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)

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.
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PMID:Failure of heparin to affect two types of experimental glomerulonephritis in rabbits. 12 30

Functional, histological and immune-histological examination were performed in altogether 64 Wistar-rats, in order to control the effect of a therapy with 2 mg/kg per body weight indomethazine lasting 2 months at the model of an experimental immune complex nephritis. In 44 rats after presensibilisation an immune complex nephritis was performed by intraperitoneal injections with human serum albumin which were repeated three times a week. 24 glomerulonephritis animals and other 20 animals without glomerulonephritis were daily administered indomethazin through a tube probe, the remaining 20 animals with glomerulonephritis served as untreated control groups. The excretion function of the kidney was tested before the beginning of the experiment, 2 weeks after the beginning of the therapy and the regular serum injections, respectively, and before the end of the experiment by determination of the biological half-life period of 131J-hippuran. In every case one day before this the proteinuria during 24 hours was determined. At the end of the experiment the kidneys were examined histologically and immune-histologically. The results showed that indomethazin does not lead to a clear influence on the proteinuria in the immune complex nephritis of the rat. The excretion of 131J-hippuran was significantly restricted, whereas the histological and immune-histological preparations in the animals with foreign serum injections showed clear changes of the glomeruli in the sense of an early stage of the immune complex nephritis, however, they did not show any essential influence by indomethazin. That is, indomethazin had altogether no favourable effect on the immune complex nephritis of the rat.
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PMID:[Treatment of experimental immune complex nephritis with indomethacin]. 15 98

Eleven rabbits were given bovine serum albumin i.v., in daily doses of 25 mg. Renal biopsy was performed on the 30th, 60th and 100th day of treatment and the specimens were subjected to light-, electron-microscopic and immunofluorescent studies, so as to follow up the dynamics of the glomerular process. Proteinuria and the serum creatinine and BUN levels were also measured. By the 100th day of treatment mesangioproliferative glomerulopathy had developed in 7, membranoproliferative glomerulopathy in 3 cases and membraneous glomerulopathy in 1 case. On the 30th day of treatment exudative glomerulopathy was demonstrable in the majority of the cases (in 9 animals). It is suggested that the earliest stage of the various glomerulopathies, regardless of their type, is marked by exudative lesions. The heaviest proteinuria was found in membraneous and membranoproliferative glomerulopathies. Changes in the serum creatinine and BUN levels indicative of a deteriorating renal function were noted in the membranoproliferative cases. The results are correlated with clinical observations of human glomerulopathies.
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PMID:Experimental glomerular lesions induced by chronic immune complex formation. II. Pathomorphological analysis. 15 42

Plasma proteins cross the glomerular basement membrane in inverse proportion to their molecular dimension; molecules larger than serum albumin are completely excluded from the glomerular filtrate. This filtration, which is purely passive, also depends of the electrical charge of the proteins; negatively charged proteins are indeed repelled by the negatively charged layer of sialogylcoproteins present along the outer surface of the epithelial cell membrane and extending to the glomerular basement membrane. The filtered proteins are selectively absorbed by the proximal tubular cells and are hydrolyzed by lysosomal enzymes. This results in a renal catabolism of proteins the importance of which depends on their ability to cross the glomerular barrier. In renal disease, proteinuria results either from an increased permeability of the glomerular basement membrane (selective or non-selective glomerular proteinuria) or from a diminished tubular reabsorption of normally filtered proteins of low molecular weight (tubular proteinuria).
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PMID:[Current concept of the mechanism of proteinuria]. 19 41

Toxicosis was induced in pregnant heifers by feeding 25,000 mg/head/day of FireMaster BP-6, a commercial blend of polybrominated biphenyls (PBB). The PBB feeding decreased dry matter intake approximately 50% by 4 days exposure. Emaciated animals became anorexic a few days prior to death at 33 to 66 days. Weight losses of heifers average 80 kg. Other clinical signs observed were dehydration, diarrhea, excessive salivation and lacrimation, fetal death, abortion, and general depression as evidenced by depressed heart and respiratory rates. Clinical signs were apparent after 10 days exposure and progressively intensified along with loss of condition until death. Clinicopathologic changes included significantly increased serum glutamic-oxaloacetic transaminase and decreased serum calcium by 30 days exposure. Lactate dehydrogenase, urea nitrogen, and bilirubin were elevated, and serum albumin decreased by 36 to 40 days. Principal urine changes were decreased specific gravity and moderate proteinuria. Pregnant heifers fed 0.25 or 250 mg/head/day for 60 days and nonpregnant heifers fed 250 mg/head/day for 180 days displayed neither clinical signs nor clinicopathologic changes indicating adverse effects from PBB exposure. Post-exposure, all heifers exposed to PBB for 60 days calved normally with zero calf mortality and were successfully rebred. Milk production was not different from control animals. Birth weights of calves from dams exposed to 250 mg PBB/head/day were significantly greater than calves of dams exposed to 0 mg or 0.25 mg/head/day. PBB exposure of dams produced no detrimental effects on calves as indicated by clinical signs, clinicopathologic changes, or performance.
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PMID:Effects of PBBs on cattle. I. Clinical evaluations and clinical chemistry. 21 5

We administered bovine serum albumin (BSA) 1 or 3 mg i.v. into hyper-immune Sprague-Dawley rats weekly for up to 6 months. Animals with free circulating antibody 1 h after BSA developed mesangial deposits of IgG and C-3 without proteinuria. Rats without free antibody at 1 h developed either mesangial or mesangial and glomerular basement membrane (GBM) deposits. Rats given 3 mg BSA tended to have GBM deposits, proteinuria and undetectable antibody at 1 h. By electronmicroscopy, all rats had mesangial and subendothelial dense deposits, while those with GBM lesions had intramembranous and subepithelial deposits with foot process obliteration. Light microscopic evaluation of kidney tissue revealed only mild histological changes similar to those in age-matched control rats. The present studies demonstrate that prolonged i.v. administration of BSA into rats results in the development of a chronic non-inflammatory nephropathy. Despite certain parallels to chronic serum sickness nephropathy in rabbits, species differences appear to modify the nephropathy in rats.
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PMID:Bovine serum albumin chronic serum sickness nephropathy in rats. 35 Feb 56

Proliferative glomerulonephritis with proteinuria was induced in Wistar rats by bovine serum albumin (BSA). Rats were first immunized with 1 mg or 2.5 mg of BSA and complete Freund's adjuvant (CFA) and eight weeks later 1 mg of BSA were given intravenously six times a week for four weeks. Immunofluorescence revealed granular deposits of IgG, C3, and BSA in the mesangial area with or without deposition of the same components along the capillary wall. Evaluation of the circulating antibody disclosed an apparent correlation between the level of antibody and histological findings. Rats with an intermediate amount of antibody production developed mesangial widening with mesangial immune deposits and no proteinuria. Rats with a low response developed proliferative glomerulonephritis with immune deposits along the capillary wall as well as in the mesangial area and proteinuria.
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PMID:Bovine serum albumin (BSA) nephritis in rats. I. Experimental model. 36 54

The nephrotic syndrome may be associated with several complications caused by severe proteinuria. The consequences of severe renal protein loss are disturbances of water and electrolyte metabolism, thromboses and thromboembolic complications, hyperlipidemia with accelerated atherosclerosis and, finally, some other complications due to the decreased oncotic pressure and the renal loss of transport globulins and immunoglobulins. Diagnosis and treatment of these complications are important in the management of patients with nephrotic syndrome. In the present study, the frequency and localization of thromboses and thromboembolic complications in 11 patients with nephrotic syndrome are described. In addition, factors which are known to be responsible for the hypercoagulable state in nephrotic syndrome were evaluated and correlated to the thromboembolic complications in these patients. An important finding was that in all patients with thromboses and thromboembolic complications, the serum albumin concentrations were below 2 g/100 ml, whereas, with one exception, serum albumin levels were above 2 g/100 ml in cases without thromboembolic complications. Our results indicate that serum albumin levels may be used as an indirect parameter to assess the risk of thromboembolic complications in patients with nephrotic syndrome.
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PMID:[Complications of nephrotic syndrome with special reference to thromboembolic accidents]. 37 Sep 77

We studied the interaction of two different forms of immune glomerular damage occurring simultaneously: anti-glomerular basement membrane (GBM) antibody fixation and immune elimination of bovine serum albumin (BSA). 125I-radiolabelled BSA anti-BSA immune complexes, formed in response to a single small intravenous dose (150 mg/kg) of 125I BSA, did not cause proteinuria in control animals within 15 days, despite evidence of immune elimination of the antigen. Similarly, a small dose of nephrotoxic globulin (NTG)(3.0 mg/kg) did not cause immediate proteinuria in controls. Test animals received the BSA injection followed by the NTG injection 5, 7 or 9 days later. In this way, antibody fixed to glomerular basement membrane antigens at various times after BSA anti-BSA complexes first appeared in the circulation. Animals were killed on day 15. Fifteen of the eighteen test animals developed moderate to severe clinical nephritis. The onset of the nephritis coincided with BSA elimination irrespective of when the NTG was given. Greatly increased amounts of nonlinear immunofluorescent deposits were demonstrated in the glomeruli of test animals. We concluded that there was a marked synergistic effect between two forms of immune glomerular damage (i.e. that mediated by anti-GBM antibody and immune complexes), which appeared to be due to the increased deposition of complex material in the presence of active fixation of anti-GBM antibody. The relevance of this finding to human glomerulonephritis is discussed.
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PMID:The interaction of anti-glomerular basement membrane antibody deposition with immune elimination of bovine serum albumin in the rabbit. 37 80

The relation of clinical and laboratory findings at the time clinical presentation to subsequent survival was investigated in 204 patients with macroglobulinaemia. It was found that the ten following clinical and laboratory parameters were of prognostic significance and a further twelve were not. The best prognoses were found amongst male patients, patients aged 50-69 years and those with serum IgM paraprotein concentrations of 20-39 g/1, type lambda paraproteins, no Bence-Jones proteinuria or cryoglobulinaemia, only one paraprotein, serum cold haemagglutinin activity, serum albumin above 40 g/1 and serum urea below 10 mmol/1.
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PMID:The relation of clinical and laboratory findings to the survival of patients with macroglobulinaemia. 40 10


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