Loss of NGAL protects against albumin-induced kidney inflammation and fibrosis

Increased albuminuria represents a risk factor for chronic kidney disease (CKD), and it is associated with the development and progression of kidney inflammation and fibrosis. The expression of neutrophil gelatinase-associated lipocalin (NGAL), a biomarker for kidney damage, is increased in CKD patients and experimental animal models of kidney damage. However, it is unknown whether NGAL is necessary for the promotion of kidney inflammation and fibrosis associated with the albumin exposition. Male C57BL6/J wild-type (WT) and NGAL (knockout) KO mice (8–12 weeks, n = 5–6) were subjected to the albumin overload (AO) model (10 mg/g/day i.p.) or Vehicle (0.9% NaCl i.p.) for 7 days. Kidney function and inflammatory and fibrotic status in the kidney were assessed. In WT and NGAL-KO mice, AO significantly increased plasma protein (1.3-fold, p p p p p p