Tubulointerstitial renal disease

Abstract

Tubulointerstitial damage, in progressive chronic renal disease of all types, arises because of a complex interplay between factors in the tubular lumen, tubular epithelial cells, peritubular capillaries, resident and infiltrating interstitial cells and extracellular matrix. Particularly in proteinuric renal disease, tubular epithelial cells play a central role in orchestrating these events. In response to mediators arising systemically, in the tubular lumen or from other renal cells, tubular epithelial cells undergo a complex series of structural and functional changes and produce a bewildering number of soluble and fixed mediators, which in turn lead to interstitial inflammation and fibrosis. Knowledge of these interactions has increased exponentially over the past decade, and has defined a number of new targets for treatment. Both expansion and consolidation of this knowledge is needed to determine which of these targets holds the most promise for future treatment.