Finerenone Reduces Renal RORγt γδ T Cells and Protects against Cardiorenal Damage

Am J Nephrol. 2022;53(7):552-564. doi: 10.1159/000524940. Epub 2022 Jun 8.

Abstract

Introduction: Chronic activation of the mineralocorticoid receptor (MR) leads to pathological processes like inflammation and fibrosis during cardiorenal disease. Modulation of immunological processes in the heart or kidney may serve as a mechanistic and therapeutic interface in cardiorenal pathologies. In this study, we investigated anti-inflammatory/-fibrotic and immunological effects of the selective nonsteroidal MR antagonists finerenone (FIN) in the deoxycorticosterone acetate (DOCA)-salt model.

Methods: Male C57BL6/J mice were uninephrectomized and received a DOCA pellet implantation (2.4 mg/day) plus 0.9% NaCl in drinking water (DOCA-salt) or received a sham operation and were orally treated with FIN (10 mg/kg/day) or vehicle in a preventive study design. Five weeks after the procedure, blood pressure (BP), urinary albumin/creatinine ratio (UACR), glomerular and tubulointerstitial damage, echocardiographic cardiac function, as well as cardiac/renal inflammatory cell content by FACS analysis were assessed.

Results: BP was significantly reduced by FIN. FACS analysis revealed a notable immune response due to DOCA-salt exposure. Especially, infiltrating renal RORγt γδ-positive T cells were upregulated, which was significantly ameliorated by FIN treatment. This was accompanied by a significant reduction of UACR in FIN-treated mice. In the heart, FIN reduced DOCA-salt-induced cardiac hypertrophy, cardiac fibrosis and led to an improvement of the global longitudinal strain. Cardiac actions of FIN were not associated with a regulation of cardiac RORγt γδ-positive T cells.

Discussion/conclusion: The present study shows cardiac and renal protective effects of FIN in a DOCA-salt model. The cardiorenal protection was accompanied by a reduction of renal RORγt γδ T cells. The observed actions of FIN may provide a potential mechanism of its efficacy recently observed in clinical trials.

Keywords: Aldosterone; Chronic kidney disease; Finerenone; Mineralocorticoid receptor antagonist.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Pressure
  • Desoxycorticosterone Acetate
  • Fibrosis
  • Hypertension* / drug therapy
  • Hypertension, Renal* / pathology
  • Kidney / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Naphthyridines* / pharmacology
  • Nuclear Receptor Subfamily 1, Group F, Member 3 / therapeutic use
  • T-Lymphocytes*

Substances

  • Naphthyridines
  • Nuclear Receptor Subfamily 1, Group F, Member 3
  • finerenone
  • Desoxycorticosterone Acetate