Tamirisa, K. P., Aaronson, K. D. & Koelling, T. K. Spironolactone-induced renal insufficiency and hyperkalemia in patients with heart failure. Am. Heart J. 148, 971-978
ABSTRACT A previous randomized controlled trial evaluating the use of spironolactone in heart failure patients reported a low risk of hyperkalemia (2%) and renal insufficiency (0%). Because treatments for heart failure have changed since the benefits of spironolactone were reported, the prevalence of these complications may differ in current clinical practice. We therefore sought to determine the prevalence and clinical associations of hyperkalemia and renal insufficiency in heart failure patients treated with spironolactone.
We performed a case control study of heart failure patients treated with spironolactone in our clinical practice. Cases were patients who developed hyperkalemia (K(+) >5.0 mEq/L) or renal insufficiency (Cr >or=2.5 mg/dL), and they were compared to 2 randomly selected controls per case. Clinical characteristics, medications, and serum chemistries at baseline and follow-up time periods were compared.
Sixty-seven of 926 patients (7.2%) required discontinuation of spironolactone due to hyperkalemia (n = 33) or renal failure (n = 34). Patients who developed hyperkalemia were older and more likely to have diabetes, had higher baseline serum potassium levels and lower baseline potassium supplement doses, and were more likely to be treated with beta-blockers than controls (n = 134). Patients who developed renal insufficiency had lower baseline body weight and higher baseline serum creatinine, required higher doses of loop diuretics, and were more likely to be treated with thiazide diuretics than controls.
Spironolactone-induced hyperkalemia and renal insufficiency are more common in our clinical experience than reported previously. This difference is explained by patient comorbidities and more frequent use of beta-blockers.
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- "Hyperkalemia and worsening renal function are serious adverse effects of MRAs, which are contraindicated in such cases according to current guidelines. These events are highly variable and are associated with advanced age, higher baseline potassium levels, decreased baseline renal function, diabetes mellitus and other treatments affecting potassium levels  . Rates of hyperkalemia admissions and mortality were increased following RALES publication , which could also be attributed to the increasing utilization of β-blockers at that time. "
ABSTRACT: Following the EPHESUS trial in 2003, mineralocorticoid receptor antagonist (MRA) therapy received a class I indication for the management of eligible high-risk post-MI patients. Our goal was to examine temporal trends in MRA use in eligible post-myocardial infarction (MI) patients. We investigated temporal trends and factors associated with MRA utilization among eligible patients enrolled in the biannual Acute Coronary Syndrome Israeli Surveys (ACSIS) 2004-2010. Among 7696 patients enrolled in the ACSIS surveys from 2004, 955 (12%) were eligible for MRA therapy. In this population, prescription of MRAs at discharge from the index event showed a modest increase from 21% to 25% over the six-year period, whereas utilization of other guideline recommended drugs, including angiotensin converting enzyme inhibitors/receptor blockers and β-blockers was >2-fold higher. Multivariate logistic regression analysis showed that independent predictors of MRA prescription at discharge included a higher degree of left ventricular dysfunction (LVEF ≤30% vs. 31-40%: OR=2.19; p=0.02), history of heart failure prior to admission (OR=1.92; p<0.004), admission Killip≥II (OR=1.78; p=0.004), and an anterior location of the index MI (OR=1.54; p=0.03). MRA utilization was not associated with an increased risk for adverse events or rehospitalization at 30days of follow-up. In a real world setting, approximately one quarter of eligible post-MI patients are treated with an MRA following the index event, without a significant time-dependent change in this management strategy. MRAs are more likely to be underutilized in eligible lower-risk patients.International journal of cardiology 07/2013; 168(4). DOI:10.1016/j.ijcard.2013.06.091 · 6.18 Impact Factor
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ABSTRACT: Summary Background: The incidence of hyperkalemia related to spironolactone use is low in stable heart failure; however, it has not been studied during decompensation. Objective: To evaluate the influence of spironolactone on serum potassium in decompensated heart failure (HF). Methods: In a cohort study, patients that had been hospitalized due to decompensated HF, with left ventricular ejection fraction (LVEF) < 0.45 and serum potassium between 3.5 and 5.5 mEq/l were selected. The patients were divided according to spironolactone use (Group S) or no use (Group C). The outcome was potassium increase (> 6.0 mEq/l) and the use of calcium polystyrene. A multivariate analysis through logistic regression was carried out and values of p < 0.05 were considered significant. Results: A total of 186 patients (group S: 56; group C: 130) were studied; LVEF of 0.25, aged 55.5 years and 65.2% of them males. The incidence of hyperkalemia was 10.7% in group S and 5.4% in group C (p = 0.862). The multivariate analysis showed that serum urea > 60.5 mg/dl during the hospitalization presents a relative risk of 9.6 (95%CI 8.03 - 11.20; p = 0.005) for the occurrence of hyperkalemia. Conclusion: The incidence of hyperkalemia was two-fold higher with spironolactone use, but it was not statistically significant. The increase in urea levels was associated to the hyperkalemia. Randomized studies are necessary to clarify this issue. (Arq Bras Cardiol 2008;91(3):177-182)
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ABSTRACT: Literature review shows that elevated serum creatinine (or diminished creatinine clearance) is frequent in patients with heart failure (40%) and prognostically bad as it indicates an independently manifold increased mortality. In addition, even renal function worsening during hospitalization (increase in serum creatinine by approximately 30 micromol/L or higher) is not a rare finding (every 4 patients with heart failure) and is an independent marker of bad outcome. The pathophysiological mechanisms involved are numerous: dehydration (including the overdiuresis-induced one), the worsening of cardiac function (including negative inotropes), too much of vasodilatation (drug-induced, i.e. Amlodipine), nephrotoxic drugs, etc. Due to methodological reasons, large heart failure trials have not included enough patients with diminished renal function, as far more of them can be found in "real-life" conditions (epidemiologically). Thus, conclusions of large trials have not proved fully applicable but should be made so by means of trials including a representative number of patients suffering from both cardiac and renal failure. In our country, the knowledge on the issue of decreased renal function in heart failure patients is far from satisfactory, which necessitates further education. Drugs and their doses should be carefully selected and adjusted to individual findings, nephrotoxic medicaments should be avoided, and all useful drugs should be administered. Each of the five basic drugs (beta blockers, ACE inhibitors, spironolactone, aspirin, statins) for heart insufficiency (primarily induced by ischemic heart disease) seems to improve prognosis (including. life span prolongation) even in patients with diminished renal function.