Tubulointerstitial damage in glomerular diseases: its role in the progression of renal damage.
The evidence that tubular damage, interstitial infiltration, and interstitial fibrosis occur in all glomerular diseases, either immunologically or non-immunologically mediated, is reviewed on the basis of personal data and data from the literature. The proposed mechanisms linking glomerular and tubular damage to the interstitial recruitment of mononuclear leukocytes and fibroblast proliferation, with abnormal extracellular matrix production leading to interstitial fibrosis, also are analyzed. The role of persistent heavy proteinuria and exposure to proinflammatory cytokines in inducing the damage of the tubular epithelial cells, with consequent acquisition by these cells of the ability to interact as antigen-presenting cells with T lymphocytes, is especially emphasized. Finally, the importance of the tubulointerstitial damage as a marker of unfavorable prognosis in glomerular diseases is documented.
D'Amico
G
G
Division of Nephrology, San Carlo Borromeo Hospital, Milano, Italy.
Ferrario
F
F
Rastaldi
M P
MP
D001284:Atrophy; D005355:Fibrosis; D005921:Glomerulonephritis / Q000276:immunology / Q000473:pathology*; D005923:Glomerulosclerosis, Focal Segmental / Q000276:immunology / Q000473:pathology; D006801:Humans; D016130:Immunophenotyping; D007668:Kidney / Q000276:immunology / Q000473:pathology*; D007684:Kidney Tubules / Q000276:immunology / Q000473:pathology*; D007963:Leukocytes, Mononuclear / Q000276:immunology; D011379:Prognosis; D011507:Proteinuria / Q000150:complications