Antiproteinuric Response to Finerenone in Diabetic Kidney Disease: Responder and Non-Responder Subgroup Analysis of the FINDKDLATAM Study
Jorge Rico Fontalvo, María Raad Sarabia, José C. De La Flor, Vicente Sánchez Polo, Jenniffer Benavides Garcia, Enrique Ramos Clason, Daniel Domínguez, Giovanny Mera Rebutti, Carlos Madrid Mancia, Rene Tabora López, Manuel Rocha Meza, Dany Tabora López, James J. Muñoz Zambrano, Eduardo Lorca Herrera, Eliana Dina-Batlle, Michael Cieza Terrones, Alvaro Pedroza Pallares, Tomas Rodríguez Yánez, Washington Osorio, Alyi Arellano Cabeza, Juan Felipe Gutiérrez, Avinash Chandu Nanwani, Celia Rodríguez Tudero, Rodrigo Daza ArnedoBackground/Objectives: Albuminuria is an early marker of kidney damage and an independent predictor of adverse outcomes, making its reduction a key therapeutic goal. Finerenone, a selective nonsteroidal mineralocorticoid receptor antagonist, has demonstrated renal and cardiovascular benefits in patients with diabetic kidney disease (DKD), although the magnitude of the antiproteinuric response may vary in clinical practice. This post hoc analysis aimed to characterize the six-month antiproteinuric response to finerenone and to descriptively explore baseline clinical and treatment characteristics across response categories in the FINDKDLATAM cohort. Methods: A subgroup analysis was performed on a real-world, multicenter, retrospective, observational study that included patients from the FINDKDLATAM study who had urinary albumin-to-creatinine ratio (UACR) measurements taken at baseline and six months. Patients were classified as absolute responders (≥50% reduction in UACR), partial responders (30–49% reduction), and non-responders (<30% reduction or no reduction in UACR) at six months of follow-up. Sociodemographic, clinical, biochemical, therapeutic, and safety variables were analyzed. Results: Of the 347 patients included in the original cohort, 334 had complete UACR data at six months and were included in the analysis. Of these, 80.2% (n = 268) were absolute responders, 11.7% (n = 39) partial responders, and 8.1% (n = 27) non-responders. Median UACR decreased from 350.7 to 67.0 mg/g among absolute responders and from 240.5 to 143.0 mg/g among partial responders (both p < 0.0001), whereas no significant change was observed among non-responders. No baseline clinical characteristic consistently distinguished responders from non-responders. Serum potassium increased during follow-up, particularly among non-responders. Conclusions: In this retrospective Latin American cohort, most patients experienced a reduction in UACR after six months of finerenone treatment. However, the uncontrolled observational design, concomitant therapies, UACR variability, and regression to the mean preclude attributing these changes exclusively to finerenone. These exploratory findings do not support selecting patients according to a particular responder phenotype but rather support prescribing finerenone according to currently approved clinical criteria. Prospective studies with adjusted analyses are needed to identify independent predictors of response.