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Can African-American Patients Take Metoprolol?
Q) One of the physicians in my practice won't use metoprolol in African-American patients. He says it causes kidney disease. Is it right, or is this an old wives' tale?
There are multiple concerns with the use of metoprolol specifically—this does not apply to all ß-blockers—in the African-American population. The main concerns are
- Lack of effective blood pressure control, compared to angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers (CCBs)
- No observable reduction in proteinuria
- The possibility of a significant increase in uric acid.
Most of the evidence-based guidelines for care of hypertensive nephrosclerosis in the African-American population were derived from the African-American Study of Kidney Disease and Hypertension (AASK) trial. This large-scale, multicenter, randomized, double-blinded study from the National Institute of Health had multiple arms to compare an ACE inhibitor (ramipril) to a CCB (amlodipine) or a ß-blocker (metoprolol) in the nondiabetic African-American population.1
In a subgroup analysis, more than 1,000 subjects with hypertensive nephrosclerosis were followed for four years, with serial glomerular filtration rate (GFR) measurements taken. Treatment with ACE inhibitors was shown to be superior to CCB and ß-blockers for hypertension and proteinuria control.1
One important take-away from the AASK trial has been that strict blood pressure control is not enough to improve kidney outcomes. Proteinuria (albuminuria) must also be controlled.1
Continue to: In a subsequent secondary analysis
In a subsequent secondary analysis of data from the AASK study, Juraschek et al showed that metoprolol significantly increased serum uric acid in African-American adults.2 It is known that hyperuricemia (> 6 mg/dL) can cause a decline in kidney function.3
Furthermore, uric acid may be a strong prognostic factor for chronic kidney disease (CKD) progression. (This association, however, remains controversial. One recent study showed that, while hyperuricemia is associated with higher risk for kidney failure, the relationship was not parallel in CKD stage 3 or 4 [GFR ≤ 60 mL/min]).4 In fact, taking uric acid–lowering medications did not slow progression of kidney disease.
In other words, your colleague seems to believe that since A (metoprolol) leads to B (hyperuricemia) and B (hyperuricemia) leads to C (kidney disease), then A leads to C. While the theory is undoubtedly logical, we have no proof that metoprolol causes increased kidney disease in African-American patients.
What we do know, thanks to AASK, is that an African-American patient with kidney disease should be treated with a diuretic and/or an ACE inhibitor as initial therapy. Furthermore, we have a blood pressure goal: < 130/80 mm Hg. And we know that CCBs are most effective for African-American patients who do not have kidney disease.5—BWM
Barbara Weis Malone, DNP, FNP-C, FNKF
Assistant Professor
Adult/Gerontology NP Program, College of Nursing
Nurse Practitioner
School of Medicine, University of Colorado Anschutz Medical Campus
1. Toto RD. Lessons from the African-American Study of Kidney Disease and Hypertension: an update. Curr Hypertens Rep. 2006;8(5):409-412.
2. Juraschek SP, Appel LJ, Miller ER III. Metoprolol increases uric acid and risk of gout in African Americans with chronic kidney disease attributed to hypertension. Am J Hypertens. 2017; 30(9):871-875.
3. Tsai C-W, Lin S-Y, Kuo C-C, Huang C-C. Serum uric acid and progression of kidney disease: a longitudinal analysis and mini-review. PLoS One. 2017;12(1):e0170393.
4. Rincon-Choles H, Jolly SE, Arrigain S, et al. Impact of uric acid levels on kidney disease progression. Am J Nephrol. 2017;46(4):315-322.
5. Armstrong C. JNC8 guidelines for the management of hypertension in adults. Am Fam Physician. 2014;90(7):503-504.
Clinician Reviews in partnership with
Renal Consult is edited by Jane S. Davis, CRNP, DNP, a member of the Clinician Reviews editorial board, who is a nurse practitioner in the Division of Nephrology at the University of Alabama at Birmingham and is the communications chairperson for the National Kidney Foundation's Council of Advanced Practitioners (NKF-CAP); and Kim Zuber, PA-C, MSPS, DFAAPA, a semi-retired PA who works with the American Academy of Nephrology PAs and is a past chair of the NKF-CAP. This month's responses were authored by Danielle S. Wentworth, MSN, FNP-BC, who practices in the Division of Nephrology at the University of Virginia Health System in Charlottesville, and Barbara Weis Malone, DNP, FNP-C, FNKF, who is an Assistant Professor in the Adult/Gerontology NP Program in the College of Nursing, and a Nurse Practitioner in the School of Medicine, at the University of Colorado Anschutz Medical Campus.
Clinician Reviews in partnership with
Renal Consult is edited by Jane S. Davis, CRNP, DNP, a member of the Clinician Reviews editorial board, who is a nurse practitioner in the Division of Nephrology at the University of Alabama at Birmingham and is the communications chairperson for the National Kidney Foundation's Council of Advanced Practitioners (NKF-CAP); and Kim Zuber, PA-C, MSPS, DFAAPA, a semi-retired PA who works with the American Academy of Nephrology PAs and is a past chair of the NKF-CAP. This month's responses were authored by Danielle S. Wentworth, MSN, FNP-BC, who practices in the Division of Nephrology at the University of Virginia Health System in Charlottesville, and Barbara Weis Malone, DNP, FNP-C, FNKF, who is an Assistant Professor in the Adult/Gerontology NP Program in the College of Nursing, and a Nurse Practitioner in the School of Medicine, at the University of Colorado Anschutz Medical Campus.
Clinician Reviews in partnership with
Renal Consult is edited by Jane S. Davis, CRNP, DNP, a member of the Clinician Reviews editorial board, who is a nurse practitioner in the Division of Nephrology at the University of Alabama at Birmingham and is the communications chairperson for the National Kidney Foundation's Council of Advanced Practitioners (NKF-CAP); and Kim Zuber, PA-C, MSPS, DFAAPA, a semi-retired PA who works with the American Academy of Nephrology PAs and is a past chair of the NKF-CAP. This month's responses were authored by Danielle S. Wentworth, MSN, FNP-BC, who practices in the Division of Nephrology at the University of Virginia Health System in Charlottesville, and Barbara Weis Malone, DNP, FNP-C, FNKF, who is an Assistant Professor in the Adult/Gerontology NP Program in the College of Nursing, and a Nurse Practitioner in the School of Medicine, at the University of Colorado Anschutz Medical Campus.
Q) One of the physicians in my practice won't use metoprolol in African-American patients. He says it causes kidney disease. Is it right, or is this an old wives' tale?
There are multiple concerns with the use of metoprolol specifically—this does not apply to all ß-blockers—in the African-American population. The main concerns are
- Lack of effective blood pressure control, compared to angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers (CCBs)
- No observable reduction in proteinuria
- The possibility of a significant increase in uric acid.
Most of the evidence-based guidelines for care of hypertensive nephrosclerosis in the African-American population were derived from the African-American Study of Kidney Disease and Hypertension (AASK) trial. This large-scale, multicenter, randomized, double-blinded study from the National Institute of Health had multiple arms to compare an ACE inhibitor (ramipril) to a CCB (amlodipine) or a ß-blocker (metoprolol) in the nondiabetic African-American population.1
In a subgroup analysis, more than 1,000 subjects with hypertensive nephrosclerosis were followed for four years, with serial glomerular filtration rate (GFR) measurements taken. Treatment with ACE inhibitors was shown to be superior to CCB and ß-blockers for hypertension and proteinuria control.1
One important take-away from the AASK trial has been that strict blood pressure control is not enough to improve kidney outcomes. Proteinuria (albuminuria) must also be controlled.1
Continue to: In a subsequent secondary analysis
In a subsequent secondary analysis of data from the AASK study, Juraschek et al showed that metoprolol significantly increased serum uric acid in African-American adults.2 It is known that hyperuricemia (> 6 mg/dL) can cause a decline in kidney function.3
Furthermore, uric acid may be a strong prognostic factor for chronic kidney disease (CKD) progression. (This association, however, remains controversial. One recent study showed that, while hyperuricemia is associated with higher risk for kidney failure, the relationship was not parallel in CKD stage 3 or 4 [GFR ≤ 60 mL/min]).4 In fact, taking uric acid–lowering medications did not slow progression of kidney disease.
In other words, your colleague seems to believe that since A (metoprolol) leads to B (hyperuricemia) and B (hyperuricemia) leads to C (kidney disease), then A leads to C. While the theory is undoubtedly logical, we have no proof that metoprolol causes increased kidney disease in African-American patients.
What we do know, thanks to AASK, is that an African-American patient with kidney disease should be treated with a diuretic and/or an ACE inhibitor as initial therapy. Furthermore, we have a blood pressure goal: < 130/80 mm Hg. And we know that CCBs are most effective for African-American patients who do not have kidney disease.5—BWM
Barbara Weis Malone, DNP, FNP-C, FNKF
Assistant Professor
Adult/Gerontology NP Program, College of Nursing
Nurse Practitioner
School of Medicine, University of Colorado Anschutz Medical Campus
Q) One of the physicians in my practice won't use metoprolol in African-American patients. He says it causes kidney disease. Is it right, or is this an old wives' tale?
There are multiple concerns with the use of metoprolol specifically—this does not apply to all ß-blockers—in the African-American population. The main concerns are
- Lack of effective blood pressure control, compared to angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers (CCBs)
- No observable reduction in proteinuria
- The possibility of a significant increase in uric acid.
Most of the evidence-based guidelines for care of hypertensive nephrosclerosis in the African-American population were derived from the African-American Study of Kidney Disease and Hypertension (AASK) trial. This large-scale, multicenter, randomized, double-blinded study from the National Institute of Health had multiple arms to compare an ACE inhibitor (ramipril) to a CCB (amlodipine) or a ß-blocker (metoprolol) in the nondiabetic African-American population.1
In a subgroup analysis, more than 1,000 subjects with hypertensive nephrosclerosis were followed for four years, with serial glomerular filtration rate (GFR) measurements taken. Treatment with ACE inhibitors was shown to be superior to CCB and ß-blockers for hypertension and proteinuria control.1
One important take-away from the AASK trial has been that strict blood pressure control is not enough to improve kidney outcomes. Proteinuria (albuminuria) must also be controlled.1
Continue to: In a subsequent secondary analysis
In a subsequent secondary analysis of data from the AASK study, Juraschek et al showed that metoprolol significantly increased serum uric acid in African-American adults.2 It is known that hyperuricemia (> 6 mg/dL) can cause a decline in kidney function.3
Furthermore, uric acid may be a strong prognostic factor for chronic kidney disease (CKD) progression. (This association, however, remains controversial. One recent study showed that, while hyperuricemia is associated with higher risk for kidney failure, the relationship was not parallel in CKD stage 3 or 4 [GFR ≤ 60 mL/min]).4 In fact, taking uric acid–lowering medications did not slow progression of kidney disease.
In other words, your colleague seems to believe that since A (metoprolol) leads to B (hyperuricemia) and B (hyperuricemia) leads to C (kidney disease), then A leads to C. While the theory is undoubtedly logical, we have no proof that metoprolol causes increased kidney disease in African-American patients.
What we do know, thanks to AASK, is that an African-American patient with kidney disease should be treated with a diuretic and/or an ACE inhibitor as initial therapy. Furthermore, we have a blood pressure goal: < 130/80 mm Hg. And we know that CCBs are most effective for African-American patients who do not have kidney disease.5—BWM
Barbara Weis Malone, DNP, FNP-C, FNKF
Assistant Professor
Adult/Gerontology NP Program, College of Nursing
Nurse Practitioner
School of Medicine, University of Colorado Anschutz Medical Campus
1. Toto RD. Lessons from the African-American Study of Kidney Disease and Hypertension: an update. Curr Hypertens Rep. 2006;8(5):409-412.
2. Juraschek SP, Appel LJ, Miller ER III. Metoprolol increases uric acid and risk of gout in African Americans with chronic kidney disease attributed to hypertension. Am J Hypertens. 2017; 30(9):871-875.
3. Tsai C-W, Lin S-Y, Kuo C-C, Huang C-C. Serum uric acid and progression of kidney disease: a longitudinal analysis and mini-review. PLoS One. 2017;12(1):e0170393.
4. Rincon-Choles H, Jolly SE, Arrigain S, et al. Impact of uric acid levels on kidney disease progression. Am J Nephrol. 2017;46(4):315-322.
5. Armstrong C. JNC8 guidelines for the management of hypertension in adults. Am Fam Physician. 2014;90(7):503-504.
1. Toto RD. Lessons from the African-American Study of Kidney Disease and Hypertension: an update. Curr Hypertens Rep. 2006;8(5):409-412.
2. Juraschek SP, Appel LJ, Miller ER III. Metoprolol increases uric acid and risk of gout in African Americans with chronic kidney disease attributed to hypertension. Am J Hypertens. 2017; 30(9):871-875.
3. Tsai C-W, Lin S-Y, Kuo C-C, Huang C-C. Serum uric acid and progression of kidney disease: a longitudinal analysis and mini-review. PLoS One. 2017;12(1):e0170393.
4. Rincon-Choles H, Jolly SE, Arrigain S, et al. Impact of uric acid levels on kidney disease progression. Am J Nephrol. 2017;46(4):315-322.
5. Armstrong C. JNC8 guidelines for the management of hypertension in adults. Am Fam Physician. 2014;90(7):503-504.
