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)

Serum hyperviscosity syndrome was diagnosed in 2 cats with multiple myeloma. Clinical signs included pale mucous membranes, dehydration, retinal hemorrhages, dilated and tortuous retinal vessels, seizures, head-tilt, nystagmus, systolic murmur, and gallop rhythm. Laboratory abnormalities included hyperglobulinemia, azotemia, hyperphosphatemia, nonregenerative anemia, and thrombocytopenia. Both cats had IgG monoclonal gammopathy, Bence Jones proteinuria, increased numbers of bone marrow plasma cells, and high values for relative serum viscosity. Renal disease was suspected in both cats. Cardiac hypertrophy was documented in 1 cat and was suspected in the other cat. Chemotherapy, using melphalan, prednisone, and vincristine, caused short-term remission in both cats, and plasmapheresis was used to lower serum protein concentration in 1 cat. Serum hyperviscosity syndrome rarely develops in cats, but should be suspected when monoclonal gammopathy exists with signs of neurologic, cardiac, or retinal disease.
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PMID:Serum hyperviscosity syndrome associated with multiple myeloma in two cats. 153 97

To determine the frequency, severity and predictors of bleeding and azotemia after envenomation in humans by Echis coloratus, a retrospective survey of 68 cases in Israel between 1970 and 1989 was carried out. We used univariate and multivariate analyses of clinical variables on admission for the outcome variables of bleeding, hemoglobin and platelet levels, and blood urea. Within hours or days after envenomation, a major bleeding episode occurred in 18% of the victims, a drop in hemoglobin to 10 g/dliter or less in 14%, and an increase in blood urea to 9 mmole/liter or more in 15%. These complications correlated with time interval between envenomation and hospital admission, and the following admission variables: degree of bleeding, hemoglobin level, platelet and white blood cell counts, blood urea and proteinuria. Complications were unlikely in patients who were presented with all of the following: a hemoglobin level of 13 g/dliter or more, a platelet count of 100,000/mm3 or more, a blood urea level of 7 mmole/liter or less, no proteinuria and no bleeding. Treatment on admission with a specific monovalent antiserum was associated with a shorter duration of hemostatic failure and a reduced incidence of anemia and thrombopenia. Infusion of fresh frozen plasma on admission did not appear to be effective in preventing complications.
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PMID:Risk indicators after envenomation in humans by Echis coloratus (mid-east saw scaled viper). 159 76

We sought to determine whether systemic administration of proteases ameliorates membranous nephritis induced in rats by immunization and challenge with cationic bovine gamma globulin, and whether targeting of protease to glomerular capillaries increases efficacy. Proteases substituted with biotin were targeted via the cationic protein avidin A, which by virtue of its charge has affinity for the glomerular basement membrane. Despite identical pretreatment proteinuria, rats given untargeted protease (biotin-conjugated without avidin, or unconjugated plus avidin) had significantly less proteinuria than saline-treated controls and nephrotic rats given avidin plus biotin-conjugated (targeted) protease had even less proteinuria and reduced glomerular rat IgG and C3. Among more severely nephrotic rats, targeted protease was again more effective than untargeted protease at reducing proteinuria, and also decreased the size of electron-dense glomerular deposits, hypercholesterolemia, and creatininemia. Inactivated targeted proteases had no effect on proteinuria, hypercholesterolemia, or azotemia. Finally, active targeted protease did not affect proteinuria in the nonimmune mediated nephrosis induced by puromycin aminonucleoside. We conclude that systemic protease can specifically diminish glomerular immune deposits, proteinuria, hyperlipidemia, and creatininemia associated with experimental immune complex glomerulonephritis but not toxic nephrosis, and that targeted protease is more effective than untargeted protease.
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PMID:Targeted enzyme therapy of experimental glomerulonephritis in rats. 170 86

The renal impairments were studied clinicopathologically in 57 patients with progressive systemic sclerosis (scleroderma). Proteinuria, hematuria, azotemia and hypertension, used as markers for renal involvements, were observed in 3 (5.3%), 4 (7.0%), 2 (3.5%) and 6 patients (10.5%) respectively, at the initial examination. Hypertension was increased 2.6 times at the last observation, although the incidence of other three markers have not changed during the follow-up period. Finally, 17 out of 57 patients (29.8) revealed more than one of these clinical markers throughout the study. The decrease of GFR (CThio) was noticed in 3 out of 36 cases (8.3%), however that of RPF (CPAH) in 11 of 36 patients (30.6%), including 5 without abnormal clinical markers. Histological studies were performed in 12 patients. One showed crescentic glomerulonephritis, two membranous nephropathy, and the remaining 9 minor glomerular abnormalities. On the other hand, the vascular changes such as intimal proliferation of interlobular arteries were frequently observed. The frequency of pulmonary involvements, skin ulcer and gastro-intestinal involvement in the patients with renal lesions were not significantly different from that of the non-renal group. The level of RPF was significantly lower in the patients with skin ulcer than that of those without skin ulcer. No significant difference was noticed in the frequency of renal involvements between the patients with or without anti-Scl-70 antibody.
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PMID:[Clinicopathological studies of renal disorders in patients with progressive systemic sclerosis]. 174 19

The clinical and necropsy findings on 7 patients with monoclonal immunoglobulin light chain deposition nephropathy are described (4 cases with a myelomatous and 3 with a non-myelomatous background). All patients had moderate proteinuria and progressive azotemia. Three myelomatous and all three non-myelomatous patients died from uremia after a mean time of 12 and 23 months, respectively, from the first presentation. Immunohistochemically, 6 patients had kappa, and one had lambda light chain deposition. Light microscopically, interstitial fibrosis, tubular atrophy and arteriolar hyalinosis were present in all cases. The glomeruli showed no changes (1 case), or displayed patterns of mesangial widening: mild (1 case), nodular (mesangial nodules, 4 cases) or global lobular expansion (1 case). Mesangial nodules were observed either with or without lamellation. Around the nodules, microaneurysms were seen in 2 cases. Mesangial nodular expansion was accompanied by crescents in 56% of the glomeruli in a male patient suffering from kappa light chain deposition nephropathy without myeloma. The present findings and a review of the literature indicate the following mesangial changes in light chain deposition nephropathy: 1. no changes, 2. mild expansion, 3. nodular expansion with and without lamellation, and 4. lobular expansion. Subtypes 2, 3 and 4 may be present in parallel, may occur with or without cellular proliferation, and may be accompanied by crescents. The term nodular glomerulosclerosis to describe mesangial nodular expansion is not completely correct, and hence its use is not recommended.
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PMID:Light chain deposition nephropathy in necropsy material. 176 89

The diagnosis of renovascular hypertension depends heavily on laboratory tests. There is no universally applicable screening test, and it should be actively sought only in patients with clinical clues suggested by the history, physical examination, and routine laboratory testing. Hyperreninemia is a characteristic finding, and acute blockade of the renin system forms the basis of diagnostic tests such as the oral captopril test and captopril renography. Other abnormal laboratory findings include hypokalemia, proteinuria, and azotemia exacerbated by angiotensin-converting enzyme inhibitors.
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PMID:The role of laboratory testing in the diagnosis of renovascular hypertension. 191 98

Diaziquone (AZQ), a synthetic quinone with demonstrated activity against acute nonlymphocytic leukemia (ANLL), primary CNS tumors, and non-Hodgkin's lymphoma (NHL), is virtually devoid of nonhematopoietic toxicity at conventional doses. As a prelude to its inclusion into bone marrow transplant (BMT) preparative regimens, a phase I study of high-dose AZQ with autologous BMT (ABMT) was performed. Patients with refractory solid tumors and lymphomas were treated with a single 24-hour infusion of AZQ at 50 to 355 mg/m2 in dose escalations of 20%. Fifty-six patients received 69 courses. Those receiving greater than 60 mg/m2 had nadir granulocyte and platelet counts less than 500/microL and 20,000/microL, respectively. Nausea, vomiting, stomatitis, and diarrhea were mild, transient, and not dose-related. Transient minimal elevations of liver function tests were seen in five patients and were also not dose-related. The maximally tolerated dose (MTD) of high-dose AZQ was found to be 245 mg/m2, with nephrotoxicity being dose-limiting. Significant azotemia was seen in four of 12 patients treated at 295 and 355 mg/m2, including fatal anuric renal failure in three of these patients. Reversible proteinuria also occurred in 24 of 26 courses above 150 mg/m2, including nephrotic range proteinuria in eight courses, all at doses of 205 to 355 mg/m2. The proteinuria was also associated with multiple proximal tubular defects including generalized aminoaciduria and proximal renal tubular acidosis. There were six early deaths including two of early renal failure (295 and 355 mg/m2), two of sepsis (205 and 245 mg/m2), one of a pulmonary embolus (85 mg/m2), and one of progressive disease (60 mg/m2). Of 50 patients who were assessable for response, there were seven responses including two of 10 with primary CNS tumors, one of 12 with malignant melanoma, one of five with non-small-cell lung carcinoma, two of two with breast carcinoma, and one of one with ovarian carcinoma. Because of its activity in ANLL and NHL and its unique toxicity spectrum, high-dose AZQ may improve the efficacy of current BMT preparative regimens without significantly increasing their nonhematopoietic toxicity.
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PMID:A phase I trial of high-dose diaziquone and autologous bone marrow transplantation: an Illinois Cancer Council study. 207 48

The acute and chronic effects of daily, oral ciclosporin (CS) therapy (25 mg/kg) on proteinuria, blood pressure, renal function and histology were studied in rats subjected to unilateral nephrectomy and 3 weekly intraperitoneal injections of the aminonucleoside of puromycin (PAN). PAN therapy resulted in heavy proteinuria by week 4 which declined by weeks 8 and 16. When CS therapy was started weeks after the last dose of PAN, acute, transient reductions in proteinuria and reversible rises in blood urea nitrogen (BUN) were observed. When CS or oil therapy was started with PAN and continued for 8 or 16 weeks, there were no differences in proteinuria; however, after 16 weeks, CS treated rats had significantly higher BUN levels [65 +/- 11 (23.2 +/- 3.9) vs. 41 +/- 5 mg/dl (14.6 +/- 1.8 mmol/l); p = 0.001], a higher percentage of sclerotic glomeruli (47 +/- 7 vs. 28 +/- 10%; p less than 0.0001) and extensive interstitial fibrosis. There was a strong correlation between glomerulosclerosis and extent of interstitial fibrosis (r = 0.951; p less than 0.0001). These studies demonstrate that rats with experimental focal glomerulosclerosis treated with CS show an acute, transient reduction in proteinuria; however, chronic (for 16 weeks) CS therapy significantly increases azotemia and results in an increase in glomerulosclerosis and interstitial fibrosis.
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PMID:The effects of ciclosporin in experimental glomerulosclerosis. 208 1

Monoclonal immunoglobulin deposition occurs in tissues as Congo Red binding fibrils in light chain amyloidosis, as less structured deposits in light chain deposition disease, and as similar but distinct deposits in light and heavy chain deposition disease. The nonamyloid forms were found in 13 patients who had evidence of plasmacytic dyscrasia by the immunohistochemical detection of immunoglobulin light chains of kappa or lambda class (with or without staining for a single heavy chain isotype) and by the absence of amyloid P component in tissue sections that did not show the birefringence characteristic of amyloid after Congo Red staining. All but two of the patients presented with proteinuria with or without azotemia. Clinical syndromes involving other organ systems were less common but occasionally severe. Four patients had overt multiple myeloma. Three others had hypercalcemia and mild bone marrow plasmacytosis but no lytic lesions. Analyses of immunoglobulin synthesis in bone marrow cells from seven patients showed excess light chains in all and incomplete light chains or heavy chain fragments in six, regardless of whether an intact monoclonal protein or related subunit was in the serum or urine. The fibrillar (amyloidotic) and nonfibrillar forms of monoclonal immunoglobulin deposition occur either in overt multiple myeloma or in the course of less neoplastically aggressive plasmacytic dyscrasias. Bone marrow cells from patients with either type produce immunoglobulin fragments that are related to those deposited in the affected tissues.
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PMID:Monoclonal immunoglobulin deposition disease: light chain and light and heavy chain deposition diseases and their relation to light chain amyloidosis. Clinical features, immunopathology, and molecular analysis. 210 17

Thrombotic thrombocytopenic purpura (TTP) is a syndrome that occurs mainly in adults with multiorgan microvascular thrombosis consisting of thrombocytopenia, microangiopathic hemolytic anemia, neurologic symptoms, renal involvement, and fever. The female to male ratio is 3:2, and peak incidence occurs in the 3rd decade of life. Clinical signs are the consequence of hyaline thrombosis and occlusion of capillaries and arterioles. Renal ailment manifests itself in hematuria and proteinuria with azotemia and even overt renal failure. In severe disease, azotemia is typical of hemolytic uremic syndrome (HUS). TTP was first described in 1925 by Moschcowitz. The clinical picture of TTP consists of a prodromal phase, a viruslike disease occurring in up to 40% of patients. 60% have neurologic disturbances, 90% have purpura initially, and fever occurs in all. Anemia is often severe with hemoglobin values of 7-9 gm/dl, renal involvement in 90%, and renal failure in 40-80% of patients. Clinical variants include the acute and fulminant variety mortality, the chronic form, and the relapsing form. Predisposing factors and triggering agents are autosomal recessive inherited traits in acute idiopathic TTP, systemic diseases, tumor antigens, pregnancy and puerperium, viruses (endotoxins for HUS), and possibly oral contraceptives and hypertension. Therapy includes corticosteroids (prednisone 100-400 mg/day); heparin for postpartum HUS; and antiplatelet agents (Dextran 70, aspirin, and dipyridamole in high doses). The infusion of PGI2 is controversial; splenectomy is also questionable; and vincristine, azathioprine, and cyclophosphamide have unproven efficacy. Fresh-frozen plasma exchange is the method of choice as it produces survival in 90%. Others are iv immunoglobulins, vitamin E, and dialysis and renal transplant. Platelet transfusions are contraindicated because of sudden death and decreased survival.
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PMID:Thrombotic thrombocytopenic purpura and related disorders. 210 74


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