Cytotoxic effect of Ochratoxin A on the renal corpuscles of rat kidney: could Ochratoxin A cause kidney failure?

Abstract

To demonstrate that Ochratoxin A can cause kidney failure as the kidney is the primary target for OTA cytotoxicity. Ochratoxin A (OTA) is a mycotoxin found in our food. The cytotoxic effect of a low cumulative dose of OTA on the renal corpuscles of the kidney tissue has been investigated in this report. This study was based on two groups in which weaning albino rats were used: (1) control; (2) OTA-treated rats (289 µg/kg/day). After 28 days of treatment, a significant decrease in body weight, kidney weight and relative weight were detected in OTA treated rats. Serum creatinine and urea level were slightly elevated. These results revealed significant histological as well as ultrastructral lesions in the OTA treated group. The lesions included global congestion in the renal tissue and loss of demarcation between the cortex and medulla. The normal architecture of the renal corpuscles was destroyed and most of the corpuscles lost their ordinary look. The most apparent histopathological changes were urinary space disappearance and hypercellularity. In addition, congested, undifferentiated, atrophied, hypertrophied, fragmented, sclerotic, degenerated, and obliterated renal corpuscles were distinct. The ultrastructural lesions observed in the renal corpuscles in OTA on treated rats included; proliferation and swelling of the endothelial cells with occasional loss of fenestrae; narrowing of the capillary lumen; damaged podocytes with deteriorated secondary foot processes, hypertrophied and proliferated mesangial cells with expanded mesangial matrix. The endothelium was clearly defected and vacuolated, and lost its fenestrations in many glomerular capillaries. In addition, the glomerular basement membrane (GBM) became visibly thickened and tortuous. Necrotic glomerular cells were frequently observed. Pre-apoptotic cells were also seen. It was concluded that the exposure to relatively low OTA concentrations induced significant lesions to the renal corpuscles. Moreover, it activated oxidative damage and necrosis which can cause extensive damage to the kidney and ultimately kidney failure.