Furthermore, studies on CLU‐knockout (KO) mice have found that (i) CLU deficiency accelerated renal fibrosis in response to IRI and unilateral ureteral obstruction21, 25 (ii) in aging mice, CLU deficiency resulted in the development of progressive glomerulopathy that has been associated with glomerular antibody deposition26 and (iii) CLU‐KO mice exhibited greater severity of renal IRI, as well as the impairment of renal repair after IRI.20, 27. This evidence concerns the gene CLU and glomerular disorder.