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In previous research, we showed that when peripheral blood mononuclear cells (PBMC) from patients with idiopathic minimal lesion nephrotic syndrome (IMLNS) in relapse were cocultured with rat glomeruli, there was an increased glomerular basement membrane (GBM) uptake of 35sulfate. This study was done to determine whether the increased uptake was due to substances secreted into the nephrotic PBMC culture supernatants. 35sulfate uptake in rat GBM was significantly higher when glomeruli were cocultured with PBMC from 12 IMLNS patients in relapse (geometric mean [GM] = 513 cpm/mg) than when simultaneous assays were done using either PBMC from eight control subjects (GM = 158) (p less than 0.05) or glomeruli incubated without PBMC (GM = 275 cpm/mg) (p less than 0.01). 35sulfate uptake did not increase when glomeruli were cocultured with PBMCs from 11 MLNS patients in remission. Rat GBM 35sulfate uptake was significantly higher when glomeruli were incubated in the supernatants of the PBMC cultures from 16 IMLNS patients in relapse (GM = 234 cpm/mg) than it was when glomeruli were cultured in the supernatants from normal control PBMC (GM = 141 cpm/mg; p less than 0.002) or from glomeruli cultured alone (GM = 141 cpm/mg) (p less than 0.04). Supernatants from PBMC cultures of 11 IMLNS patients in remission did not increase rat GBM 35sulfate uptake. These data suggest that PBMC from IMLNS patients in relapse secrete a factor(s) released into supernatants that increases the 35sulfate rat GBM uptake. Since sulfated compounds in the GBM play a role in glomerular permeability, this finding may have pathogenic significance.

Effect of Supernatants from Nephrotic Peripheral Blood Mononuclear Cells on 35Sulfate Incorporation in Rat Glomerular Basement Membrane