g in 24 h).  Severe preeclampsia develops with the addition of worsening hypertension and proteinuria, oliguria less than 500 mL in 24 h, thrombocytopenia, hemolysis, el­e­vated liver enzymes, low platelets, pulmonary edema, and fetal growth restriction. Eclampsia is when seizures occur in addition to preeclampsia.² Gestational hypertension has also been linked with a higher risk for ischemic heart disease, myocardial infarcts and death, heart failure, ischem-
ic stroke, kidney disease, and diabetes.³

Because of the association between hypertension during pregnancy and subsequent development of CKD, it is very important that mothers who have hypertension during pregnancy continue to have their renal function monitored after delivery.

Mandy Trolinger, MS, RD, PA-C

Denver Nephrology
Denver, CO

Personal Note: Mandy is a two-time kidney transplant recipient. She delivered a healthy baby boy in 2012.

REFERENCES

1. Wang I-K, Muo C-H, Liang C-C, et al.  Association between hypertensive disorders during pregnancy and end-stage renal disease: a population-based study. CMAJ. 2013;85: 207-213.

2. McPhee SJ, Papadakis MA, Tierney LM, et al. Current Medical Diagnosis and Treatment. 47th ed. New York, NY: McGraw-Hill/Lange; 2008.

3. Männistö T, Mendola P, Vääräsmäki M, et al. Elevated blood pressure in pregnancy and subsequent chronic disease risk. Circulation. 2013;127:681-690.

4. Nevis IF, Reitsma A, Dominic A, et al. Pregnancy outcomes in women with chronic kidney disease: a systematic review. Clin J Am Soc Nephrol. 2011;6:2587-2598.

5. Hou S. Pregnancy in chronic renal insufficiency and end-stage renal disease. Am J Kidney Dis. 1999;33:235-252.

6. Davison JM. Dialysis, transplantation, and pregnancy. Am J Kidney Dis. 1991;17:127-132.

7. Asamiya Y, Otsubo S, Matsuda Y, et al. The importance of low blood urea nitrogen levels in pregnant patients undergoing hemodialysis to optimize birth weight and gestational age. Kidney Int. 2009;75:1217-1222.

8. Giatras I, Levy DP, Malone FD, et al. Pregnancy during dialysis: case report and management guidelines. Nephrol Dial Transplant. 1998;13:3266-3272.

9. McKay DB, Josephson MA. Pregnancy in recipients of solid organs—effects on mother and child. N Engl J Med. 2006;354:1281-1293.

10. Sifontis NM, Coscia LA, Constantinescu S, et al. Pregnancy outcomes in solid organ transplant recipients with exposure to mycophenolate mofetil or sirolimus. Transplantation. 2006;82:1698-1702.

11. Kainz A, Harabacz I, Cowlrick IS, et al. Review of the course and outcome of 100 pregnancies in 84 women treated with tacrolimus. Transplantation. 2000;70:1718-1721.

12. Josephson MA. Pregnancy in renal transplant recipients: more questions answered, still more asked. Clin J Am Soc Nephrol. 2013;8: 182-183.

Q If a pregnant woman has mild hypertension  (eg, 140/90 mm Hg) but no albuminuria, is she at higher risk for kidney disease as she ages?

Gestational hypertension and preeclampsia are two types of hypertension that occur during pregnancy. Both occur after 20 weeks’ gestation and include a blood pressure reading greater than 140/90 mm Hg and no maternal history of hypertension. Proteinuria does not occur in gestational hypertension as it does in preeclampsia (proteinuria ≥ 300 mg in a 24-h urine collection).

One study evaluated more than 26,000 Taiwanese women with hypertension during pregnancy and compared them to more than 200,000 women without hypertension during pregnancy. It was found that hypertension during pregnancy increased the risk for chronic kidney disease (CKD) and end-stage renal disease (ESRD) later in life. Preeclampsia and ­eclampsia were even more likely to increase the risk for ESRD, ­compared with gestational hypertension.¹

Preeclampsia occurs after 20 weeks’ gestation and includes elevated blood pressure (≥ 140 mm Hg systolic or ≥ 90 mm Hg diastolic) and proteinuria (≥ 0.3 g in 24 h).  Severe preeclampsia develops with the addition of worsening hypertension and proteinuria, oliguria less than 500 mL in 24 h, thrombocytopenia, hemolysis, el­e­vated liver enzymes, low platelets, pulmonary edema, and fetal growth restriction. Eclampsia is when seizures occur in addition to preeclampsia.² Gestational hypertension has also been linked with a higher risk for ischemic heart disease, myocardial infarcts and death, heart failure, ischem-
ic stroke, kidney disease, and diabetes.³

Because of the association between hypertension during pregnancy and subsequent development of CKD, it is very important that mothers who have hypertension during pregnancy continue to have their renal function monitored after delivery.

Mandy Trolinger, MS, RD, PA-C

Denver Nephrology
Denver, CO

Personal Note: Mandy is a two-time kidney transplant recipient. She delivered a healthy baby boy in 2012.

REFERENCES

1. Wang I-K, Muo C-H, Liang C-C, et al.  Association between hypertensive disorders during pregnancy and end-stage renal disease: a population-based study. CMAJ. 2013;85: 207-213.

2. McPhee SJ, Papadakis MA, Tierney LM, et al. Current Medical Diagnosis and Treatment. 47th ed. New York, NY: McGraw-Hill/Lange; 2008.

3. Männistö T, Mendola P, Vääräsmäki M, et al. Elevated blood pressure in pregnancy and subsequent chronic disease risk. Circulation. 2013;127:681-690.

4. Nevis IF, Reitsma A, Dominic A, et al. Pregnancy outcomes in women with chronic kidney disease: a systematic review. Clin J Am Soc Nephrol. 2011;6:2587-2598.

5. Hou S. Pregnancy in chronic renal insufficiency and end-stage renal disease. Am J Kidney Dis. 1999;33:235-252.

6. Davison JM. Dialysis, transplantation, and pregnancy. Am J Kidney Dis. 1991;17:127-132.

7. Asamiya Y, Otsubo S, Matsuda Y, et al. The importance of low blood urea nitrogen levels in pregnant patients undergoing hemodialysis to optimize birth weight and gestational age. Kidney Int. 2009;75:1217-1222.

8. Giatras I, Levy DP, Malone FD, et al. Pregnancy during dialysis: case report and management guidelines. Nephrol Dial Transplant. 1998;13:3266-3272.

9. McKay DB, Josephson MA. Pregnancy in recipients of solid organs—effects on mother and child. N Engl J Med. 2006;354:1281-1293.

10. Sifontis NM, Coscia LA, Constantinescu S, et al. Pregnancy outcomes in solid organ transplant recipients with exposure to mycophenolate mofetil or sirolimus. Transplantation. 2006;82:1698-1702.

11. Kainz A, Harabacz I, Cowlrick IS, et al. Review of the course and outcome of 100 pregnancies in 84 women treated with tacrolimus. Transplantation. 2000;70:1718-1721.

12. Josephson MA. Pregnancy in renal transplant recipients: more questions answered, still more asked. Clin J Am Soc Nephrol. 2013;8: 182-183.

Q If a pregnant woman has mild hypertension  (eg, 140/90 mm Hg) but no albuminuria, is she at higher risk for kidney disease as she ages?

Gestational hypertension and preeclampsia are two types of hypertension that occur during pregnancy. Both occur after 20 weeks’ gestation and include a blood pressure reading greater than 140/90 mm Hg and no maternal history of hypertension. Proteinuria does not occur in gestational hypertension as it does in preeclampsia (proteinuria ≥ 300 mg in a 24-h urine collection).

One study evaluated more than 26,000 Taiwanese women with hypertension during pregnancy and compared them to more than 200,000 women without hypertension during pregnancy. It was found that hypertension during pregnancy increased the risk for chronic kidney disease (CKD) and end-stage renal disease (ESRD) later in life. Preeclampsia and ­eclampsia were even more likely to increase the risk for ESRD, ­compared with gestational hypertension.¹

Preeclampsia occurs after 20 weeks’ gestation and includes elevated blood pressure (≥ 140 mm Hg systolic or ≥ 90 mm Hg diastolic) and proteinuria (≥ 0.3 g in 24 h).  Severe preeclampsia develops with the addition of worsening hypertension and proteinuria, oliguria less than 500 mL in 24 h, thrombocytopenia, hemolysis, el­e­vated liver enzymes, low platelets, pulmonary edema, and fetal growth restriction. Eclampsia is when seizures occur in addition to preeclampsia.² Gestational hypertension has also been linked with a higher risk for ischemic heart disease, myocardial infarcts and death, heart failure, ischem-
ic stroke, kidney disease, and diabetes.³

Because of the association between hypertension during pregnancy and subsequent development of CKD, it is very important that mothers who have hypertension during pregnancy continue to have their renal function monitored after delivery.

Mandy Trolinger, MS, RD, PA-C

Denver Nephrology
Denver, CO

Personal Note: Mandy is a two-time kidney transplant recipient. She delivered a healthy baby boy in 2012.

REFERENCES

1. Wang I-K, Muo C-H, Liang C-C, et al.  Association between hypertensive disorders during pregnancy and end-stage renal disease: a population-based study. CMAJ. 2013;85: 207-213.

2. McPhee SJ, Papadakis MA, Tierney LM, et al. Current Medical Diagnosis and Treatment. 47th ed. New York, NY: McGraw-Hill/Lange; 2008.

3. Männistö T, Mendola P, Vääräsmäki M, et al. Elevated blood pressure in pregnancy and subsequent chronic disease risk. Circulation. 2013;127:681-690.

4. Nevis IF, Reitsma A, Dominic A, et al. Pregnancy outcomes in women with chronic kidney disease: a systematic review. Clin J Am Soc Nephrol. 2011;6:2587-2598.

5. Hou S. Pregnancy in chronic renal insufficiency and end-stage renal disease. Am J Kidney Dis. 1999;33:235-252.

6. Davison JM. Dialysis, transplantation, and pregnancy. Am J Kidney Dis. 1991;17:127-132.

7. Asamiya Y, Otsubo S, Matsuda Y, et al. The importance of low blood urea nitrogen levels in pregnant patients undergoing hemodialysis to optimize birth weight and gestational age. Kidney Int. 2009;75:1217-1222.

8. Giatras I, Levy DP, Malone FD, et al. Pregnancy during dialysis: case report and management guidelines. Nephrol Dial Transplant. 1998;13:3266-3272.

9. McKay DB, Josephson MA. Pregnancy in recipients of solid organs—effects on mother and child. N Engl J Med. 2006;354:1281-1293.

10. Sifontis NM, Coscia LA, Constantinescu S, et al. Pregnancy outcomes in solid organ transplant recipients with exposure to mycophenolate mofetil or sirolimus. Transplantation. 2006;82:1698-1702.

11. Kainz A, Harabacz I, Cowlrick IS, et al. Review of the course and outcome of 100 pregnancies in 84 women treated with tacrolimus. Transplantation. 2000;70:1718-1721.

12. Josephson MA. Pregnancy in renal transplant recipients: more questions answered, still more asked. Clin J Am Soc Nephrol. 2013;8: 182-183.

Q) I was having a “discussion” over lunch about CKD, pregnancy, and transplant. I said that dialysis patients cannot get pregnant, but someone said I was wrong. A friend said that transplant patients should not get pregnant because of the toxicity of the immunosuppressant medications they take, but another practitioner said that was in the “olden days.” What is the current state of the CKD, dialysis, and transplant patient and pregnancy? 

The first healthy baby delivered by a pregnant kidney transplant patient was born in 1958. With the advances in treatment of kidney disease, we are now seeing more pregnancies in these patients. However, they are still considered high risk and should be monitored by a transplant nephrologist and a high-risk obstetrician.⁴

 CKD patients (not on dialysis) are at increased risk for pregnancy complications. Maternal risks include gestational hypertension, preeclampsia/eclampsia, ESRD, or death. Fetal complications include prematurity, small-for-gestational-age babies, and stillbirth. It is very important to control hypertension because it is directly linked to fetal outcome; however, not all blood pressure medications are safe in pregnancy. ACE inhibitors, for example, are teratogenic and absolutely contraindicated.⁴

Fertility is decreased in dialysis patients; however, pregnancy occurs in 0.3% to 1.5% of women of childbearing age on dialysis. Pregnancy should be confirmed with an ultrasound because serum β-human chorionic gonadotropin can be falsely elevated in ESRD.⁵

It also can be difficult to monitor pregnancy weight gain due to fluid gains between dialysis treatments. Dialysis prescriptions should be increased either in time or frequency (or both), with a goal of keeping the blood urea nitrogen concentration below 50 mg/dL to improve maternal and fetal outcomes.^6,7 Other important factors to control are metabolic acidosis, hypocalcemia, and anemia (increased erythropoietin-stimulating agents may be needed). Frequent uterine and fetal monitoring is also indicated to prevent preterm labor due to the dialysis process. Preeclampsia, prematurity, low birth weight, and hypertension are the most common risks in these pregnancies.⁸

Renal transplantation often returns fertility to normal and allows pregnancy to occur; however, it is recommended that female patients wait until one year post-transplant if the transplanted kidney is from a living related donor (two years if from a deceased donor), have a serum creatinine level less than 1.5 mg/dL, and a urinary protein level less than 500 mg/d.⁹ The immunosuppression regimen usually needs adjustment because certain immunosuppressants are contraindicated in pregnancy and have been linked to teratogenic effects; however, data is still limited in this area.^10,11 Pregnant transplant recipients are at higher risk for preeclampsia, gestational diabetes, preterm delivery, small-for-gestational-age babies, miscarriage, stillbirth, neonatal death, and congenital abnormalities.¹²

The National Transplantation Pregnancy Registry (www.ntpr.giftoflifeinstitute.org/) is an ongoing registry in the United States that reports on transplant pregnancies and their outcomes.  Data collected by the registry show that there have been many healthy pregnancies without any adverse maternal or fetal outcomes among transplant recipients.

Mandy Trolinger, MS, RD, PA-C

Denver Nephrology
Denver, CO

Personal Note: Mandy is a two-time kidney transplant recipient. She delivered a healthy baby boy in 2012.

REFERENCES

1. Wang I-K, Muo C-H, Liang C-C, et al.  Association between hypertensive disorders during pregnancy and end-stage renal disease: a population-based study. CMAJ. 2013;85: 207-213.

2. McPhee SJ, Papadakis MA, Tierney LM, et al. Current Medical Diagnosis and Treatment. 47th ed. New York, NY: McGraw-Hill/Lange; 2008.

3. Männistö T, Mendola P, Vääräsmäki M, et al. Elevated blood pressure in pregnancy and subsequent chronic disease risk. Circulation. 2013;127:681-690.

4. Nevis IF, Reitsma A, Dominic A, et al. Pregnancy outcomes in women with chronic kidney disease: a systematic review. Clin J Am Soc Nephrol. 2011;6:2587-2598.

5. Hou S. Pregnancy in chronic renal insufficiency and end-stage renal disease. Am J Kidney Dis. 1999;33:235-252.

6. Davison JM. Dialysis, transplantation, and pregnancy. Am J Kidney Dis. 1991;17:127-132.

7. Asamiya Y, Otsubo S, Matsuda Y, et al. The importance of low blood urea nitrogen levels in pregnant patients undergoing hemodialysis to optimize birth weight and gestational age. Kidney Int. 2009;75:1217-1222.

8. Giatras I, Levy DP, Malone FD, et al. Pregnancy during dialysis: case report and management guidelines. Nephrol Dial Transplant. 1998;13:3266-3272.

9. McKay DB, Josephson MA. Pregnancy in recipients of solid organs—effects on mother and child. N Engl J Med. 2006;354:1281-1293.

10. Sifontis NM, Coscia LA, Constantinescu S, et al. Pregnancy outcomes in solid organ transplant recipients with exposure to mycophenolate mofetil or sirolimus. Transplantation. 2006;82:1698-1702.

11. Kainz A, Harabacz I, Cowlrick IS, et al. Review of the course and outcome of 100 pregnancies in 84 women treated with tacrolimus. Transplantation. 2000;70:1718-1721.

12. Josephson MA. Pregnancy in renal transplant recipients: more questions answered, still more asked. Clin J Am Soc Nephrol. 2013;8: 182-183.

Q) I was having a “discussion” over lunch about CKD, pregnancy, and transplant. I said that dialysis patients cannot get pregnant, but someone said I was wrong. A friend said that transplant patients should not get pregnant because of the toxicity of the immunosuppressant medications they take, but another practitioner said that was in the “olden days.” What is the current state of the CKD, dialysis, and transplant patient and pregnancy? 

The first healthy baby delivered by a pregnant kidney transplant patient was born in 1958. With the advances in treatment of kidney disease, we are now seeing more pregnancies in these patients. However, they are still considered high risk and should be monitored by a transplant nephrologist and a high-risk obstetrician.⁴

 CKD patients (not on dialysis) are at increased risk for pregnancy complications. Maternal risks include gestational hypertension, preeclampsia/eclampsia, ESRD, or death. Fetal complications include prematurity, small-for-gestational-age babies, and stillbirth. It is very important to control hypertension because it is directly linked to fetal outcome; however, not all blood pressure medications are safe in pregnancy. ACE inhibitors, for example, are teratogenic and absolutely contraindicated.⁴

Fertility is decreased in dialysis patients; however, pregnancy occurs in 0.3% to 1.5% of women of childbearing age on dialysis. Pregnancy should be confirmed with an ultrasound because serum β-human chorionic gonadotropin can be falsely elevated in ESRD.⁵

It also can be difficult to monitor pregnancy weight gain due to fluid gains between dialysis treatments. Dialysis prescriptions should be increased either in time or frequency (or both), with a goal of keeping the blood urea nitrogen concentration below 50 mg/dL to improve maternal and fetal outcomes.^6,7 Other important factors to control are metabolic acidosis, hypocalcemia, and anemia (increased erythropoietin-stimulating agents may be needed). Frequent uterine and fetal monitoring is also indicated to prevent preterm labor due to the dialysis process. Preeclampsia, prematurity, low birth weight, and hypertension are the most common risks in these pregnancies.⁸

Renal transplantation often returns fertility to normal and allows pregnancy to occur; however, it is recommended that female patients wait until one year post-transplant if the transplanted kidney is from a living related donor (two years if from a deceased donor), have a serum creatinine level less than 1.5 mg/dL, and a urinary protein level less than 500 mg/d.⁹ The immunosuppression regimen usually needs adjustment because certain immunosuppressants are contraindicated in pregnancy and have been linked to teratogenic effects; however, data is still limited in this area.^10,11 Pregnant transplant recipients are at higher risk for preeclampsia, gestational diabetes, preterm delivery, small-for-gestational-age babies, miscarriage, stillbirth, neonatal death, and congenital abnormalities.¹²

The National Transplantation Pregnancy Registry (www.ntpr.giftoflifeinstitute.org/) is an ongoing registry in the United States that reports on transplant pregnancies and their outcomes.  Data collected by the registry show that there have been many healthy pregnancies without any adverse maternal or fetal outcomes among transplant recipients.

Mandy Trolinger, MS, RD, PA-C

Denver Nephrology
Denver, CO

Personal Note: Mandy is a two-time kidney transplant recipient. She delivered a healthy baby boy in 2012.

REFERENCES

1. Wang I-K, Muo C-H, Liang C-C, et al.  Association between hypertensive disorders during pregnancy and end-stage renal disease: a population-based study. CMAJ. 2013;85: 207-213.

2. McPhee SJ, Papadakis MA, Tierney LM, et al. Current Medical Diagnosis and Treatment. 47th ed. New York, NY: McGraw-Hill/Lange; 2008.

3. Männistö T, Mendola P, Vääräsmäki M, et al. Elevated blood pressure in pregnancy and subsequent chronic disease risk. Circulation. 2013;127:681-690.

4. Nevis IF, Reitsma A, Dominic A, et al. Pregnancy outcomes in women with chronic kidney disease: a systematic review. Clin J Am Soc Nephrol. 2011;6:2587-2598.

5. Hou S. Pregnancy in chronic renal insufficiency and end-stage renal disease. Am J Kidney Dis. 1999;33:235-252.

6. Davison JM. Dialysis, transplantation, and pregnancy. Am J Kidney Dis. 1991;17:127-132.

7. Asamiya Y, Otsubo S, Matsuda Y, et al. The importance of low blood urea nitrogen levels in pregnant patients undergoing hemodialysis to optimize birth weight and gestational age. Kidney Int. 2009;75:1217-1222.

8. Giatras I, Levy DP, Malone FD, et al. Pregnancy during dialysis: case report and management guidelines. Nephrol Dial Transplant. 1998;13:3266-3272.

9. McKay DB, Josephson MA. Pregnancy in recipients of solid organs—effects on mother and child. N Engl J Med. 2006;354:1281-1293.

10. Sifontis NM, Coscia LA, Constantinescu S, et al. Pregnancy outcomes in solid organ transplant recipients with exposure to mycophenolate mofetil or sirolimus. Transplantation. 2006;82:1698-1702.

11. Kainz A, Harabacz I, Cowlrick IS, et al. Review of the course and outcome of 100 pregnancies in 84 women treated with tacrolimus. Transplantation. 2000;70:1718-1721.

12. Josephson MA. Pregnancy in renal transplant recipients: more questions answered, still more asked. Clin J Am Soc Nephrol. 2013;8: 182-183.

Q) I was having a “discussion” over lunch about CKD, pregnancy, and transplant. I said that dialysis patients cannot get pregnant, but someone said I was wrong. A friend said that transplant patients should not get pregnant because of the toxicity of the immunosuppressant medications they take, but another practitioner said that was in the “olden days.” What is the current state of the CKD, dialysis, and transplant patient and pregnancy? 

The first healthy baby delivered by a pregnant kidney transplant patient was born in 1958. With the advances in treatment of kidney disease, we are now seeing more pregnancies in these patients. However, they are still considered high risk and should be monitored by a transplant nephrologist and a high-risk obstetrician.⁴

 CKD patients (not on dialysis) are at increased risk for pregnancy complications. Maternal risks include gestational hypertension, preeclampsia/eclampsia, ESRD, or death. Fetal complications include prematurity, small-for-gestational-age babies, and stillbirth. It is very important to control hypertension because it is directly linked to fetal outcome; however, not all blood pressure medications are safe in pregnancy. ACE inhibitors, for example, are teratogenic and absolutely contraindicated.⁴

Fertility is decreased in dialysis patients; however, pregnancy occurs in 0.3% to 1.5% of women of childbearing age on dialysis. Pregnancy should be confirmed with an ultrasound because serum β-human chorionic gonadotropin can be falsely elevated in ESRD.⁵

It also can be difficult to monitor pregnancy weight gain due to fluid gains between dialysis treatments. Dialysis prescriptions should be increased either in time or frequency (or both), with a goal of keeping the blood urea nitrogen concentration below 50 mg/dL to improve maternal and fetal outcomes.^6,7 Other important factors to control are metabolic acidosis, hypocalcemia, and anemia (increased erythropoietin-stimulating agents may be needed). Frequent uterine and fetal monitoring is also indicated to prevent preterm labor due to the dialysis process. Preeclampsia, prematurity, low birth weight, and hypertension are the most common risks in these pregnancies.⁸

Renal transplantation often returns fertility to normal and allows pregnancy to occur; however, it is recommended that female patients wait until one year post-transplant if the transplanted kidney is from a living related donor (two years if from a deceased donor), have a serum creatinine level less than 1.5 mg/dL, and a urinary protein level less than 500 mg/d.⁹ The immunosuppression regimen usually needs adjustment because certain immunosuppressants are contraindicated in pregnancy and have been linked to teratogenic effects; however, data is still limited in this area.^10,11 Pregnant transplant recipients are at higher risk for preeclampsia, gestational diabetes, preterm delivery, small-for-gestational-age babies, miscarriage, stillbirth, neonatal death, and congenital abnormalities.¹²

The National Transplantation Pregnancy Registry (www.ntpr.giftoflifeinstitute.org/) is an ongoing registry in the United States that reports on transplant pregnancies and their outcomes.  Data collected by the registry show that there have been many healthy pregnancies without any adverse maternal or fetal outcomes among transplant recipients.

Mandy Trolinger, MS, RD, PA-C

Denver Nephrology
Denver, CO

Personal Note: Mandy is a two-time kidney transplant recipient. She delivered a healthy baby boy in 2012.

REFERENCES

1. Wang I-K, Muo C-H, Liang C-C, et al.  Association between hypertensive disorders during pregnancy and end-stage renal disease: a population-based study. CMAJ. 2013;85: 207-213.

2. McPhee SJ, Papadakis MA, Tierney LM, et al. Current Medical Diagnosis and Treatment. 47th ed. New York, NY: McGraw-Hill/Lange; 2008.

3. Männistö T, Mendola P, Vääräsmäki M, et al. Elevated blood pressure in pregnancy and subsequent chronic disease risk. Circulation. 2013;127:681-690.

4. Nevis IF, Reitsma A, Dominic A, et al. Pregnancy outcomes in women with chronic kidney disease: a systematic review. Clin J Am Soc Nephrol. 2011;6:2587-2598.

5. Hou S. Pregnancy in chronic renal insufficiency and end-stage renal disease. Am J Kidney Dis. 1999;33:235-252.

6. Davison JM. Dialysis, transplantation, and pregnancy. Am J Kidney Dis. 1991;17:127-132.

7. Asamiya Y, Otsubo S, Matsuda Y, et al. The importance of low blood urea nitrogen levels in pregnant patients undergoing hemodialysis to optimize birth weight and gestational age. Kidney Int. 2009;75:1217-1222.

8. Giatras I, Levy DP, Malone FD, et al. Pregnancy during dialysis: case report and management guidelines. Nephrol Dial Transplant. 1998;13:3266-3272.

9. McKay DB, Josephson MA. Pregnancy in recipients of solid organs—effects on mother and child. N Engl J Med. 2006;354:1281-1293.

10. Sifontis NM, Coscia LA, Constantinescu S, et al. Pregnancy outcomes in solid organ transplant recipients with exposure to mycophenolate mofetil or sirolimus. Transplantation. 2006;82:1698-1702.

11. Kainz A, Harabacz I, Cowlrick IS, et al. Review of the course and outcome of 100 pregnancies in 84 women treated with tacrolimus. Transplantation. 2000;70:1718-1721.

12. Josephson MA. Pregnancy in renal transplant recipients: more questions answered, still more asked. Clin J Am Soc Nephrol. 2013;8: 182-183.