Molecular basis of IgA nephropathy

Curr Mol Med. 2005 Aug;5(5):475-87. doi: 10.2174/1566524054553450.


IgA nephropathy (IgAN) is the most common glomerulonephritis worldwide and remains an important cause of end-stage renal failure. However, the basic molecular mechanism(s) underlying abnormal IgA synthesis, selective mesangial deposition with ensuing mesangial cell proliferation and extracellular matrix expansion remains poorly understood. Notably, the severity of tubulointerstitial lesions better predicts the renal progression than the degree of glomerular lesions. The task of elucidating the molecular basis of IgAN is made especially challenging by the fact that both environmental and genetic components likely contribute to the development and progression of IgAN. This review will summarize the earlier works on the structure of the IgA molecule, mechanisms of mesangial IgA deposition and pathophysiologic effects of IgA on mesangial cells following mesangial deposition. Recently, a series of important advances in the area of communication between the glomerular mesangium and renal tubular cells have emerged. These novel findings regarding the molecular pathogenesis of IgAN will be helpful in designing future directions for therapy.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Communication
  • Glomerular Mesangium / metabolism*
  • Glomerular Mesangium / pathology
  • Glomerulonephritis, IGA / metabolism*
  • Glomerulonephritis, IGA / pathology
  • Glomerulonephritis, IGA / therapy
  • Humans
  • Immunoglobulin A / metabolism*
  • Kidney Failure, Chronic / metabolism
  • Kidney Failure, Chronic / mortality
  • Kidney Failure, Chronic / pathology
  • Kidney Tubules / metabolism*
  • Kidney Tubules / pathology


  • Immunoglobulin A