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Results for “NEPHROSIS, LIPOID”

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At least 145 records · Page 8Linked to original sources
PubMed1981

Concanavalin A-induced suppressor cell activity in lipoid nephrosis.

Suppressor cell activity (SCA) was analysed in 28 patients with lipoid nephrosis (LN) and 11 patients with chronic proliferative glomerulonephritis (CGN). We have assessed the ability of peripheral blood lymphocytes (PBL) stimulated by concanavalin A (Con A) to inhibit the proliferative response of normal allogeneic lymphocytes by both Con A and phytohaemagglutinin (PHA). It was found that the LN patients in the earlier phase of relapse had significantly increased levels of suppression index (SI) were compared with the values obtained with normal controls. In contrast, the mean suppression values in the PBL from LN patients in remission and CGN patients with or without nephrotic syndrome, whether the mitogen used was Con A or PHA, were similar to those of the control subjects. Moreover, when individual patients were followed through their clinical illness, LN patients had high levels of SI, particularly in the beginning of acute exacerbations; the SI levels than decreased sharply in the latter phase of relapse and again increased to relatively normal levels with the onset of clinical remission. These in vitro findings suggest that there exists an alteration in Con A-induced SCA in a group of patients with LN.

Adolescent↗
PubMed1989

Decreased production of interleukin-1 by monocytes from patients with lipoid nephrosis.

In order to further characterize monocyte function in patients with lipoid nephrosis (LN), we studied the production of interleukin-1 (IL-1). In this study we examined the ability of peripheral blood monocytes (PBM) from LN patients to produce this monokine in vitro under the stimulus of bacterial lipopolysaccharide (LPS). The levels of IL-1 were decreased in patients with LN compared with those in normal controls and lower in LN patients with nephrotic syndrome (NS) than in those without NS. In contrast, the values in IgA nephropathy (IgAN) patients with or without NS did not differ from normal subjects. The addition of indomethacin, an inhibitor of prostaglandin synthesis, partially restored this defect. These results suggest that the impaired IL-1 production of LN PBM is probably attributable, at least in part, to increased prostaglandin production and possibly influences the immune status of LN patients.

Adolescent↗
PubMed1995

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 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.

Adolescent↗
PubMed2000

T-cell lineage acute lymphoblastic leukemia with chromosome 5 abnormality in a patient with Crohn's disease and lipoid nephrosis.

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.

Adolescent↗
PubMed1998

Anti-interleukin 8 antibody abolishes effects of lipoid nephrosis cytokine.

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.

Adolescent↗
PubMed1982

Fenoprofen nephropathy: lipoid nephrosis and interstitial nephritis. A possible T-lymphocyte disorder.

Five patients are presented, each of whom had an acute idiosyncratic reaction to fenoprofen calcium (Nalfon) characterized by acute renal failure and marked proteinuria. Renal pathology was similar in all patients. Light microscopy revealed marked lymphocytic inflammatory infiltrates and normal glomeruli. Immunofluorescent staining was minimal or absent. Electron microscopy showed fusion of podocytes in otherwise normal glomeruli. Two patients were studied using T-cell and B-cell specific fluorescent staining, which revealed that the interstitial infiltrates were composed exclusively of T-lymphocytes. This finding is considered in relation to prior experimental and theoretic work. It is suggested that the various clinical and pathologic findings in fenoprofen nephropathy are all manifestations of a disordered cell-mediated immunity.

Acute Kidney Injury↗