Open AccessIL‐1‐like production in adriamycin‐induced nephrotic syndrome in the rat
Author(s) -
BRICIO T.,
MOLINA A.,
EGIDO J.,
GONZALEZ E.,
MAMPASO F.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb06423.x
Subject(s) - proteinuria , nephrotic syndrome , cytokine , nephrosis , glomerulonephritis , immunology , mediator , lipopolysaccharide , renal glomerulus , medicine , endocrinology , biology , kidney
SUMMARY Rats receiving a single dose of adriamycin (7·5 mg/kg) develop heavy proteinuria and morphological abnormalities similar to those observed in minimal change nephrotic syndrome in humans. IL‐1‐concomitance between enhanced I‐a display by resident glomerular macrophages. IL‐1‐like cytokine secreted by whole isolated rat glomeruli and proteinuria was observed in adriamycin‐injected rats during the experimental protocol. In addition, in vitro studies have shown that after stimulation with adriamycin or lipopolysaccharide (LPS) this cytokine is mainly produced by resident glomerular macrophages in culture. Although the precise mechanism of proteinuria in this model needs to be further studied, our results indicate that IL‐1‐like cytokine could be an important mediator implicated in the structural and functional disturbances occurring at the glomerular capillary wall level in adriamycin nephrosis.