Hyperkalemia in congestive heart failure patients aged 63 to 85 years with subclinical renal disease

Prolonged treatment with an angiotensin-converting enzyme (ACE) inhibitor does not permanently suppress aldosterone production. Increased aldosterone production often resumes after a variable interval. The failure to suppress aldosterone production permanently is termed "aldosterone escape."(1,2) The addition of spironolactone to ACE inhibitor therapy in patients with refractory congestive heart failure has been advocated because of this escape phenomenon.(3) However, it was not until the landmark Randomized Aldactone Evaluation Study (RALES) by Pitt et al(4) that widespread use of this combination therapy became uniformly practiced by cardiologists and general internists. The incidence of dangerous hyperkalemia was 2% and insignificant in the RALES study,(4) but patients with insulin-dependent diabetes mellitus and those with serum creatinine greater than or equal to2.0 mg/dl (greater than or equal to176.8 mumol/L) were excluded. There are increasing reports of hyperkalemic complications in elderly patients with pre-existing renal disease after,exposure to this combination of drugs.(5-7) Because serum creatinine may be normal in elderly patients who may already have moderate to severe reduction of their glomerular filtration rate and they also have altered electrolyte homeostasis, elderly patients are therefore at risk for hyperkalemia and other electrolyte derangements.(8) Underappreciation of the presence of a reduced glomerular filtration rate in the, elderly potentially places them at great risk for hyperkalemia and acute renal failure when exposed to this combination therapy. In this report, we present 18 patients (aged 63 to 85 years) whose serum creatinine levels were apparently normal but who had significantly reduced glomerular filtration rates. They developed hyperkalemia after exposure to combination therapy with spironolactone and ACE inhibitors.