EFFECT OF LIPOID NEPHROSIS CYTOKINE ON GLOMERULAR SULFATED COMPOUNDS AND ALBUMINURIA

Supernatants from peripheral blood mononuclear cells cultures of 30 idiopathic, minimal lesion, nephrotic syndrome (IMLNS) patients in relapse and the same patients in remission were fractionated by gel filtration chromatography. Fractions eluting with carbonic anhydrase (29 kilodaltons) were infused for 5 days at the rate of 10 mu l/h into the left renal artery of Wistar rats using an Alter osmotic pump. On the last day of infusion, rats were injected with (35)sulfate (1.0 mCi/200 g) intraperitoneally and killed after 8 h. Glomeruli were isolated and glomerular basement membrane (GEM) obtained. There was a significant increase in (35)sulfate uptake by GEM of the infused kidney (302 +/- 92 cpm/mg dry glomerular weight, mean +/- SEM) compared with the uptake seen in the contralateral kidney (157 +/- 36, P < 0.01) when the fraction from IMLNS patients in relapse was infused. No significant differences in (35)sulfate incorporation were seen between infused kidney (166 +/- 41) and contralateral kidney (172 +/- 64) when the same fraction from patients in remission was administered. A significant increase in albuminuria was seen on the last day of infusion (14.2 +/- 1.0 mg/24 h, mean +/- SEM) when supernatant factor from IMLNS patients in relapse was used. No significant differences in urinary albumin excretion prior to and after infusion were seen when the same fraction from IMLNS patients in remission was administered. The in vivo infusion of supernatant factor from IMLNS patients in relapse increased the (35)sulfate uptake by GEM and augmented albuminuria, suggesting that the factor may have pathogenic significance in the proteinuria of IMLNS.