[Serum level and urinary excretion of soluble Fas (sFas) in patients with primary glomerulopathies].
Fas ligand (Fas-L) is a lethal cytokine that promotes apoptosis, as well as the immune and inflammatory responses through cross-linking of the Fas receptor. Soluble Fas (sFas) blocks apoptosis by inhibition of binding between Fas and Fas-L or soluble Fas-L. The aim of the work was to investigate the prognostic significance and role of the serum levels and urinary excretion of sFas in various types of adult chronic primary glomerular diseases. We studied 53 patients with primary glomerular diseases (5 minimal change--MC; 4 focal glomerulosclerosis--FS; 4 membranous nephropathy--MN; 12--mesangial proliferative GN--MesPGN; 18 IgA nephropathy--IgAN; 6 membranoproliferative GN--MPGN, and 4 extracapillaris GN--ExGN) and 10 healthy persons. Renal biopsies were evaluated by light and fluorescence microscopy. Concentrations of sFas were measured by ELISA (BIOSOURCE international kits). The treatment of patients consisted of 3 to 5 i.v. methylprednisolone pulses (1.0 g per single dose, average total 1.0 g/20 kg given alternate days) followed by oral prednisone 20 to 25 mg/day and six monthly i.v. cyclophosphamide 0.6 g/l m2/month. The serum levels and urinary excretion of sFas in the patients with MC, and MN were similar to controls. However, the serum levels and urinary excretion of sFas were insignificantly elevated in patients with MesPGN, MPGN, FS, and ExGN, but significantly elevated in patients with IgAN as compared with control and patient groups. In patient groups serum Cr showed significant correlations with interstitial volume in renal biopsy, and urinary excretion of sFas, but serum levels of sFas with interstitial volume. Serum levels and urinary secretion of sFas in patients with renal insufficiency (Cr > 1.3 mg%) and reduction of proteinuria < 50% after 1-year treatment was higher before treatment than in another patient groups. These results suggest that increased serum and urinary excretion of sFas in proliferative glomerulonephritis PGN (particularly in IgAN) may inhibit apoptosis in glomeruli and may be one of the progressing factors in PGN.
Kacprzyk
Feliks
F
Klinika Nefrologiczna Instytutu Medycyny Wewnetrznej AM w Łodzi.
D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood / Q000652:urine; D016022:Case-Control Studies; D004359:Drug Therapy, Combination; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005921:Glomerulonephritis / Q000188:drug therapy / Q000276:immunology*; D006801:Humans; D007166:Immunosuppressive Agents / Q000008:administration & dosage; D008297:Male; D008775:Methylprednisolone / Q000008:administration & dosage; D008875:Middle Aged; D011241:Prednisone / Q000008:administration & dosage; D012995:Solubility; D013997:Time Factors; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019014:fas Receptor / Q000097:blood* / Q000652:urine*
D015415:Biomarkers; D007166:Immunosuppressive Agents; D014409:Tumor Necrosis Factor-alpha; D019014:fas Receptor; D011241:Prednisone; D008775:Methylprednisolone