# Finerenone is associated with pronounced uric acid reduction in hyperuricemic diabetic kidney disease: a real-world analysis

## TL;DR

Finerenone significantly lowers uric acid in diabetic kidney disease patients, especially those with high baseline levels, while also reducing albuminuria.

## Contribution

This study demonstrates finerenone's pronounced uric acid-lowering effect in hyperuricemic diabetic kidney disease patients in a real-world setting.

## Key findings

- Finerenone reduced serum uric acid by 47.9 μmol/L in DKD patients, with a larger effect in those with baseline hyperuricemia.
- Albuminuria decreased by 39.4% with finerenone treatment, independent of other therapies like SGLT2 inhibitors.
- A small but significant decline in eGFR was observed, but hyperkalemia occurred in only 0.8% of patients.

## Abstract

Diabetic kidney disease (DKD) is a critical complication of type 2 diabetes, often compounded by hyperuricemia, which may accelerate renal function decline. While finerenone, a nonsteroidal mineralocorticoid receptor antagonist (MRA), provides renal and cardiovascular benefits, its impact on uric acid (UA) metabolism in real-world DKD patients, particularly those with high baseline SUA, remains controversial.

In this retrospective, single-center study, we included 124 patients with type 2 DKD (baseline eGFR ≥60 mL/min/1.73 m2) who initiated finerenone. Patients with recent gout or urate-lowering therapy were excluded. Changes in SUA, urinary albumin-to-creatinine ratio (UACR), and eGFR were assessed before and after 1–3 months of treatment. Statistical analyses employed linear mixed models for longitudinal data and multivariable regression.

Linear mixed model analysis showed finerenone treatment was associated with a significant reduction in SUA (adjusted mean difference: −47.9 μmol/L, 95% CI: −63.5 to −32.3; p < 0.001). This reduction was substantially greater in patients with baseline hyperuricemia (−88.6 μmol/L) than in those without (−16.6 μmol/L; p for interaction = 0.003). UACR decreased by 39.4% (p < 0.001), while eGFR showed a small but significant decline (−2.7 mL/min/1.73 m2, p = 0.019). The SUA-lowering association was independent of concomitant SGLT2 inhibitor or GLP-1 receptor agonist use in multivariable analyses. Hyperkalemia (potassium ≥5.5 mmol/L) occurred in 0.8% of patients.

In this real-world cohort, finerenone use was associated with significant reductions in albuminuria and SUA, particularly among patients with hyperuricemia. These findings suggest a potential dual benefit in this high-risk subgroup and highlight the importance of baseline SUA in interpreting finerenone’s metabolic effects. The observed SUA reduction warrants further prospective investigation.