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

The objective of this study was to characterize the hemostatic defect in dogs with infectious canine hepatitis (ICH), a naturally occurring viral disease of dogs. Five littermate dogs were inoculated with 10(3) TCID50 of ICH virus intravenously. Two littermates were controls. The clinicopathologic manifestations of ICH were fever, depression, anorexia, hematemesis, melena, widespread mucocutaneous petechiae, prolonged bleeding from venipunctures, faceial edema, leukopenia, and proteinuria. The hemostatic defect of ICH was characterized by thrombocytopenia, abnormal platelet function, prolonged one-stage prothrombin time and activated partial thromboplastin time, normal thrombin times, depressed factor VIII activity, and increased fibrin-fibrinogen degradation products. These findings suggested that the central pathologic mechanism of the abnormal hemostasis in ICH was disseminated intravascular coagulation (DIC). ICH is an example of DIC induced by viral infection. This disease is a suitable model for investigation of the detection, pathogenesis, and therapy of DIC.
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PMID:Infectious canine hepatitis: animal model for viral-induced disseminated intravascular coagulation. 124 23

Carbetimer (carboxyimamidate) was administered at a dose of 6,500 mg/m2/day intravenously for 5 consecutive days to 14 patients with measurable metastatic or recurrent colorectal cancer in a single institution phase II study of the Northern California Oncology Group. A total of 38 cycles of therapy were administered; nine patients completed at least three cycles of treatment. No partial or complete responses were observed. One patient did have a greater than 50% response in the liver while developing new retroperitoneal lymphadenopathy and is considered a nonresponder. Carbetimer was well tolerated with elevations of calcium from 10.2 to 12.5 mg/dl in nine patients, prolongation of prothrombin time and partial thromboplastin time in 14 patients, proteinuria in 10 patients, dizziness in six patients, nausea in two patients, and venous pain during infusion in three patients. Myelosuppression was not observed. Carbetimer at this dose and schedule is inactive in the treatment of colorectal cancer.
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PMID:A phase II trial of carbetimer for the treatment of colorectal cancer. A trial of the Northern California Oncology Group. 219 95

Carbetimer (carboxyimamidate) is a low molecular weight derivative of ethylene/maleic anhydride polymer. This compound has demonstrated antitumor activity against several animal models with a daily x 5 schedule appearing most effective. A phase I clinical study of the daily x 5 schedule repeated every 28 days was therefore performed. Forty-one evaluable patients received 66 evaluable cycles of Carbetimer at daily doses ranging from 100-11,000 mg/m2. Hypercalcemia was the dose limiting toxicity with both patients at the 11,000 mg/m2 daily dose level and one patient who received 6 cycles of drug at the 4200 mg/m2 dose level developing severe hypercalcemia not explained by the underlying malignancy. Mild nausea, concentration and rate dependent arm pain at the site of infusion, proteinuria, and coagulopathy were also seen. Calcium balance studies revealed hypercalciuria, suggesting increased mobilization of calcium rather than renal retention. In vitro coagulation studies revealed concentration dependent prolongation of the partial thromboplastin time and thrombin time. No complete or partial responses were seen. However mixed response or biochemical response (reduction in serum lactic dehydrogenase) were seen in 5 patients with melanoma or renal cancer. Due to unacceptable toxicity at the 11,000 mg/m2 daily dose level, Carbetimer 8500 mg/m2 is the recommended dose for a 5-day treatment schedule every 28 days. Special attention should be directed toward possible activity against melanoma and renal cancer.
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PMID:Phase I trial of a 5-day course of carbetimer. 238 16

1. Female Wistar rats received a single subnephrotoxic dose of guinea pig anti-glomerular basement membrane (GBM) IgG1, 2.5 mg, followed by infusion of preformed immune complexes (BSA, 5.0 mg/rabbit anti-BSA, 6 mg), 10 X antigen excess. Control groups received guinea-pig IgG1 anti-GBM, or preformed immune complexes alone, or isotonic saline. Systemic reactions were observed clinically during the first 24 h, and 24 h urine was collected for the measurement of proteinuria and hematuria. 2. Blood was collected before and 2 h after the above treatment for the determination of complement (50% hemolytic assay), kininogen (isolated guinea pig assay of released bradykinin-like spasmogenic activity) and activated partial thromboplastin time (APTT). Kidney and lung tissue was examined by light microscopy, immunofluorescence and electron microscopy. 3. Rats treated with guinea pig anti-GBM IgG1 followed by BSA immune complex presented a severe systemic picture, with macroscopic hematuria (9/14), several deaths (8/14), slight proteinuria (24.6 +/- 5.2 mg/day), marked complement consumption (delta = 49.4 +/- 2.4 UCH50/ml), intravascular coagulation and severe diffuse interstitial pneumonia, obliteration of glomerular capillary walls by edema of endothelial cells, without deposition of immune complexes in kidneys or lungs. The control groups showed no signs of systemic reaction (isotonic saline alone) or slight dyspnea (guinea pig anti-GBM IgG1 or immune complexes alone), without proteinuria or macroscopic hematuria, and with foci of interstitial pneumonia. 4. Complement consumption was significant in rats receiving immune complexes alone (delta = 31.1 +/- 1.3 UCH50/ml) and even higher when associated with infusion of guinea pig anti-GBM IgG1 (delta = 49.3 +/- 2.4 UCH50/ml). APTT was significantly lengthened only for the group treated with guinea pig anti-GBM IgG1 plus immune complexes (delta = 18.5 +/- 1.9 s), with no alterations in the other groups. Kininogen consumption was demonstrable for all groups except the saline control and was more extensive in rats which received immune complexes alone or preceded by guinea pig IgG1. 5. These data show that previous infusion of a subnephrotoxic dose of guinea pig IgG1 anti-GBM aggravated the pathological effects of preformed immune complexes by promoting marked complement consumption and activation of the coagulation system, rather than by enhancing tissue deposition.
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PMID:Potentiation of immune complex injury in rats by pretreatment with subnephrotoxic doses of guinea pig anti-glomerular basement membrane IgG1. 296 89

The mechanism involved in glomerular fibrin deposition was investigated during mercuric chloride (HgCl2)-induced autoimmune glomerulonephritis in the Brown Norway rat. To ascertain whether the local hemostatic system was activated secondarily to the immunological conflict, the ability of glomerular lysates to induce coagulation in vitro was assessed in treated and control rats. Glomerular procoagulant activity (PCA) of HgCl2-injected rats was measured on day 12 (latent phase of the disease), day 20 (acme), and days 32 and 42 (recovery phase) after the first mercury injection. PCA rose 3-fold (p less than 0.02) at day 20 and then almost returned to control values. Proteinuria, PCA, and the incidence of glomerular fibrin deposits peaked concomitantly at day 20. Glomerular PCA was characterized as thromboplastin. The number of Ia positive cells detected by monoclonal OX-6 antibody was not different from the control number at any phase of the disease; the number of macrophages per glomerular section detected by electron microscopy at day 20 in HgCl2-injected rats was 1.80 +/- 0.60, versus 0.30 +/- 0.11 in the controls. No correlation was found between glomerular PCA and either the number of monocytes/macrophages or of Ia-positive cells present in the glomeruli. Since glomerular PCA was maximal at the onset of fibrin formation in the glomeruli and then decreased toward its basal level, and since the fibrin disappeared, it is concluded that increased production of thromboplastin by glomeruli, with activation of the extrinsic coagulation pathway, may contribute to intraglomerular fibrin deposition in HgCl2-induced glomerulonephritis.
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PMID:Enhanced glomerular procoagulant activity and fibrin deposition in rats with mercuric chloride-induced autoimmune nephritis. 347 99

Calves (n = 4) were given neomycin (2.25 or 4.5 mg/kg) twice daily IM and were compared with 2 calves given penicillin IM. The 2 hallmarks of aminoglycoside toxicosis, nephrotoxicosis and ototoxicosis, were seen with both dosages of parenterally administered neomycin. Nephrotoxicosis was confirmed by abnormal findings in urinalysis (granular casts, proteinuria, low specific gravity), renal biopsy results (tubular degeneration and necrosis), and increased 24-hour amounts of urinary enzymes (alanine aminopeptidase and gamma-glutamyltranspeptidase). Azotemia, decreased creatinine clearance, polyuria, and polydipsia also were documented in calves given neomycin. Clinically, deafness was suspected in 2 calves and was documented by electrical auditory-evoked response tests. Abnormalities in partial thromboplastin times and renal residues of neomycin were seen in all 4 calves that were given neomycin, but not in calves that were given penicillin.
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PMID:Neomycin toxicosis in calves. 611 66

Twelve patients with acquired immunodeficiency syndrome were treated with a natural product, highly purified human interleukin-2. Doses ranged from 250 to 250,000 units. No clinical responses were seen. Minimal toxicity was noted and consisted of mild prolongation of partial thromboplastin time and proteinuria. Immunologic changes during the study included a decrease in the number of circulating T8 lymphocytes, increased skin test reactivity, and a decline in serum immunoglobulin levels.
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PMID:Use of interleukin-2 in patients with acquired immunodeficiency syndrome. 633 38

In 57 patients with pregnancy-induced or aggravated hypertension, antithrombin III levels correlated inversely with maternal morbidity. Morbidity was determined by the maximal diastolic blood pressure, disturbance of renal and liver function, and thrombocytopenia. Antithrombin III levels and platelet counts correlated inversely with the degree of placental infarction. Proteinuria (grams per 24 hours) was most predictive of fetal outcome, which was considered to be either favorable if a healthy baby could be discharged with its mother or unfavorable in case of perinatal death or a prolonged stay in the neonatal intensive care unit. Plasma antithrombin III and serum glutamic oxaloacetic transaminase levels, in that order, augmented the number of correct predictions. Antithrombin III inhibits blood coagulation by forming irreversible complexes with activated clotting enzymes, notably with factor Xa and thrombin. Evidence is presented which suggests that antithrombin III levels in preeclampsia are depressed as a result of increased consumption in the maternal vascular tree, rather than decreased synthesis or increased urinary loss.
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PMID:Antithrombin III levels in preeclampsia correlate with maternal and fetal morbidity. 671 44

Renal biopsy was performed in 31 cases of primary glomerulonephritis and the effect of Hirudo in these patients observed. The results revealed that proteinuria decreased significantly, serum albumin increased significantly and cholesterol, triglyceride reduced significantly 4 weeks after treatment with Hirudo (P < 0.01 or P < 0.05); Fibrinogen and platelet aggregation reduced significantly (P < 0.01). However, platelet count, partial thromboplastin time, bleeding and clotting time did not change (P > 0.05); urine NAGase decreased significantly (P < 0.01). It is concluded that Hirudo may decrease proteinuria and alleviate renal parenchymal damage.
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PMID:[The effect of hirudo on proteinuria, lipid metabolism and coagulation system in the patients with chronic glomerulonephritis]. 758 5


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