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)

Normal rats were injected with guinea pig anti-rat glomerular basement membrane antibodies of the IgG1 or IgG2 class or with their F (ab') 2 fragments, in order to study which antibody site triggers the alternate complement pathway in vivo. Both IgG classes were able to induce a heavy proteinuria and led to C3 deposition in the glomeruli in a pattern similar to their own distribution along the glomerular basement membrane, as shown by the immunofluorescence technique. The Fab(ab')2 fragment of IgG2 did not produce C3 binding or proteinuria. The F(ab')2 fragment of IgG1 was difficult to obtain devoid of Fc determinants. A F(ab')2 fragment of IgG1 still bearing Fc determinants led to C3 binding and proteinuria, whereas the true F(ab')2 fragment of IgG1 had none of these effects in two out of three animals.
J Immunol 1975 Sep
PMID:Further studies on the biologic properties of guinea pig IgG1 antibodies. II. In vivo activation of C3 by anti-glomerular basement membrane antibodies. 5 Mar 74

Cells from human glomeruli explanted in tissue culture were grown and subcultivated up to 12 to 13 times. Light and electron microscopic studies revealed these cells to be morphologically distinct from fibroblasts. By electron microscopy, an extracellular material resembling basal lamina was seen and prominent intracellular microfilaments were evident. Immunofluorescent microscopy demonstrated reactivity of heterologous antiglomerular basement membrane antibody with aggregates of extracellular material. Absorption experiments using antiglomerular basement membrane antibody showed that the extracellular materiial shared some antigenic components with glomerular basement membrane. Antibody to cultured glomerular cells stained the mesangium and glomerular basement membrane of normal human kidney. This antibody was nephrotoxic in monkeys, induced proteinuria with proliferative glomerulonephritis, and localized to the mesangium and glomerular basement membrane of monkey glomeruli. These findings and the presence of prominent intracellular microfilaments (contractile elements) suggest that the glomerular cells may be of mesangial origin.
Lab Invest 1975 Sep
PMID:Human glomerular cells in tissue culture. 5 Nov 34

Although the precise etiologic incitant of the minimal lesion idiopathic nephrotic syndrome of childhood is not known, it is likely that a host mechanism mediates the permeability alterations of the glomerular capillary wall resulting in massive proteinuria. As a first step in examining the possibility that local kinin release may account for the proteinuria in this disorder, two parameters of the plasma kinin-generating system, plasma prekallikrein and kallikrein inhibitor, were assayed during 27 nephrotic episodes in 21 corticosteroid-responsive children. Plasma kallikrein was assayed by means of its esterase activity on a synthetic arginine ester substrate, N-alpha-tosyl-L-arginine methyl ester (TAMe), after activation of Hageman factor by kaolin. This activity, after subtraction of spontaneous arginine esterase activity (i.e., TAMe esterase activity measured in plasma not exposed to kaolin) is derived from prekallikrein. Plasma prekallikrein activity in 11 normal children was 99.6 +/- 2.9 mumol TAMe hydrolyzed/ml plasma/hr (mean +/- SEM). Kallikrein inhibitor was quantified in arbitrary units. Kallifrein inhibitor activity in 11 normal children was 0.94 +/- 0.04 units. During the overt nephrotic syndrome, before initiation of intensive daily corticosteroid treatment, mean values were: prekallikrein, 58.5 +/- 7.24 mumol/ml/hr; and kallikrein inhibitor, 0.35 +/- 0.06 units. After corticosteroid-induced remission occurred, mean values were: plasma prekallikrein, 118.6 +/- 3.2 mumol/ml/hr; and kallikrein inhitor, 0.78 +/- 0.03 mumol/ml/hr. Both parameters were again assayed in 14 of the 21 children after complete cessation of corticosteroid treatment. Plasma prekallikrein was normal, 99.6 +/- 4.8 mumol/ml/hr; but kallikrein inhibitor was still somewhat depressed, 0.84 +/- 0.03 units. A subset of 9 patients had marked depression of plasma prekallikrein to levels less than 20 mumol/ml/hr and essentially undetectable inhibitor activity. Serum alpha-2 macroglobulin was elevated in nephrotic patients: mean value during relapse, 862 +/- 29 mg/100 ml; during corticosteroid-maintaining remission, 615 +/- 29 mg/100 ml. After cessation of corticosteroids, mean serum level was 481 +/- 20 mg/100 ml. The proportional reduction of plasma prekallikrein and kallikrein inhibitor suggested that an enzyme-inhibitor complex formed in vivo, perhaps at a local site of activation in proximity to the glomerular basement membrane. These data suggest that the plasma kinin-generating system may be the host effector mechanism subserving the increased glomerular capillary permeability in the minimal lesion nephrotic syndrome of childhood.
Pediatr Res 1975 Sep
PMID:A study of the plasma kinin-generating system in children with the minimal lesion, idiopathic nephrotic syndrome. 5 8

Anti-beta 2 microglobulin sera (beta2m AS) rendered specific after extensive absorptions were obtained following immunization of rabbits with highly purified beta2m prepared from urine of tubular proteinuria. beta2m AS were cytotoxic upon addition of selected rabbit complement for human T and B lymphocytes. Partial inhibition of sheep red blood cells receptor recognition on T lymphocytes (E rosettes) and C3 component recognition on B lymphocytes (EAC rosettes) was obtained only with high concentrations of Fab'2 anti-beta2m, eliminating a direct association of beta2m and those receptors. Fab'2 anti-beta2 induced very little inhibition of Fc portion receptor recognition (EA rosettes), but they had no effect on lysis of targets covered with IgG anti-targets (ADCC), a function mediated through that receptor. Anti-beta2m antibodies in excess inhibited antigen-induced proliferation (PPD) and the mixed lymphocyte reaction (MLR) performed in AB serum and fetal calf serum containing media ; whereas a potentiation of the response occurred in the presence of an antigen excess (beta2m) brought by the culture medium (AB serum) suggesting involvement of immune complexes. Pretreatment of responding cells with beta2m AS did block unilateral MLR ; conversely, treatement of stimulating cells had no effect. Independent migration of T cell membrane antigens (HTLA) and beta2m upon addition of suitable ligands, as well as the lack of inhibition by Fab'2 anti-beta2m of complement dependent lysis with IgG anti-HTLA, excluded possible association of HTLA and beta2m.
Pathol Biol (Paris) 1978 Sep
PMID:[Study of lymphocyte membrane antigens and receptors with antibodies to beta2-microglobulin (author's transl)]. 8 67

The results of low molecular weight (LMW) proteinuria test in urines of patients and suspect subjects in an endemic area of Balkan endemic nephropathy (BEN) in Yugoslavia are reported. An accordance between the positive LMW test and the clinical diagnosis of BEN has been found in more than 70%. The authors claim that LMW immunodiffusion test is a very useful procedure for detecting BEN and a great aid in the epidemiological work in the endemic field. The results of determining beta2-microglobuline (beta2m) in serums and urines by radioimmunoassay technique as well as counting of clearances of endogenous creatinine in healthy persons, "endangered" subjects in endemic area, and BEN patients without azotemia, with azotemia and uremia are reported. The group of 17 patients suffering of BEN without azotemia having slightly or more markedly lowered creatinine clearances showed higher serum and much higher urinary concentration of beta2m which are not in proportion with creatinine clearance. The results are interpreted so far as a consequence of the predominant tubular lesion in BEN. In groups of patients with azotemia and uremia no differences in beta2m handling have been found. The report has a preliminary character and requires further study.
Pathol Biol (Paris) 1978 Sep
PMID:beta2-Microglobulin in Balkan endemic nephropathy. 8 72

For the range of exposure to heavy metals sustained by the different groups of workers, a significant increase in the urinary excretion of low and/or high molecular weight proteins was found in the workers exposed to cadmium or to lead + cadmium, but no in those exposed to lead only and those exposed to mercury. Our observations suggest that the classical "tubular" proteinuria induced by cadmium has two not necessarily concomitant components : a "tubular type" component with increased excretion of low molecular weight proteins and a "glomerular type" component with increased excretion of high molecular weight proteins.
Pathol Biol (Paris) 1978 Sep
PMID:Urinary excretion of beta2-microglobulin and other proteins in workers exposed to cadmium, lead or mercury. 8 75

Anticoagulation has been reported to ameliorate antiglomerular basement membrane glomerulonephritis (anti-GBM-GN) while its effect on chronic immune complex glomerulonephritis (IC-GN) as studied in the NZB mouse is unclear. Chronic serum sickness IC-GN was induced in rabbits by injecting bovine serum albumin (BSA) daily. Anti-GBM-GN was induced by i.v. injection of a known amount of heterologous anti-GBM antibody. Heparin was administered beginning at two to six weeks after the first BSA injections or before the administration of anti-GBM antibody, on various schedules from 5000 U every 12 hr to 8000 U every 8 hr. With this dosage the partial thromboplastin time remained greater than 1-1/2 to 2-1/2 times the control at the time of the subsequent heparin injection. Heparinized and nonheparinized groups were matched according to duration of disease, maximum anti-BSA concentrations or anti-GBM antibody dosage--and no significant differences were found in proteinuria; severity of the glomerular histologic lesions; or immunofluorescence patterns of immunoglobulin G (IgG), third component of complement (C3), BSA or fibrinogen-related antigen(s) (FRA). Crescent formation was not prevented. This study shows that heparin in the maximum permissible dosage is ineffective in preventing glomerular FRA deposition or altering the progression of experimental IC-GN or anti-GBM-GN in rabbits.
Kidney Int 1975 Sep
PMID:Failure of heparin to affect two types of experimental glomerulonephritis in rabbits. 12 30

A 22-year-old man with a ventriculojugular shunt had edema, hematuria, proteinuria, hypocomplementemia, azotemia, and S epidermidis bacteremia. Initial percutaneous renal biopsy showed a diffuse proliferative glomerulonephritis. Subendothelial and intramembranous deposits were seen on electron microscopy. Immunofluorescent studies were positive for IgG and C3. A repeat percutaneous renal biopsy six weeks after cessation of antibiotic therapy revealed a mild proliferative glomerulonephritis with some evidence of resolution. No deposits were seen on electron microscopy and immunofluorescent studies were negative. At elective shunt revision three months after cessation of therapy, culture of the jugular portion of the removed shunt revealed S epidermidis. Early recognition of immune complex glomerulonephritis occurring with an infected ventriculovascular shunt should permit early treatment (antibiotic therapy and removal of the infected foreign body) and a favorable outcome.
South Med J 1977 Sep
PMID:Immune complex disease associated with an infected ventriculojugular shunt: a curable form of glomerulonephritis. 14 64

Immunocomplex nephritis as one of the serious side-effects is dealt with on the basis of 41 patients with Wilson's Disease who have been treated for many years and were stabilised on D-penicillinamine. In one quarter of the patients, proteinuria was found 1 to 5 years after the beginning of the therapy. Until now, an immunocomplex nephritis with diffuse granular, mainly epimembranous IgG and C3 deposits on the glomerular basement membran was found in four patients. No circulating antibodies against cell nuclei were found. The finding of immunocomplex nephritis calls for the discontinuation of the therapy for an at present unknown period of time.
Psychiatr Neurol Med Psychol (Leipz) 1979 Sep
PMID:[Serious side effects with D-penicillamine therapy for Wilson's disease]. 16 3

Glomerular epithelial slit alterations and their relation to proteinuria have not been studied in detail in New Zealand Black/White (NZB/W) mice. The kidneys of proteinuric and nonproteinuric female NZB/W mice and normal Swiss albino mice were perfusion-fixed with tannic acid-glutaraldehyde and studied by light and electron microscopy. Semiquantitative studies were performed on full montages of glomeruli enlarged 10,000 times. Fine structural alterations of the epithelial slits, with emphasis on the slit diaphragm, were studied on semiserial thin sections. Proteinuric NZB/W mice with features of membraneous nephropathy exhibited: (1) wedging of electron-dense deposits below the slit diaphragm, (2) enlargement and distortion of interpedicel spaces, (3) displacement, folding, and stacking of slit diaphragms, (4) formation of occluding junctional complexes in residual slits, and (5) variable loss of foot processes. Similar alterations were not observed in controls or nonproteinuric NZB/W mice, including animals having complexes inglomerular mesangia but not in epithlialslits. These studies show that in NZB/W mice, abnormal protein excretion is associated with structural modification of the slit pore and suggest a role for such a component in the process of protein ex
Lab Invest 1976 Sep
PMID:An ultrastructural study of the glomerular slit diaphragm in New Zealand black/white mice. 18 54


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