Does finerenone improve proteinuria and affect serum potassium levels in patients with diabetic kidney disease already receiving RAS inhibitors and SGLT2 inhibitors?
Finerenone significantly reduces proteinuria without causing severe hyperkalemia in patients with diabetic kidney disease already receiving RAS and SGLT2 inhibitors, with efficacy potentially influenced by sodium intake.
Finerenone has been shown to exert renoprotective effects in patients with diabetic kidney disease. However, the effects of finerenone on proteinuria and serum potassium levels in patients already receiving renin–angiotensin system inhibitors and sodium-glucose cotransporter 2 inhibitors have not been fully elucidated. A total of 47 patients with diabetic kidney disease already treated with angiotensin receptor blocker, angiotensin-converting-enzyme inhibitor or angiotensin receptor-neprilysin inhibitors and sodium-glucose cotransporter 2 inhibitors and newly started treatment with finerenone were analyzed to identify predictors of finerenone-induced changes in proteinuria and serum potassium levels. After 57.8 ± 25.3 days of treatment with finerenone, urinary protein was significantly decreased from 2.61 ± 2.34 g/gCr to 2.29 ± 2.44 g/gCr and serum potassium was significantly elevated from 4.27 ± 0.36 mmol/L to 4.47 ± 0.42 mmol/L, respectively. There were no patients whose serum potassium levels reached 5.5 mmol/L. The amount of estimated sodium excretion was significantly correlated with the finerenone-induced changes in proteinuria and was the only significant predictive factor for the proteinuria-reducing effect of finerenone. Lower baseline serum potassium level was associated with a greater increase in serum potassium levels after finerenone administration. Proteinuria-lowering effect of finerenone may be influenced by the amount of sodium intake in patients with diabetic kidney disease.
Kidoguchi et al. (Tue,) studied this question.