Diabetic kidney disease, biomarkers, and finerenone

Abstract Diabetic kidney disease (DKD), the leading cause of kidney failure worldwide, is associated with an increased risk of cardiovascular disease (CVD). A complex pathobiology involving hemodynamic, metabolic, and immune dysregulation promotes inflammatory and fibrotic pathways that contribute to kidney disease progression and CVD in individuals with DKD. While the standard treatment approach incorporating renin‐angiotensin‐aldosterone system (RAAS) blockers and sodium‐glucose cotransporter‐2 inhibitors (SGLT2i) reduces the risk for kidney disease progression and CVD, the high residual risk that persists despite these treatments underscores the need for novel therapies for DKD. Finerenone, a nonsteroidal mineralocorticoid receptor antagonist (MRA), is a proven therapeutic option for DKD that targets inflammatory and fibrotic pathways involved in its progression. Furthermore, finerenone has been evaluated for DKD outcomes in phase 3 clinical trials, has a favourable side effect profile compared to steroidal MRAs, reduces the risks of major kidney and CVD outcomes in clinical trials when used with RAAS blockers, and is the only MRA specifically approved for DKD and recommended for DKD in treatment guidelines. The integration of novel biomarkers of CKD and CVD into the clinical management of DKD may improve early identification of at‐risk individuals and allow for patient‐specific therapeutic strategies. This review provides a brief overview of the pathogenesis of DKD and the role of mineralocorticoid receptor activation in DKD pathobiology, summarises the role of finerenone in the treatment paradigm of DKD, evaluates current and emerging biomarkers of DKD and finerenone's impact on these biomarkers, and provides forward‐looking guidance on future research for biomarker‐driven precision medicine in DKD.