Decay-Accelerating Factor Expression Modulates the Severity of Experimental Focal Segmental Glomerulosclerosis

Kidney360. 2023 Mar 1;4(3):381-386. doi: 10.34067/KID.0005312022.

Sofia Bin^{1

2}, Kelly Budge¹, Micaela Gentile^{1

3}, Manuel Alfredo Podestà⁴, Yaseen Khan¹, Jamil R Azzi⁵, Luis Sanchez Russo^{1

6}, Gaetano La Manna², Paolo Cravedi¹

¹ Translational Transplant Research Center and Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
² Nephrology, Dialysis and Renal Transplant Unit, IRCCS-Azienda Ospedaliero-Universitaria di Bologna, Alma Mater Studiorum University of Bologna, Bologna, Italy.
³ Unità Operativa Nefrologia, Azienda-Ospedaliero Universitaria di Parma & Dipartimento di Medicina e Chirurgia, Università di Parma, Parma, Italy.
⁴ Renal Division, Department of Health Sciences, Università degli Studi di Milano, Milan, Italy.
⁵ Transplantation Research Center, Division of Nephrology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
⁶ Renal Division, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.

Abstract

Genetically induced decay-accelerating factor (DAF) overexpression prevents adriamycin (ADR)-induced focal segmental glomerulosclerosis (FSGS) in mice.
Pharmacologic inhibition of DAF cleavage reduces complement activation in the glomeruli and albuminuria in murine ADR-induced FSGS.
Inhibition of complement activation represents a valuable therapeutic strategy for FSGS and, potentially, other glomerular diseases.