Relationship between interstitial infiltrates and steroid responsiveness of proteinuria in membranous nephropathy.
Mononuclear inflammatory cells were retrospectively analysed using monoclonal antibodies in the interstitium and glomeruli of 16 renal biopsy specimens from patients with nephrotic syndrome due to idiopathic membranous nephropathy (IMN). The aim of the study was to determine the composition of the infiltrate and to assess the ability to predict the response of proteinuria to corticosteroids. All patients had received prednisolone as a sole treatment. Nine patients had shown a complete or partial remission of proteinuria (group A) and seven did not respond at all (group B). Both groups were matched for age and degree of proteinuria; also both groups had normal renal function at the time of biopsy. Very few intraglomerular leukocytes, mostly monocytes/macrophages (MM) were found. The majority of interstitial T cell population and B cells were a minor component. No significant differences were found between the two groups regarding the types of the intraglomerular cells. However, interstitial T-cells, CD4+ve T helper/inducer cells, CD8+ve T cytotoxic/suppressor cells and MM were significantly higher in group A than in group B. Also HLA-DR expressing interstitial cells were much in excess in group A. In addition patients with complete remission of proteinuria had higher numbers of interstitial cells compared to those with partial response. There was no correlation between the numbers of types of intraglomerular and interstitial cells and the degree of proteinuria at presentation. Also no association was found between intraglomerular or interstitial cell population and subsequent relapse of proteinuria. In conclusion, interstitial but not intraglomerular mononuclear cells seem to determine the initial response of proteinuria to corticosteroids in patients with IMN.
Department of Nephrology, Aristotelian University of Thessaloniki, Greece.
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E
Alexopoulos
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M
Leontsini
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M
Papadimitriou
D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal; D001706:Biopsy; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D005260:Female; D015433:Glomerulonephritis, Membranous / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D016130:Immunophenotyping; D007249:Inflammation / Q000209:etiology / Q000473:pathology; D007678:Kidney Glomerulus / Q000276:immunology / Q000473:pathology*; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011239:Prednisolone / Q000627:therapeutic use*; D011507:Proteinuria / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D012189:Retrospective Studies
D000911:Antibodies, Monoclonal; D011239:Prednisolone