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)

A new case of acquired von Willebrand syndrome (AvWS) with Hashitoxicosis and pernicious anemia combined in a 73-years-old male is reported. He was admitted because of appetite loss and general malaise. Physical examination showed severe anemia and general edema. The red-cell count was 103 X 10(4)/microliters with a MCV of 122 fl; the white-cell count was 2,900/microliters with 24.5% hypersegmented neutrophils; the platelet count was 17.2 X 10(4)/microliters. the lactate dehydrogenase was 9,513 U/ml and vitamin B12 was 87 pg/dl. An aspirated specimen of bone marrow was diagnostic of megaloblastic anemia. The thyroid hormones were decreased with the thyroid stimulating hormone increased. From the immunological findings, the thyroid-test, microsome-test, and anti-intrinsic factor were positive, but M proteinemia and Bence Jones proteinuria were absent. Histology of the thyroid gland and the gastric mucosa established the diagnosis of chronic thyroiditis and chronic atrophic gastritis. Subcutaneous hemorrhages after veni-puncture were observed on admission. He had a normal bleeding time, but the coagulation studies indicated the presence of von Willebrand disease, but as his family and past history were negative, this suggested the presence of an AvWS. The analysis of von Willebrand factor (vWF) multimeric composition had showed the lack of the larger multimers in the plasma, but it was normalized after the administration of levothyroxine sodium and hydroxocobalamin with vWF: Ag/RCo ratio paralleled. As far as we know, this is the first report of AvWS with Hashitoxicosis and pernicious anemia combined.
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PMID:[Acquired von Willebrand syndrome associated with Hashitoxicosis and pernicious anemia combined]. 267 35

2-Bromo-(diglutathion-S-yl)hydroquinone [2-Br-(diGSyl)HQ] causes severe necrosis of the proximal renal tubules in the rat, elevations in blood urea nitrogen (BUN) and increased urinary excretion of protein, glucose, and lactate dehydrogenase. In contrast, 2-Br-3-(GSyl)HQ, 2-Br-5-(GSyl)HQ, and 2-Br-6-(GSyl)HQ caused differentially less toxicity than the diglutathionyl conjugate. None of these conjugates had any apparent effect on liver pathology and serum glutamate-pyruvate transaminase remained within the normal range. Pretreatment of rats with probenecid, an organic anion transport inhibitor, offered only slight protection against 2-Br-(diGSyl)HQ-mediated elevations in BUN, proteinuria, or glucosuria. In contrast, quinine, an organic cation transport inhibitor, potentiated the nephrotoxicity of 2-Br-(di-GSyl)HQ. Thus, in contrast to other nephrotoxic sulfur conjugates, probenecid-sensitive organic ion transport systems do not contribute to the kidney-specific toxicity of 2-Br-(diGSyl)HQ. However, inhibition of renal gamma-glutamyl transpeptidase by AT-125 completely protected rats from the nephrotoxic effects of 2-Br-(diGSyl)HQ. Aminooxyacetic acid, an inhibitor of cysteine conjugate beta-lyase, caused a 20-25% decrease in 2-Br-(diGSyl)HQ-mediated elevations in BUN and urinary excretion parameters. The isomeric 35S conjugates covalently bound to rat kidney 10,000 x g homogenate in the order 2-Br-6-(GSyl)HQ greater than 2-Br-5-(GSyl)HQ greater than 2-Br-3-(GSyl)HQ greater than 2-Br-(diGSyl)HQ. AT-125 (0.4 mM) decreased covalent binding by 25%, 17%, 33%, and 28%, respectively. Aminooxyacetic acid (0.1 mM) inhibited covalent binding by 26%, 10%, 17%, and 17% respectively. Ascorbic acid (1.0 mM) inhibited covalent binding by 63%, 87%, 62%, and 28%, respectively, and this inhibition correlated, inversely, with the redox potential of the conjugates. Thus, the covalent binding is mediated preferentially by oxidation of the quinol moiety, although the formation of reactive thiols cannot be excluded. In addition, the initial conjugation of 2-BrHQ with GSH does not result in the formation of a less redox-active species. However, the subsequent addition of a second molecule of GSH results in the formation of a more redox-stable compound, which, paradoxically, enhances toxicity. The metabolism of 2-Br-(diGSyl)HQ by renal proximal tubular gamma-glutamyl transpeptidase and trans-membrane transport of the cysteine conjugate(s) followed by oxidation of the quinol moiety is probably responsible for the target organ toxicity of this compound.
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PMID:2-Bromo-(diglutathion-S-yl)hydroquinone nephrotoxicity: physiological, biochemical, and electrochemical determinants. 317 33

The nephrotoxic potential of alpha-interferon (IFN alpha-2b) was analysed in 21 patients with chronic myeloid leukemia. As particularly sensitive parameters in the detection of subclinical renal injury we measured the excretion of the following urinary enzymes: lactate dehydrogenase (LDH), gamma-glutamyltransferase (GGT), leucine arylaminidase (LAP), beta-galactosidase (GAL) and N-acetyl-beta-glucosaminidase (NAG). Additionally, protein excretion and urinary sediment were analysed. In 18 of 21 patients a significant increase in the excretion of LDH, LAP, GGT and NAG was found, in 6 patients there was an additional rise in the output of GAL. Eleven patients developed proteinuria up to 2 g/l, one patient excreted up to 9 g/l. Enzymuria and protein excretion decreased in all patients after reduction of the IFN alpha-2b dosage and disappeared in two patients following cessation of therapy. The high incidence of nephrotoxic events in patients with CML during IFN alpha-2b therapy might be mostly due to immunological or substance-specific effects.
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PMID:[Detection of nephrotoxicity of human alpha 2b interferon with special reference to the analysis of urine enzymes in patients with chronic myeloid leukemia]. 347 5

The effect of nickel on cadmium nephro-toxicity and hepato-toxicity in rats was investigated. The administration of nickel (6 mg per kg, i.p., three days) or cadmium (6 mg per kg, i.m., once) significantly enhanced the urinary excretion of alkaline phosphatase (ALP), lactate dehydrogenase (LDH), glutamate oxaloacetate transaminase (GOT), amino acids, and proteins. In addition, it increased the activity of serum ALP, GOT, and glutamate pyruvate transaminase (GPT). These biochemical alterations in urine and serum were used as a measure of kidney and liver damage. Cadmium-induced enzymuria, proteinuria, amino aciduria and increase in the activity of serum enzymes were significantly less marked in animals pretreated with nickel than in controls. However, the accumulation of cadmium in kidneys and liver and its urinary excretion were unaffected by nickel pretreatment. The results suggest protection by nickel against cadmium nephro- and hepato-toxicity.
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PMID:Preventive effects of nickel on cadmium hepatotoxicity and nephrotoxicity. 647 83

The protean manifestations of Legionnaires' disease are described in an analysis of 12 sporadic cases. Two forms of the disease have been delineated. One variant (Group A) consisted of six patients who had a mild form of non-progressive pneumonia with minimum extra-pulmonary involvement. Six patients (Group B) were differentiated by rapidly progressive pulmonary infiltrates, severe hypoxia and respiratory failure, plus a higher frequency of band neutrophils and extra-pulmonary manifestations. Particularly notable were evidence of severe myositis (elevated creatinine phosphokinase and lactate dehydrogenase), anaemia, and neurological findings which included alterations in the sensorium, meningitis, and convulsions. Cerebrospinal fluid (CSF) abnormalities were seen frequently in patients with neurological manifestations, and necropsy findings in one patient suggested that the Legionnaires' bacillus was capable of producing a fatal leucoencephalitis. Renal findings included haematuria, proteinuria and oliguric renal failure. Hepatic transaminases (SGPT, SGOT) were elevated in six patients and serum bilirubin was abnormal in five. Alkaline phosphatase values were normal to minimally elevated. The gastrointestinal symptoms commonly considered to be a frequent initial manifestation of Legionnaires' disease were rare in this series. Recommendations for instituting empirical therapy, based upon recognition of a clinical syndrome which should suggest the diagnosis of Legionnaires' disease, are included.
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PMID:The protean manifestations of Legionnaires' disease. 663 Oct 29

A single s.c. injection of 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU; 20-140 mg/kg) resulted in rapid decreases in renal function as well as leading to a chronic progressive nephropathy in male Fischer 344 rats. Disturbances in renal function were proportional to the dose of MeCCNU administered and included impaired tubular transport of p-aminohippuric acid, a decrease in urine concentrating ability, an increase in urine pH, polyuria, proteinuria and enzymuria. The tubular accumulation of p-aminohippuric acid by kidney slices was decreased as early as 1 hr after MeCCNU administration (100 mg/kg), was maximal within 12 hr and remained depressed for at least 28 days after a single injection of either 40 or 80 mg/kg. Changes in other measures of renal function (increased lactate dehydrogenase excretion, alkalinuria and decreased urine concentrating ability) were delayed from 1 to 6 days after MeCCNU administration and in some cases progressed in severity throughout the 28-day duration of the experiment. The delay between the first evidence of renal damage (decreased p-aminohippuric acid uptake) and the subsequent appearance of enzymuria, proteinuria, polyuria and alkalinuria appears to correspond to a similar delay between the initial insult and the eventual development of cellular necrosis and other histopathological changes. These results demonstrate that MeCCNU is a nephrotoxicant in rats and indicate that even a single acute dose may lead to chronic and irreversible effects on the kidney. The in vivo toxicity model defined herein appears to be an appropriate one for further study of the mechanism of nephrotoxicity of MeCCNU.
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PMID:Nephrotoxicity of 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU) in the Fischer 344 rat. 663 21

Protection by fosfomycin of the nephrotoxicity of dibekacin was studied using Fischer 344 rats and urinary parameters such as volume, osmolality, protein, N-acetyl-beta-D-glucosaminidase, leucine aminopeptidase, lactate dehydrogenase and nucleated cells were determined as markers of nephrotoxicity. The duration of treatment was 11 d. Fosfomycin reduced polyuria, proteinuria, enzymuria and cyturia induced by dibekacin best by the concomitant administration, followed by pre-treatment, but not by post-treatment. Protection was effective in the dose ratio of dibekacin: fosfomycin = 1:2 - 1:32, regardless of administration routes. As judged from urinalysis, protection by fosfomycin (320 mg/kg) was almost complete for the experimental nephrotoxicity induced by 10 mg/kg of dibekacin, and still significant for that by 40 mg/kg. This was supported by the histo-pathological and ultrastructural improvement of proximal tubules and by suppressed blood urea nitrogen and creatinine values. Protective activity of fosfomycin was more potent than that of cephalothin, when compared on the weight basis.
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PMID:Protective effect of fosfomycin on the experimental nephrotoxicity induced by dibekacin. 715 39

Following experimental rhabdomyolysis, animals become resistant to heme protein-induced acute renal failure (ARF). The goals of this study were to: (a) ascertain whether this resistance, previously documented only in vivo, is expressed directly at the proximal tubular cell level; (b) determine whether heme proteinuria (vs. other consequences of rhabdomyolysis) is its trigger; and (c) ascertain some of its subcellular determinants. Rats were injected with a borderline toxic dose of glycerol and 24 hours later proximal tubular segments (PTS) were isolated for study. Their vulnerability to diverse forms of injury (FeSO4-induced oxidant stress, hypoxia, Ca2+ ionophore, cytochalasin D, PLA2) was compared to that found in normal PTS. Post-glycerol PTS manifested significant resistance to each insult (decreased lactate dehydrogenase +/- N-acetyl-beta-D-glucosaminidase release). Protection against FeSO4 was virtually complete and it was associated with a 50% decrease in membrane lipid peroxidation. No decrease in hydroxyl radical generation was noted during the FeSO4 challenge (salicylate trap assessment), suggesting a primary increase in membrane resistance to attack. That PLA2 addition caused less deacylation, plasma membrane enzyme (alanine aminopeptidase) release, and LDH leakage from post-glycerol versus normal tubules supported this hypothesis. To test whether cytoresistance was specifically triggered by heme proteins (vs. being a non-specific filtered protein effect, or a result of endotoxin cascade activation), rats were injected with purified myoglobin, non-heme containing filterable proteins, or endotoxin. Only myoglobin induced cytoresistance. In vivo heme oxygenase inhibition (tin-protoporphyrin) did not block the emergence of cytoresistance and it was expressed despite Na,K-ATPase inhibition (ouabain) or cytoskeletal disruption (cytochalasin D). In vivo heat shock failed to protect. In conclusion, (1) rhabdomyolysis induces broad based proximal tubular cytoresistance; (2) heme proteinuria is its trigger; and (3) it is most easily explained by a primary increase in plasma membrane resistance to attack.
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PMID:Heme protein-induced tubular cytoresistance: expression at the plasma membrane level. 763 63

Rats were injected intraperitoneally with saline or fumonisin B1 (FB1) at doses of 7.5 and 10.0 mg FB1/kg for 4 days. For each day of dosing, 24-hr urine samples were collected and analyzed for creatinine and protein content and the enzymes gamma-glutamyl-transpeptidase, lactate dehydrogenase, and N-acetyl-beta-D-glucosaminidase. Twenty-four hours after the last dose, animals were killed and kidneys removed for ion transport measurement and histopathology. Significant increases in urine volume and decreases in urine osmolality were observed in both FB1 dose groups. Creatinine excretion was decreased only in the 10 mg FB1/kg group on the final day of the study. Urine protein excretion was elevated in both treated groups and found to be due primarily to high-molecular-weight proteins indicative of increased glomerular permeability. Enzymuria, a marker of tubular cell damage, was also observed with increases in the urinary excretion of all three enzymes measured. In renal cortical slices tubular transport of the anion p-aminohippuric acid was reduced by 75-80% and cationic transport of tetraethylammonium was reduced by 40% in the FB1-treated animals. While these results suggest significant alterations in renal function, only minor histopathologic changes were observed in the kidneys of both dose groups. Results of the present study indicate that urine volume, proteinuria, enzymuria, and ion transport are sensitive indicators of early FB1-induced nephrotoxicity.
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PMID:The effects of fumonisin B1 on several markers of nephrotoxicity in rats. 764 15

A number of laboratory tests are available for the evaluation of the hypertensive gravida. These tests can be used to either predict and/or prognosticate between preeclampsia and other hypertensive disorders of pregnancy. These laboratory tests were evaluated based on published experience with special attention to its ability to facilitate identification of the patient with preeclampsia apart from other hypertensive disorders that co-exist with and occur as a complication of pregnancy. Hypocalciuria and increased cellular plasma fibronectin seem to be good tests to differentiate preeclampsia from chronic hypertension. The management of preeclampsia with its increased risk of perinatal morbidity and mortality renders this differentiation clinically very important. Hyperuricemia, proteinuria, increased serum beta-thromboglobulin concentration, abnormal red blood cell morphology with increased hemoglobin/hematocrit, and increased serum iron individually and collectively reflect the severity of preeclampsia. Platelets and total serum lactate dehydrogenase are the best tests to reflect the severity of HELLP syndrome. Circulating hCG and serum thromboglobulin seem to be the most promising future predictors for preeclampsia.
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PMID:The laboratory evaluation of hypertensive gravidas. 773 26


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