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Predictors of hyperkalemia risk after hypertension control with aldosterone blockade according to the presence or absence of chronic kidney disease.
BACKGROUND/AIMS: Aldosterone antagonists have been proven to be efficient in the management of hypertension and the reduction of proteinuria; however, they are not widely used because of the risk of hyperkalemia. We assessed the predictors of hyperkalemia risk following hypertension control using aldosterone blockade in the presence or absence of chronic kidney disease (CKD).
METHODS: A total of 6,575 patients with hypertension treated between January 1, 2000, and November 30, 2012, were evaluated for the safety of an aldosterone-blocking agent (spironolactone) added to preexisting blood pressure-lowering regimens. Hyperkalemia was defined as a serum potassium level ≥5.0 mEq/l. All patients used 3 mechanistically complementary antihypertensive agents, including a diuretic and a RAAS blocker. Patients were evaluated after 4 and 8 weeks of treatment. The incidence of hyperkalemia, significant renal dysfunction [a reduction of the estimated glomerular filtration rate (eGFR) ≥30%], and adverse effects was assessed.
RESULTS: The incidence of hyperkalemia in the presence or absence of CKD was 50.4 and 42.6% after 4 weeks (p = 0.001) and 3.8 and 3.0% after 8 weeks, respectively (p = 0.371). A logistic regression analysis revealed that medication, CKD, basal hyperkalemia, reduction in eGFR, and diabetes were all predictive of a hyperkalemia risk following spironolactone use.
CONCLUSION: Spironolactone was well tolerated by selected CKD patients. The risk of serious hyperkalemia or a significant reduction of eGFR appears to be low. Strict monitoring over the first month of treatment followed by standard surveillance for angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers is suggested.
METHODS: A total of 6,575 patients with hypertension treated between January 1, 2000, and November 30, 2012, were evaluated for the safety of an aldosterone-blocking agent (spironolactone) added to preexisting blood pressure-lowering regimens. Hyperkalemia was defined as a serum potassium level ≥5.0 mEq/l. All patients used 3 mechanistically complementary antihypertensive agents, including a diuretic and a RAAS blocker. Patients were evaluated after 4 and 8 weeks of treatment. The incidence of hyperkalemia, significant renal dysfunction [a reduction of the estimated glomerular filtration rate (eGFR) ≥30%], and adverse effects was assessed.
RESULTS: The incidence of hyperkalemia in the presence or absence of CKD was 50.4 and 42.6% after 4 weeks (p = 0.001) and 3.8 and 3.0% after 8 weeks, respectively (p = 0.371). A logistic regression analysis revealed that medication, CKD, basal hyperkalemia, reduction in eGFR, and diabetes were all predictive of a hyperkalemia risk following spironolactone use.
CONCLUSION: Spironolactone was well tolerated by selected CKD patients. The risk of serious hyperkalemia or a significant reduction of eGFR appears to be low. Strict monitoring over the first month of treatment followed by standard surveillance for angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers is suggested.
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