Finerenone in kidney transplantation: an underinvestigated agent: review of available evidence, existing gaps, and future directions

Emerging data on finerenone have drawn significant interest from nephrologists and cardiologists for its clinical potential in patient management. Its nonsteroidal structure, greater receptor selectivity, and reduced risk of hyperkalemia make it a distinctive choice for clinicians. Mineralocorticoid receptors (MRs) are expressed in the collecting ducts, endothelial and vascular smooth muscle cells of the interlobar arteries, as well as in podocytes, mesangial cells, and renal fibroblasts. These receptors are also present in cardiovascular and inflammatory cells. MR activation contributes to ischemia-reperfusion injury (IRI) and mediates calcineurin inhibitor (CNI) toxicity, proteinuria, and fibrosis in both the cardiovascular system and kidneys. Blocking MR activation with finerenone may exert therapeutic effects in renal allografts by mitigating IRI, preventing CNI toxicity, reducing proteinuria and renal fibrosis, and lowering the risk of renal and cardiovascular events. Preclinical and clinical studies in the general population with diabetes have demonstrated that finerenone effectively reduces proteinuria and improves renal and cardiovascular outcomes. However, clinical evidence in kidney transplant recipients remains extremely limited, and the efficacy and safety of finerenone in this population are yet to be established. To date, no clinical trials specifically investigating finerenone in kidney transplantation have been published, with only the EFFEKTOR trial currently underway. This review discusses the mechanistic rationale, extrapolates evidence from nontransplant populations, identifies key knowledge gaps, and proposes future research directions to evaluate the safety and efficacy of finerenone in kidney transplant recipients.