Interestingly, pro-fibrotic TGF-β was downregulated in mouse kidneys. Grading of lesions revealed higher scores in hamsters compared to the slight alterations observed in the mouse kidneys, irrespective of the bacterial load. Hamsters developed morphological alterations in the kidneys with tubulointerstitial nephritis and fibrosis. borgpetersenii serogroup Ballum to assess chronic infection. Animals were monitored until 28 days after injection with a virulent L. Herein, we studied the renal morphological alterations in relation with the regulation of inflammatory cytokines and chemokines, comparing two experimental models of chronic leptospirosis, the golden Syrian hamster that survived the infection, becoming carrier of virulent leptospires, and the OF1 mouse, a usual reservoir of the bacteria. Chronic Kidney Disease (CKD) is considered as a possible AKI-residual sequela but little is known about the renal pathophysiology consequent to leptospirosis infection. In contrast, accidental hosts may present an acute form of leptospirosis with a range of clinical symptoms including the development of Acute Kidney Injury (AKI). Humans can be infected after exposure to contaminated urine of reservoir animals, usually rodents, regarded as typical asymptomatic carriers of leptospires. Leptospirosis is caused by pathogenic spirochetes of the genus Leptospira.
