Interstitial Nephritis

Chronic nephropathies with higly enhanced glomerular permeability to proteins are accompanied by tubulointerstitial inflammation and scarring and time progression to renal function deterioration. Proteins filtered through the glomerular capillary in excessive amount have intrinsic renal toxicity possibly linked to the subsequent process of proximal tubular reabsorption. Protein overloading of proximal tubular cells regulates transcription of nuclear factor-κB-dependent and nuclear factor-κB-independent genes. This forms endothelin-1, chemokines, and cytokines that are secreted into the renal interstitium and incite inflammatory and fibrogenic reaction. Autocrine pathways of activation of tubular epithelial cells contribute to interstitial injury and fibrosis.