Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Light chain proteinuria was found in 9 of 17 tuberculosis patients treated with rifampin. Concomitant assay of cellular mediated immunity in these patients using skin test antigen and a lymphokine in vitro test provided results that were different. Response to Varidase skin test antigen was negative for all eight tuberculosis patients tested, but there occurred a hyper-responsiveness of the lymphocytes of these eight patients to phytomitogen (PHA-P). as well as of those of seven other tuberculous patients. This last finding may be related to time of testing and/or endogenous serum binding of rifampin which could have inhibited mitogen activity for the lymphocyte.
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PMID:Light chain proteinuria and cellular mediated immunity in rifampin treated patients with tuberculosis. 80 91

Lymphocytes from N.S. patients, in culture and stimulated by PHA or Con A, release a lymphokine which increases vascular permeability; this factor is not present in normal subject and in control supernatants. Pharmacological and biological properties of this factor are similar to the guinea pig S.R.F. (PICK, TURK, MAILLARD). Modifications observed with meclofenamate, DTTC and addition of N.H.S. suggest that it could be an activator of the kinin system. Physicochemical studies show that it is a protein migrating as albumin. We have also recently demonstrated (unpublished data) the relationship of this factor with proteinuria: injections of active supernatants in rats renal artery is immediately followed by increase in proteinuria from 0,8 mg/h to 3,5 mg/h. Up to date, lymphokines have been studied in animals but seldom in human. Our results show that in human, variations in lymphokine production may be present. Pathogenic implications are now under study.
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PMID:Lymphokine 'skin reactive factor' (SRF) and the nephrotic syndrome. 123 73

In 2 patients with the nephrotic syndrome, unsuspected solid tumors were found. One was a small cell lung carcinoma, accompanied with the syndrome of inappropriate ADH secretion. The other was a cancer of the breast with lymph node and bone metastases. In both, renal biopsy showed minimal change disease without immune complex deposits. There are only 14 other reported cases of paraneoplastic lipoid nephrosis complicating solid tumors. Such cases lead to the discussion on the respective roles of tumor cell gene product(s) inducing proteinuria and of lymphokine secretion by lymphocytes directed against the tumor itself. Cancer should be considered as a possible etiology of the minimal change nephrotic syndrome in the adult.
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PMID:Minimal change nephrotic syndrome revealing solid tumors. 813 50

Minimal change nephrotic syndrome has been reported to be a lymphocyte-mediated disorder. It has been suggested that the secretion of lymphokine(s) is involved in the pathogenesis of MCN and in determining proteinuria. The presence of a soluble form of IL-2 receptor (sIL-2R) has been previously described in the sera of patients with some autoimmune disorders. In this work, we report the detection of high sIL-2R levels, both in the plasma (mean value 844 +/- 436 U/ml versus normal value 276 +/- 86 U/ml) and urine of patients with MCN during the nephrotic phase alone. Instead, when the patients achieve stable remission, sIL-2R levels decrease to within normal values (mean value 332 +/- 272 U/ml). Furthermore, during the nephrotic syndrome we observed a significant inverse relationship between sIL-2R plasma levels and the mitogenic response to PHA (p less than 0.005). Since sIL-2R exerts a down-modulation on T-proliferative expansion, sIL-2R might represent one of the inhibitory serum factors extensively reported in the serum of patients with MCN-induced nephrotic syndrome.
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PMID:Lymphocyte release of soluble IL-2 receptors in patients with minimal change nephropathy. 158 55

We report a transient neonatal nephrotic syndrome in two infants born to a mother with idiopathic nephrotic syndromes (INS). The mother, born in Mali in 1966, had a normal first pregnancy, with a normal live child. Six months later a nephrotic syndrome appeared with normal renal function; renal biopsy disclosed slight lesions of focal and segmental glomerulosclerosis. Prednisone and ciclosporin were totally ineffective. In 1986 and 1988 two pregnancies occurred with normal gestation outcome; however, the two births were premature (35 weeks) with hypotrophic infantas (2.160 and 2.080 kg). In both cases urine analysis revealed neonatal heavy proteinuria, with low serum protein and hypoalbuminemia; proteinuria decreased and disappeared within 2 and 3 weeks respectively; simultaneously protidemia and albuminemia were normalized. Thus, a transitory nephrotic syndrome, resolving spontaneously, occurred in two successive offsprings of a patient with INS. These cases are in keeping with the hypothesis that heavy proteinuria in nephrotic syndrome might be linked to a circulating humoral factor and that INS is a disorder linked to T-lymphocyte function with enhanced production of a lymphokine acting on vascular permeability.
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PMID:[Transmission of nephrotic syndrome to two neonates. Spontaneous regression]. 182 64

Monocytes have been demonstrated to play an important role in acute serum sickness (AcSS) nephritis. Because accumulation of monocytes within the glomeruli could be the result of local lymphokine production, we studied migration inhibition factor (MIF) activity in supernatants from glomerular cultures, analyzed its temporal relationship with monocyte and lymphocyte accumulation, and tested the effect of anti-T lymphocyte monoclonal antibody on local MIF production. AcSS was induced in 12 rabbits, and one additional rabbit had antigen elimination without proteinuria. Single nephrectomy was performed at the time of antigen elimination in all animals; the remaining kidney was removed four days (4 rabbits) or 14 days afterwards (5 rabbits). In glomerular cross sections (gcs), lymphocytes were identified using monoclonal antibody M108, and monocytes by nonspecific esterase stain (ES). MIF activity was determined in supernatants of cultures of isolated glomeruli by the agarose microdroplet method. Peak of MIF activity (84.3 +/- 2.6%, SEM) was observed the first day of proteinuria in association with peak of lymphocyte infiltration (1.15 +/- 0.1 lymphocytes/gcs) and monocyte infiltration (2.4 +/- 0.3 mean ES score/gcs). MIF activity diminished by day 4 (66.0 +/- 6.3%) and reached control levels by day 14 (12.8 +/- 3.2%). There was a significant correlation between lymphocyte infiltration and MIF activity (r = 0.776, P less than 0.0001) as well as between MIF activity and monocyte accumulation (r = 0.858, P less than 0.0001). In five additional rabbits with AcSS, glomeruli were isolated, treated successively with M108 and normal rabbit serum, and supernatants harvested from 24-hour cultures were tested for MIF activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Migration inhibition factor in acute serum sickness nephritis. 207 55

We have previously described a significant increase in 35sulfate uptake in rat glomerular basement membrane (GBM) when glomeruli were cocultured with peripheral blood mononuclear cells (PBMC) from patients with idiopathic minimal-lesion nephrotic syndrome (IMLNS) in relapse, but not with PBMC of IMLNS patients in remission. In the present study we examined the effect of prednisone therapy on the PBMC-mediated increase in 35sulfate GBM uptake. The GBM 35sulfate uptake after rat glomeruli were cocultured with PBMC from 11 IMLNS patients in relapse (geometric mean 437 cpm/mg dry glomerular weight) was significantly higher than the incorporation observed in glomeruli cultured alone (geometric mean 229 cpm/mg dry glomerular weight; p less than 0.01). However, no significant differences in 35sulfate uptake were seen between glomeruli cultured alone and glomeruli cocultured with PBMC from IMLNS patients when PBMC were obtained from the 11 patients on treatment with prednisone (2 mg/kg/day) or the same patients in remission and off prednisone therapy. Prednisone therapy abolished the PBMC-mediated increased 35sulfate uptake by rat GBM. GBM sulfated compounds seem to play a role in glomerular permeability. The temporal relationship between inhibition of GBM sulfate incorporation by prednisone and resolution of the proteinuria support the hypothesis that PBMC from IMLNS patients in relapse could secrete a lymphokine which by altering the metabolism of the GBM sulfated compounds may subsequently increase glomerular permeability to plasma proteins.
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PMID:Effect of prednisone on nephrotic peripheral blood mononuclear cell mediated increase in 35sulfate uptake in rat glomerular basement membrane. 279 47

The role of serum soluble immune response suppressor (SIRS) lymphokine in the prediction of steroid responsiveness in idiopathic nephrotic syndrome was investigated. Serum SIRS was detected by its capacity to suppress the induction of plaque forming cells in pokeweed mitogen-stimulated in vitro lymphocyte culture in a dose dependent manner, and specificity was determined by the ability of monoclonal anti-SIRS coated beads to specifically absorb the suppressor activity. Serum SIRS was present in 7 of 18 patients with steroid responsive nephrotic syndrome and in 1 of 6 patients with nephrotic syndrome who were resistant to steroid treatment. It was also found in 2 of 4 patients with nephrotic syndrome which would be expected to be resistant to steroid treatment, in 2 of 10 patients with steroid responsive nephrotic syndrome in remission and in 2 of 8 normal healthy controls but was absent in 8 patients with non-nephrotic proteinuria secondary to a variety of renal disease. It was concluded that, although serum SIRS was present more often in patients with steroid responsive nephrotic syndrome, it is not a sensitive enough assay for predicting the response to treatment.
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PMID:The role of soluble immune response suppressor lymphokine in the prediction of steroid responsiveness in idiopathic nephrotic syndrome. 280 58

Classically, the histological lesion observed in a drug-or heavy metal-induced nephrotic syndrome is membranous glomerulonephritis. We report two cases of "toxic" nephrotic syndrome with unusual histological features. One was secondary to mercury intoxication and the other, to D-penicillamine in a patient with rheumatoid arthritis. In both cases, renal biopsy revealed minimal glomerular changes. The proteinuria rapidly disappeared after exposure to the toxic agent was discontinued. Genetic factors and a disregulation of the immune system with lymphokine production may be responsible for these renal changes. This study demonstrates that renal biopsy is necessary in this clinical setting.
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PMID:[Lipoid nephrosis of toxic origin. 2 cases]. 294 17

Idiopathic nephrotic syndrome (INS) is associated with a disorder of T-lymphocyte function, and an enhanced production of a vasoactive lymphokine, the vascular permeability factor (VPF). In an attempt to evaluate lymphocyte activation in various phases of INS, we measured beta 2-microglobulin (beta 2m) levels in lymphocyte culture supernatants (LCS). In 23 cases of untreated active INS, beta 2m levels in unstimulated LCS were significantly increased in comparison with those of 13 cases of untreated INS in complete remission (p less than 0.001), of 17 cases of active membranous nephropathy (p less than 0.01) and of 14 controls (p less than 0.001). In 13 patients treated with cyclosporine (Cs) (3-4.5 mg/kg/d) during 3 months, beta 2m levels were within the normal range. Although the beta 2m of 7 Cs patients without proteinuria was lower than 5 Cs patients with residual proteinuria, the difference was not statistically significant. In 15 prednisone(Pr)-treated INS patients, beta 2m levels were normalized. However their beta 2m levels were lower in 8 cases of complete remission than in 7 cases of persistent proteinuria (p less than 0.05). Concanavalin-A stimulation increased beta 2m amounts in all groups with a similar magnitude. In vitro addition of Cs (100 ng/ml) inhibited both beta 2m and VPF elevations observed in active INS. beta 2m level and VPF activity were significantly correlated (r = 0.54, p less than 0.01). High levels of beta 2m in LCS from INS are the consequence of an enhanced cellular synthesis and they are inhibited by Pr and Cs. Thus beta 2m increase in INS indeed reflects lymphocyte activation.
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PMID:Enhanced beta 2-microglobulin levels in lymphocyte culture supernatants from patients with idiopathic nephrotic syndrome: inhibition of lymphocyte activation by cyclosporine. 306 18


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