How prevalent is hyperkalemia and renal dysfunction during treatment with spironolactone in patients with congestive heart failure?

Svensson, M.; Gustafsson, Finn; Galatius, Søren; Hildebrandt, Per; Atar, Dan

doi:10.1016/j.cardfail.2003.10.012

Cited by 107 publications

(76 citation statements)

References 13 publications

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“…1,2 Although spironolactone is generally well tolerated, hyperkalemia is a potentially life-threatening adverse effect of the drug in clinical practice. [3][4][5] Strategies for mitigating the risk of serious hyperkalemia include cautious dosing of spironolactone, close monitoring of electrolyte levels and avoidance of other drugs that cause hyperkalemia.…”

mentioning

confidence: 99%

Trimethoprim–sulfamethoxazole and risk of sudden death among patients taking spironolactone

Antoniou

Hollands

Macdonald

et al. 2015

CMAJ

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T he use of spironolactone increased considerably following publication of the Randomized Aldactone Evaluation Study, which showed that the drug improved morbidity and mortality in carefully selected patients with severe systolic heart failure.1,2 Although spironolactone is generally well tolerated, hyperkalemia is a potentially life-threatening adverse effect of the drug in clinical practice.3-5 Strategies for mitigating the risk of serious hyperkalemia include cautious dosing of spironolactone, close monitoring of electrolyte levels and avoidance of other drugs that cause hyperkalemia.The widely used antibiotic trimethoprim has pharmacologic similarities to the potassium-sparing diuretic amiloride. It reduces urinary potassium excretion by about 40% and can increase the risk of life-threatening hyperkalemia in susceptible individuals, including those taking spironolactone.6,7 In combination with sulfamethoxazole, trimethoprim is most often used for the treatment of urinary tract infections. More than 20 million prescriptions are written for the combination each year in the United States. 8 We have previously shown that the use of trimethoprim-sulfamethoxazole in patients receiving spironolactone increased the risk of hospital admission with hyperkalemia more than 12-fold relative to amoxicillin.9 However, we did not examine whether the drug interaction was associated with an increased risk of sudden cardiac death, a predictable consequence of severe hyperkalemia. 10,11 This is important because sudden death in patients taking spironolactone may erroneously be attributed to intrinsic heart disease.Because treatment with trimethoprimsulfamethoxazole can precipitate life-threatening hyperkalemia in patients receiving spironolactone, we conducted a study to determine whether

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mentioning

confidence: 99%

Trimethoprim–sulfamethoxazole and risk of sudden death among patients taking spironolactone

Antoniou

Hollands

Macdonald

et al. 2015

CMAJ

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“…Hyperkalemia, with possibility of subsequent arrhythmias and sudden cardiac death, represents one of the potential risks associated with the use of MR antagonist in heart failure [68][69][70][71][72][73].…”

Section: Hyperkalemia Potential Risks and Preventionmentioning

confidence: 99%

Mineralocorticoid receptor activation in myocardial infarction and failure: recent advances

Galuppo

Bauersachs

2012

Eur J Clin Investigation

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The classical view of aldosterone actions via the mineralocorticoid receptor (MR) limited to control of fluid balance and blood pressure homoeostasis has been progressively overcome by clinical and experimental evidence emphasizing the pleiotropic role of MR activation in the pathogenesis of cardiovascular disease. Clinical studies have shown the benefit of MR blockade in patients with left ventricular dysfunction and heart failure after myocardial infarction (MI), hypertension or diabetic nephropathy. Deleterious effects of MR activation include cardiac structural and electrical remodelling, cardiovascular fibrosis, inflammation and oxidative stress. Complexity of pathophysiological role of MR derives from the presence of circulating glucocorticoids at higher concentrations than aldosterone and the equal affinity of the MR for aldosterone, cortisol and corticosterone. Recent experimental studies using different animal models and genetic tools have deeply explored the cell-specific functional role of MR in cardiovascular pathology. This review addresses emerging preclinical studies as well as ongoing clinical trials regarding MR activation in MI and failure.

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“…This is in contrast to the acute intravenous administration of a betablocker to naïve patients in the acute myocardial infarction setting. There are no data regarding the use of beta blockade in cardiogenic shock because in most cases, clinicians will withhold in this setting (100,(106)(107)(108)(109)(110)(111)(112)(113)128).…”

Section: Practical Tipsmentioning

confidence: 99%

“…• When diuretics are reduced, especially in the setting of a concomitant ACE inhibitor, ARB or spironolactone, serum electrolytes should be rechecked within two to four weeks to assess serum potassium levels (109).…”

Section: Practical Tipsmentioning

confidence: 99%

Canadian Cardiovascular Society Consensus Conference recommendations on heart failure update 2007: Prevention, management during intercurrent illness or acute decompensation, and use of biomarkers

Arnold¹,

Howlett²,

Dorian³

et al. 2007

Canadian Journal of Cardiology

124

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How prevalent is hyperkalemia and renal dysfunction during treatment with spironolactone in patients with congestive heart failure?

Cited by 107 publications

References 13 publications

Trimethoprim–sulfamethoxazole and risk of sudden death among patients taking spironolactone

Trimethoprim–sulfamethoxazole and risk of sudden death among patients taking spironolactone

Mineralocorticoid receptor activation in myocardial infarction and failure: recent advances

Canadian Cardiovascular Society Consensus Conference recommendations on heart failure update 2007: Prevention, management during intercurrent illness or acute decompensation, and use of biomarkers

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