CD44 expression in renal tubules during maladaptive repair is a potential marker for the transition from acute kidney injury to chronic kidney disease in rats

tubules remained enclosed by a laminin-positive basement membrane. Pathway analysis predicted CD44 as a putative upstream regulator of fibrosis-related genes including Fn1; increased Fn1 mRNA in dilated/atrophic TECs with peritubular fibronectin accumulation suggested a possible tubular contribution to matrix deposition. Together, these findings support tissue CD44 as a candidate marker of maladaptive tubular repair during the AKI-to-CKD transition and suggest serum CD44 as a candidate circulating indicator in cisplatin nephrotoxicity.