Tubular and interstitial renal disease due to immunologic mechanisms

Abstract

There is now compelling evidence, derived from experimental models as well as human disease, that tubular and interstitial lesions can result from immune complexes or from autoantibodies against tubular basement membrane constituents (anti TBM disease). Moreover, in contrast to the glomerulus, it appears that the renal interstitium is an area where cell mediated reactions can occur, accounting for some forms of interstitial nephritis. The authors describe the experimental models of immunologically mediated tubular and interstitial renal disease as well as evidence concerning the occurrence and importance of similar lesions in man.