Chronic tubulointerstitial disease in IgA nephropathy

Abstract

Summary: Considerable clinical and experimental evidence points to the functional importance of tubulointerstitial disease (TID) in IgA nephropathy (IgAN). Current thinking is that the proteinuria/haematuria in IgAN causes tubular injury and that this is followed by tubular cell neoantigen expression (human leucocyte antigens [HLA] ICAM‐1 and VCAM‐1), with T cell (γδ cell) activation, macrophage recruitment, the release of cytokines (notably transforming growth factor‐β [TGF‐β] and platelet derived growth factor [PDGF]), and the growth of interstitial fibroblasts. Agents that have been effective in preventing experimental TID in animals include anti‐TGF‐β, decorin, IL‐1 receptor antagonists and angiotensin converting enzyme (ACE) inhibitors. Thus the tubulointerstitial component of IgAN might well provide an important new window of opportunity for therapeutic intervention in this disease. Tubulointerstitial disease must be monitored more closely as a prognostic factor in future clinicopathological studies of IgAN.