Mineralocorticoid receptor antagonists confer antiproteinuric effect in CKD
Treatment with mineralocorticoid receptor antagonists (MRA) alone or in addition to renin–angiotensin system (RAS) blockade is associated with significant antiproteinuric effects, with a slight increase in mean potassium levels, in patients with chronic kidney disease (CKD), a study has shown.
A systematic review and meta-analysis was conducted to determine the effects of MRAs on albuminuria/proteinuria and adverse events, such as change in renal function and hyperkalaemia incidence. The investigators searched electronic databases, clinical trial registries and grey literature to retrieve randomized controlled trials (RCTs) that compared MRA alone or on top of RAS blockade with placebo or active treatment.
Forty-five studies with a total of 2,767 participants were initially identified, of which 31 were included in the analysis.
Compared with placebo, MRAs (alone or with RAS blockade) reduced urine albumin-to-creatinine ratio (UACR) by –24.55 percent (95 percent confidence interval [CI], –29.57 to –19.53 percent), urine protein-to-creatinine ratio by –53.93 percent (95 percent CI, –79 to –28.86 percent) and 24-h albumin excretion by –32.47 percent (95 percent CI, –41.1 to –23.85 percent).
MRAs, compared with calcium-channel blockers, also reduced UACR by –22.48 percent (95 percent CI, –24.51 to –20.44 percent), but there were no differences when compared with a second RAS blockade or nonpotassium-sparing diuretics.
The addition of an MRA resulted in a change in estimated glomerular filtration rate of –2.38 ml/min per 1.73 m2 (95 percent CI, −3.51 to −1.25), an increase in potassium by 0.22 mEq/l (95 percent CI, 0.16–0.28 mEq/l) and a 2.6-fold rise in the risk of hyperkalaemia (risk ratio, 2.63, 95 percent CI, 1.69–4.08) compared with placebo or active control.