[DIABETES IN A CHILD WITH LIPOID NEPHROSIS].
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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 microliters/h into the left renal artery of Wistar rats using an Alzet osmotic pump. On the last day of infusion, rats were injected with 35sulfate (1.0 mCi/200 g) intraperitoneally and killed after 8 h. Glomeruli were isolated and glomerular basement membrane (GBM) obtained. There was a significant increase in 35sulfate uptake by GBM 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 35sulfate 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 35sulfate uptake by GBM and augmented albuminuria, suggesting that the factor may have pathogenic significance in the proteinuria of IMLNS.
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Alterations in phagocytosis have been studied in 25 patients with idiopathic nephrotic syndrome (INS). At the time of investigation all patients had normal renal function.
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We describe a 17-year-old patient with a documented history of Crohn's disease (CD) and of minimal-change nephrotic syndrome (MCNS) in whom a diagnosis of T-cell acute lymphoblastic leukemia (ALL) was made. The diagnosis of ALL was established by morphological examination of bone-marrow aspirates and confirmed by means of immunophenotypic analysis showing the involvement of T-cell lineage leukemic cells. The lymphoid clone showed a karyotypic abnormality involving the long arm of chromosome 5 in a translocation (5;6). Few cases of CD complicated by ALL have been previously reported. The present one is the first case combining CD and ALL in a patient with a past history of MCNS. This raises the possibility of a relationship among those diseases. The possible mechanisms for such a relationship are discussed here.
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Supernatant factor from peripheral blood mononuclear cell (PBMC) cultures of idiopathic minimal lesion nephrotic syndrome (IMLNS) patients in relapse induces in vivo albuminuria and increases 35sulfate uptake by glomerular basement membrane (GBM) in rats. The purpose of this study was to evaluate the effect of anti-interleukin 8 (IL8) neutralizing antibody on the effects induced by the supernatant factor. Supernatant factor collected from six cultures of PBMC from IMLNS patients in relapse were combined and aliquotted into two samples. Anti-IL8 neutralizing antibody (750 ng) was added to one. Supernatant factor or supernatant factor and anti-IL8 antibody were infused for 5 days into the left renal artery of Wistar rats using an osmotic pump. On the last day of infusion, rats were injected with 35sulfate (1.0 mCi/200 g) intraperitoneally and killed after 8 h. Glomeruli were isolated and GBM obtained. There was a significant increase in 35sulfate uptake of the infused kidney (169 +/- 52 cpm/mg dry glomerular weight, mean +/- SEM) compared with the uptake seen in the contralateral kidney (116 +/- 41, P < 0.05) when the supernatant factor was infused alone. No significant differences in 35sulfate incorporation were seen between infused kidney (173 +/- 5) and contralateral kidney (190 +/- 49) when supernatant factor and anti-IL8 antibody were administered. A significant increase in albuminuria was seen on the last day of infusion (0.43 +/- 0.11 albumin/ creatinine ratio, mean +/- SEM) compared with the ratio prior to infusion of the supernatant factor alone (0.18 +/- 0.03, P <0.05). No significant differences in urinary albumin/creatinine ratios prior to and on the 5th day of infusion were seen when the supernatant factor was administered with anti-IL8 antibody. Supernatant factor effects were abolished by the addition of anti-IL8 neutralizing antibody, suggesting that the described effects are mediated by IL8.