Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:Nephrotoxicity of 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU) in the Fischer 344 rat. 663 21

Thrombotic thrombocytopenic purpura (TTP) is usually accompanied by renal disfunction presumable due to diffuse thrombotic occlusions in the microcirculation. Two patients with TTP and slight renal failure with proteinuria and microscopic hematuria, were treated by repeated plasma exchanges with fresh frozen plasma, associated with prednisone and cyclophosphamide in one case, and prednisone alone in the other one. Platelet count, hematocrit and lactic dehydrogenase reverted to normal values within the fourth exchange; circulating immune complexes were never detected. Plasma factor stimulating prostacyclin activity lacked in only one patient and returned to normal levels after plasma exchange without being affected during a hematologic relapse. Renal function and urinary abnormalities reverted to normal by the end of plasma exchange and nine and six months renal and hematologic follow-up is still negative. Renal abnormalities in TTP seem to take advantage of early treatment by plasma exchange, which further to replacement of missing plasma factors, can account for the removal of toxic substances to be further investigated on.
 ...
PMID:Renal abnormalities reverted by plasma exchange in thrombotic thrombocytopenic purpura. 668 92

The presence of tubular involvement, as a marker for the detection of urinary tract infection (UTI) site, was examined in 19 patients with pyelonephritis and in 15 patients with cystitis or asymptomatic bacteriuria. The urinary excretion of four markers of tubular proteinuria, beta 2-microglobulin (beta 2M), lysozyme (LZ), lactic dehydrogenase isoenzyme V (LAD-5) and N-acetyl-beta D-glucosaminidase (NAG), was investigated. LAD-5 appeared particularly valuable for the early detection of upper UTI. However, the overall diagnostic accuracy appeared to be further strengthened using, besides LAD-5, one additional variable. A set of simple and noninvasive biochemical tests on urine samples can reliably help to identify the site of UTI.
 ...
PMID:Contribution of four markers of tubular proteinuria in detecting upper urinary tract infections. A multivariate analysis. 675 51

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.
 ...
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.
 ...
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.
 ...
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.
 ...
PMID:The laboratory evaluation of hypertensive gravidas. 773 26

Two dogs were seen at the University Veterinary Teaching Hospital, Nairobi, Kenya, both having histories of dyspnoea, progressively enlarging abdomens, anasarca, ascites, pleural and pericardial effusion, and pulmonary oedema. One of the dogs had a mild neutrophilic leucocytosis, elevated levels of alkaline phosphatase, alanine aminotransferase, lactate dehydrogenase and proteinuria. Histopathological examination of the myocardium revealed some damage to myocytes and a mononuclear cellular infiltration involving the myocardium, liver and kidneys. The two dogs had a fondness for avocado fruits and, as the presenting syndrome is identical to that seen in goats, sheep and horses poisoned by avocados, a comparison is made and the probable manifestation of this poisoning presented.
 ...
PMID:Putative avocado toxicity in two dogs. 789 92

Halogenated anilines and aminophenols are nephrotoxicants and hepatotoxicants in mammals. The purpose of this study was to determine the in vivo and in vitro nephrotoxic and hepatotoxic potential of 4-amino-2,6-dichlorophenol, a putative metabolite of 3,5-dichloroaniline. In the in vivo experiments, male Fischer 344 rats (four/group) were administered a single intraperitoneal (i.p.) injection of 4-amino-2,6-dichlorophenol (0.25, 0.38 or 0.50 mmol/kg) or vehicle (dimethylsulfoxide (DMSO), 1.0 ml/kg) and renal and hepatic function monitored for 48 h. Only minor changes in function or morphology were observed in the 0.25 mmol/kg treatment group. However, in the 0.38 mmol/kg treatment group evidence of both nephrotoxicity and hepatotoxicity were evident. Nephrotoxicity was characterized by increased proteinuria, glucosuria, hematuria, elevated blood urea nitrogen (BUN) concentration and kidney weight, decreased p-aminohippurate (PAH) accumulation and proximal tubular necrosis in the corticomedullary region of the kidney. Hepatotoxicity was characterized by elevated plasma alanine aminotransferase (ALT/GPT) activity and liver weight. Animals administered the 0.5 mmol/kg dose died within 24 h. In the in vitro experiments, the effect of 4-amino-2,6-dichlorophenol on organic ion accumulation, gluconeogenesis and lactate dehydrogenase (LDH) leakage was quantitated in liver and/or renal cortical slices. Organic anion accumulation was inhibited in renal cortical slices by 4-amino-2,6-dichlorophenol bath concentrations of 5 x 10(-6) M or higher, while organic cation uptake was decreased at 4-amino-2,6-dichlorophenol bath concentrations of 1 x 10(-5) M or greater. Renal and hepatic pyruvate-stimulated gluconeogenesis were inhibited and renal LDH leakage increased at 4-amino-2,6-dichlorophenol bath concentrations of 5 x 10(-5) M or greater. Increased LDH leakage from liver slices was not observed. These results demonstrate that 4-amino-2,6-dichlorophenol is a nephrotoxicant and hepatotoxicant in vivo and in vitro and that the kidney is more susceptible to 4-amino-2,6-dichlorophenol toxicity than the liver.
 ...
PMID:In vivo and in vitro 4-amino-2,6-dichlorophenol nephrotoxicity and hepatotoxicity in the Fischer 344 rat. 802 37

Four hundred and fifty-four gravid women were identified with the HELLP syndrome from January, 1980 to May, 1992. The peak systolic and diastolic blood pressures, proteinuria, and uric acid were recorded for each patient during the peripartal course. Patients were classified according to disease severity with, in addition to elevated lactate dehydrogenase (LDH) values, laboratory evidence of haemolysis and hepatic dysfunction, a peripartal platelet count < or = 50,000/microliters was depicted Class I, Class II as a platelet count > 50,000 and < or = 100,000/microliters and Class III as > 100,000 and < or = 150,000/microliters. Patients with Class I HELLP syndrome had peak antepartum systolic blood pressures < 150 mm Hg significantly more often than the Class II (p < 0.0091) or Class III (p < 0.04) HELLP syndrome. Class I HELLP syndrome had significantly more patients with 1+ to 2+ proteinuria than Class II (p < 0.02) and Class III HELLP syndrome (p < 0.009). Uric acid levels were not different among nor proportionately related to increasing severity of the HELLP syndrome.
 ...
PMID:Standard parameters of preeclampsia: can the clinician depend upon them to reliably identify the patient with the HELLP syndrome? 798 Mar 24


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>