Nephrol Dial Transplant (2002) 17: 57-63
© 2002 European Renal Association-European Dialysis and Transplant Association
C5b–9 and adhesion molecules in human idiopathic membranous nephropathy
Department of Nephrology and Department of Pathology, Hippokration General Hospital, Thessaloniki, Greece
Background. Cellular immune responses and C5b–9 seem to play an important role in the pathogenesis and progression of idiopathic membranous nephropathy (IMN). The aim of the study was to investigate the role of C5b–9 and adhesion molecules in the pathogenesis of the disease.
Methods. The clinical and pathological data of 35 patients with biopsy-proven IMN were correlated with immunohistochemical findings using monoclonal antibodies against T lymphocytes, monocytes/macrophages (MM), HLA-DR antigens, C5b–9, and adhesion molecules such as 
3ß1, LFA-1ß, and ICAM-1.
Results. In the glomeruli, C5b–9 deposits showed a significant correlation with the intensity of IgG and C3 deposition. The stage of the disease had a significant negative relationship with the glomerular 3ß1 expression. In the tubulointerstitium (TIN), the number of HLA-DR(+) cells was highly correlated with the numbers of total T lymphocytes, MM, and LFA-1ß(+) cells, as well as with the percentage of tubules with C5b–9 deposits. The extent of ICAM-1 expression in the TIN was significantly correlated with the numbers of interstitial MM, HLA-DR(+), and LFA-1ß(+) cells, as well as with the extent of tubular C5b–9 deposition. The severity of tubular atrophy and interstitial fibrosis had a relationship with the numbers of total T lymphocytes, MM, HLA-DR(+), and LFA-1ß(+) cells and with the extent of tubular C5b–9 deposition and ICAM-1 expression in the TIN. Serum creatinine (Scr) was highly correlated with the numbers of interstitial total T lymphocytes, MM, HLA-DR(+), and LFA-1ß(+) cells. Moreover, Scr had a significant relationship with the severity of tubular atrophy and interstitial fibrosis, as well as with the extent of tubular C5b–9 deposition and ICAM-1 expression in the TIN. Proteinuria was significantly correlated with the extent of tubular 3ß1 expression.
Conclusions. In IMN, C5b–9 formation may be secondary to IgG and C3 deposition. Proteinuria may contribute to the TIN damage by altering the expression of 3ß1 integrins in tubular cells. De novo ICAM-1 and C5b–9 expression within the TIN as well as the activated interstitial cells may be important factors leading to renal damage and renal function impairment.
Keywords: adhesion molecules; C5b–9; interstitial damage; membranous nephropathy
Correspondence and offprint requests to: Aikaterini A. Papagianni, MD, Department of Nephrology, Hippokration General Hospital, 50 Papanastasiou Str, 54642 Thessaloniki, Greece. Email: aikpapag{at}otenet.gr
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