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Management Specifics in Kidney Disease: Rise in SCr

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.

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Kim Zuber, PA-C, MSPS, DFAAPA, Jane S. Davis, CRNP, DNP, Department Editors

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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.

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