Kidney Failure

Kidney Function Restoration Program

Foods not to eat when you have Kidney Problems

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Acute renal failure (ARF) as complication of the systemic inflammatory response is a clinical entity characterized by an abrupt decline in the glomerular filtration rate (GFR), resulting in oliguria and azotemia, all of which have been detected in the CLP-induced MODS rats, but not in those with blockade of C5a (19) (Figure 3C). Though the presence of C5aR has been described on human glomerular mesangial cells and more recently on renal tubular cells, the linkage between C5a and development of ARF during MODS is obscure. There are suggestions that infusion of C5a leads to a significant fall in renal blood flow by increasing the vascular resistance in the afferent and efferent arterioles (50). Proteinuria was observed in CLP-induced MODS, reflective of the presence in urine of proteins larger than the glomerular filtration barrier of 60 kDa. In CLP rats there were morphological changes in podocytes, including fusion of their foot processes and flattening of their cell surfaces, and necrosis of proximal convoluted tubular cells (19). In an ARF model in dogs induced by norepinephrine infusion into the renal artery, similar morphological changes of podocytes were found together with development of tubular necrosis, mainly involving the proximal convoluted tubules (51). The morphological changes in kidneys of CLP-induced MODS rats were absent in rats treated with anti-C5a antibody (19). In a model of immunological glomerulonephritis in mice, a genetic deficiency of C5 was associated with reduced glomerular injury when compared to C5-intact mice (52), suggesting that activated complement products may be linked to development of glomerular injury.

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