Mineralocorticoid receptor antagonist (MRA) treatment is associated with increased risk of hyperkalemia in patients with chronic kidney disease (CKD), but the drugs do not increase their risk for death, according to data presented at the European Renal Association (ERA) 59th Congress.
MRAs are often not recommended in patients with advanced CKD due to perceived risk of hyperkalemia and death, investigators noted.
From the 2008-2021 Danish population, investigators identified 34,442 adults with hyperkalemia (serum potassium exceeding 6 mmol/L) and matched them 1:4 to 131,410 adults without hyperkalemia based on age, sex, hypertension, and diabetes status. Of the cohort, 57% were male. The median age was 73.5 years and median estimated glomerular filtration rate (eGFR; in mL/min/1.73 m2) was 74.
MRA use vs nonuse was significantly associated with 8.3-, 4.6-, and 2.0-fold increased risk of hyperkalemia in patients with an eGFR of more than 60, 30-60, and less than 30, respectively, Morten Lindhardt, MD, PhD, of Steno Diabetes Center Copenhagen in Gentofte, Denmark and colleagues reported. MRA use, however, was significantly associated with a 16% and 33% lower risk of death within 30 days in patients with an eGFR of more than 60 and 30-60, respectively. For patients with an eGFR less than 30, the reduced mortality risk after MRA treatment was not significant.
“Although mineralocorticoid receptor antagonist treatment was associated with increased risk of hyperkalaemia for all strata of kidney impairment, subsequent 30-day mortality was lower compared with patients with corresponding kidney function without mineralocorticoid receptor antagonist treatment,” Dr Lindhardt’s team concluded.
In patients with CKD, the renal protective benefits of an MRA may outweigh the hyperkalemia risk.
Møller S, Torp C, Schou M, Gislason G, Carlson N, Lindhardt M. Mineralocorticoid receptor antagonist treatment in patients with renal insufficiency and associated risk of hyperkalemia and death. Presented at: ERA 59th Congress, May 19-22, 2022. Abstract FC 084.