Biomedical subjects

C Sapin

Publications and source records attributed to C Sapin.

75 records · Page 5Linked to original sources

PubMedDate not supplied

[Induction of anti-glomerular basement membrane antibodies in BN rats: genetic control].

Mercuric chloride induces anti-glomerular basement membrane antibodies in Brown Norway rats (Ag B3) and not in Lewis rats (Ag B1). Studies on (Lewis X BN) F1 and F2 and with back-crosses (Lewis X BN) F1 X Lewis demonstrate a genetic control for this immune response. This genetic control probably depends on two non-linked, autosomal and dominant genes. One of these genes is linked to the major histocompatibility locus.

Animals↗

PubMedDate not supplied

Complement studies in BN rats with mercuric chloride-induced immune glomerulonephritis.

Whole complement haemolytic activity (CH50) changes were examined in 71 rats, developing and HgCl2-induced biphasic immune glomerulonephritis. In some rats, serum C4 level was also studied. Whole CH50 level was compared with proteinuria and C3 glomerular deposits. In control rats or in rats injected with low doses of HgCl2, there was no complement decrease. In rats injected with a high dose, after an initial increase (also observed in controls), CH50 level decreased between day 12 and day 20, sometimes dramatically. This decrease, observed during the first phase, was transient, CH50 levels returning to normal before day 30. Serum C4 level varied in accordance with CH50, indicating a classical pathway activation of complement. Fall in CH 50 and proteinuria was correlated: the heavier the proteinuria, the greater the fall in complement (p < 0.01). Whether proteinuria is or is not the consequence of the complement activation, remains to be demonstrated.

Animals↗

PubMedDate not supplied

Immune type glomerulonephritis induced by HgCl2 in the Brown Norway rat.

HgCl2 chronically injected in the Brown-Norway rat induced a biphasic renal disease. The first stage was characterized by anti-glomerular basement membrane antibodies. The second stage by the appearance of immune complexe type deposits in the glomerular tufts and in the small renal arteries. These immune complexes were constituted of a basement membrane component and anti-basement membrane antibodies. Other immune complexes were perhaps involved. In most of the rats, a proteinuria and a nephrotic syndrome appeared, as a consequence of this immune disease. No abnormalities were observed in Lewis rats, suggesting a role for a genetic control of this immune response.

Animals↗