Recent advances in IgA nephropathy--the glomerulopodocytic-tubular communication

IgA nephropathy (IgAN) is characterized by mesangial deposition of pathogenic polymeric IgA1 with rare deposits in the tubular epithelial cells (TEC). Recently, a novel mechanism involving a glomerulopodocytictubular cross-talk in the development of tubulointerstitial damage in IgAN has been revealed. Podocytes are positioned strategically along the glomerulotubular axis and plays an important role in mediating the glomerulotubular cross-talk. In IgAN, podocyte markers are reduced in the glomeruli. In vitro study implicates humoral factors (predominantly tumor necrosis factor-α and transforming growth factor-β) released from mesangial cells alter the glomerular permeability in the event of proteinuria and tubulointerstitial injury in IgAN. These mediators released from mesangial cells after IgA deposition further activate TEC leading to subsequent inflammatory changes in the renal tubulointerstitium.