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)

The authors examined, by means of disc electrophoresis, urine, obtained from football players before and after a match of the championship of the "A" republican football group. Proteinuria after effort was manifested by a considerable excretion of albumin, but there were also serum proteins: postalbumin, transferin, gamma-globulins and fractions found at the place of alpha2-macroglobulins till a complete resemblence of serum electrophoresis. Electrophoresis of lactate-dehydrogenase revealed the presence only of two quick fractions, mainly LDH-1, which increased after effort as well. The fractions of nonspecific esterases were of predominantly tissue origin but after effort of serum origin. The results were discussed in connection with various mechanisms, which could cause proteinuria after physical effort.
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PMID:[Disc electrophoresis of urinary proteins. Changes after exertion]. 5 60

Ten male rhesus monkeys, each weighing 3.5 kg, were divided into four groups of 3, 3, 2, and 2, and were fed daily with 100 g pelleted food containing 300, 30, 3, and 0 ppm cadmium, respectively. Urine samples were collected every 2 weeks and blood samples every 4 weeks. One monkey each of the 300 and 30 ppm groups was autopsied for pathological examination and tissue cadmium determination at the week 24 of the experiment; the remaining 8 animals were killed after 55 weeks. The lowest exposed group (3 ppm) did not show any specific biological response to cadmium over a period of 55 weeks. In the 30 ppm group, no significant changes were observed for up to 24 weeks, although cadmium concentration in the renal cortex and urine at 24 weeks were 300 mug/g wet weight and 18 mug/l., respectively. Plasma urea nitrogen and urine protein (quantitative determination) increased after 30 and 36 weeks. At 55 weeks of the experiment, qualitative tests were negative for low molecular weight proteinuria and glycosuria, and the results remained normal for renal and liver function tests and blood analysis, although cadmium concentrations in the renal cortex of two monkeys were 460 and 730 mug/g wet weight and those in the liver were 110 and 160 mug/g wet weight, respectively. In the highest exposure group (300 ppm), urine cadmium increased to 250 mug/l. by 11 weeks, and urine retinol-binding protein, plasma GOT, GPT, and LDH increased after 12 weeks. Proteinuria (quantitative determination), glycosuria, aminoaciduria (panaminoaciduria), and erythrocytopenia were observed after 16 weeks, when urine cadmium was 500-900 mug/l. Hypohemoglobinopathy and proteinuria (qualitative determination) were observed after 20 and 24 weeks, while cadmium concentrations in the renal cortex and the liver were 760 and 430 mug/g wet weight at 24 weeks, respectively. Slightly depressed tubular reabsorption of phosphate, increased urine beta(2)-microglobulin, increased plasma urea nitrogen, and increased plasma alpha(2)-globulin fraction (electrophoresis) were observed between 28 and 30 weeks of the experiment. Creatinine clearance and plasma cholinesterase decreased after 47 and 54 weeks, respectively. Cadmium concentrations in the renal cortex and the liver of two monkeys at 55 weeks were 350 and 580 mug/g wet weight and 410 and 630 mug/g wet weight, respectively. Pathological examinations revealed denaturation, destruction, and regeneration of the epithelial cells in renal proximal tubules, but no pathological changes in osseous tissues. Critical cadmium concentration in the renal cortex was estimated to be 380 mug/g wet weight for low molecular weight proteinuria and 470 mug/g wet weight for proteinuria, glycosuria, and aminoaciduria. Critical concentration in the liver was also estimated to be 210 mug/g wet weight. The apparent biological half-time of cadmium in monkeys at autopsied stage was calculated to be 0.66, 6.4, 5.2, and 22.4 years for the 300, 30, 3, and 0 ppm groups, respectively.
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PMID:Effects of dietary cadmium on rhesus monkeys. 11 86

A prospective study was carried out in 25 patients following visceral angiography using, on average, 3.5 (2.3 to 4.3) ml/kg. of sodium methyl glucamine diatrizoate 76%. No significant changes were found in the liver enzymes (SGTP, LDH and alkaline phosphatase). On the other hand, there was a significant but temporary rise of serum creatinine from 0.9 +/- 0.2 mg% to 1.2 +/- 0.3 mg% as well as transient proteinuria (7 cases) and microhaematuria (6 cases). With the usual contrast doses for visceral angiography, the kidney appears to be the critical organ. In order to reduce the risks of renal complications, contrast doses should be kept to below 4 ml/kg. if possible; angiography should be carried out only if the patient is well hydrated and the indications for angiography should be particularly stringent if there is previous renal damage.
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PMID:[Evaluation of hepatic and renal function after visceral angiography (author's transl)]. 15 51

The function of canine kidneys stored with hypothermic solutions (Rheomacrodex, Collins4, Sacks) was studied in acute autologous reperfusion models. Changes in the perfusates (increase in LDH level and minor increase in K+ level), as well as the quantitative and qualitative properties (proteinuria) of the urine produced by the graft may be ascribed to storage and revascularization which affect the cells and their membranes. The alterations of the circulatory parameters demonstrable at the outset and during revascularization are due to an increase in renovascular resistance of hypothermic origin on the one hand, and to acute tubular epithelial damage inherent in the procedure, on the other.
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PMID:Description and interpretation of functional changes in canine kidneys after preservation with hypothermic perfusates and subsequent reperfusion. 36 24

An 8-year-old boy underwent general anesthesia and experienced an episode of malignant hyperthemia, characterized by elevated temperature, cardiac arrhythmias, markedly elevated serum enzymes (SGOT, LDH, and CPK), proteinuria, and hemoglobinuria. Sixty-six days after anesthesia a skeletal muscle biopsy was obtained for examination by electron and light microscopy, which showed skeletal muscle cells with abnormally numerous mitochondria, enlarged, and variable in shape. Some contained abnormal cristae. There were more lysosomes than normal, and lipofuscin was increased in quantity. Myelin-like bodies were also present. Previous reports of muscle abnormalities are reviewed and compared with the data in this case.
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PMID:Morphologic abnormalities in a case of malignant hyperthermia. 62 31

This paper reports on a 26 year old male who died of toxic diphtheria with all typical features such as: Bullneck, paralysis of the soft palate, renal failure accompanied by proteinuria and--most notably--myocarditis (very typical microscopically) with circulatory disturbances and finally left and right hand failure. The myocarditis hat caused increases of SGOT, SGPT, CPK, LDH and HBDH to values not seen before by us in the course of myocarditis. The patient had been immunized against diphtheria as a child. Initial treatment consisted of the application of ampicillin which caused rapid regression of the local symptoms in the pharyngeal region including the bullneck-symptom; of course the course of intoxication was not influenced, even after the patient had been admitted to the hospital, the disease correctly diagnosed and antitoxin given three days before death.
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PMID:[Fatal diphtheria in a 26-year-old man. Repetitorium; Known and current aspects of diphtheria]. 101 48

This is a study of the changes, both in serum and urine, of a wide enzymatic pattern whose origin is well known to be the renal parenchyma (LDH, LAP, AP and lysozyme), in the course of two experimental prototype lesions induced in rats. Simultaneously a similar enzymatic study was carried out in a group of patients with nephropathies. The experimental lesions were a toxic tubular dysfunction using a mercury salt and an immune glomerulonephritis of two types: by foreign proteins (human albumin) and by rabbit nephrotoxic serum. In all these cases, there has been a convincing evidence, both direct (histological and inmunofluorescent) and indirect (marked proteinuria), of the induced lesions which were similar to the experimental models reported in the literature. The isolated enzymatic changes we observed in serum made us conceed less value to this pattern in comparison to the urinary one which proved to be more important in our study. It was possible to define the following urinary enzymatic patterns for each of the experimental groups: a) The acute toxic tubular dysfunction has a marked rise in the activity of LDH and LAP, and less so in the activity of AP and lysozyme. The retarded tubular lesion has a moderate rise in LAP. b) The glomerular lesion has a moderate and exclusive rise in the activity of LDH and LAP. Likewise the clear similarity between each experimental group and its clinical equivalent was demonstrated as refers to the urinary enzymatic pattern.
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PMID:[Renal enzymology: experimental patterns and clinical symptoms]. 123 86

HELLP syndrome continues to be a clinical entity of difficult diagnosis. Weinstein first defined it in 1982 giving the practicing obstetrician a sequence of useful initials (H = hemolysis; EL = elevated liver enzymes; LP = low platelets). Since then a lot has been written and it has become clear that the syndrome is a form of severe preeclampsia. The American College of Obstetrics and Gynecology does not include HELLP in the description of severe pre-eclampsia as such but does accept each of its components as being part of severe pre-eclampsia. The case presented deals with a 33 year old white female, admitted at 27 weeks gestation with nausea, epigastric pain resembling acute abdomen, nose bleeding and mild hypertension. The analysis revealed an abnormal liver profile with elevated GOT, GPT and LDH, heavy proteinuria (14.4 g/day), decreased platelet count (92000/mm3) and elevated total bilirubin. Pregnancy was terminated by cesarean section 24 hours after admission because the patient's condition was deteriorating. Obviously in pre-eclampsia/eclampsia there is a systematic injury to all tissues. Proof of this is the hypertension as a consequence of vascular spasm and proteinuria due to glomerular injury. In HELLP the sequence of events is probably altered; hepatic injury precedes vascular and renal injury of conventional preeclampsia. The syndrome results from many clinical and pathological symptoms derived from endothelial microvascular injury which determine a rapid platelet activation causing vascular spasm, platelet aggregation and further endothelial injury through a feedback mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Massive proteinuria and HELLP syndrome]. 130 8

A total of 99 cases of viridans streptococcal endocarditis encountered during the period of 1973 and 1990 at the Veterans General Hospital-Taipei were reviewed to evaluate its prognostic factors. Applying strict clinical and laboratory criteria, 24 cases were categorized as definite, 44 probable, 23 possible and 8 likely. The symptoms were frequently subtle and atypical but initial laboratory tests gave useful indications: 69.1% with leukocytosis, 78% with anemia, 58.5% with elevation of LDH level, 88.9% with elevation of ESR value and 100% with elevation of CRP level. Furthermore, 32.4% of the cases demonstrated proteinuria and 67.4% microscopic hematuria. Seventy-three of the subjects had a history of underlying heart disease, predominantly rheumatic heart disease. Histological examination and echocardiography revealed that 51 patients suffered from vegetative endocarditis, 7 (13.7%) of whom were found to have anatomically confirmed vegetations without initial echocardiographic evidence, Vascular events were seen in 61 cases (61.6%): peripheral stigmata (32 cases), cerebral vascular accidents (17 cases), pulmonary embolism (10 cases) and others (2 cases). The overall mortality rate was 18.2%. Congestive heart failure with embolization was the most common cause of death in this group. The presence of vegetation was not well correlated with embolic events. There was no statistically significant association between the mortality and the following characteristics: age, sex, underlying heart disease, evidence of echocardiographically detected vegetations, major surgical intervention and recurrent cases except for embolic events (p less than 0.01). In conclusion, viridans streptococcal endocarditis complicated embolic events usually presented with a fulminant course and a grave outcome.
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PMID:Overview of viridans streptococcal endocarditis: clinical analysis of 99 cases. 165 35

A 60-year-old man was admitted to our hospital because of fever, hemorrhagic tendency, anemia and neurological abnormality. A blood count revealed that the hemoglobin was 6.8 g/dl, the reticulocyte was 17.3 percent with 2 erythroblasts per 100 white cells, the white cell count was 7,100/microliters and the platelet count was 0.8 x 10(4)/microliters. Peripheral blood smear demonstrated marked fragmentation of red cells. Bone marrow examination disclosed the marked erythroid hyperplasia. Although the bleeding time was prolonged (14 minutes 30 seconds), the other hemostatic data were within normal limits. The serum bilirubin level was 1.57 mg/dl; LDH level, 1,437 U/l; creatinine level, 0.92 mg/dl; BUN level 14.7 mg/dl. Haptoglobin was below 10 mg/dl. Results of immunological tests were all negative except the result of PAIgG (576.6 ng/10(7) cells). The urinalysis showed proteinuria, microhematuria and trace granular and hyaline casts. A diagnosis of thrombotic thrombocytopenic purpura was made. The patient was initially treated with prednisolone (60 mg), aspirin (1,000 mg), dipyridamole (150 mg), gabexate mesilate (1.5 g), sodium oxagrel (80 mg) daily with little response. The thirty days after admission, infusion of gamma globulin (20 g, daily) was given for 3 days. The clinical state and laboratory findings became dramatically improved shortly after the administration of gamma globulin and the laboratory data came to be normalized after 1 month. After ten months of this treatment, the patient is remained asymptomatic and the hematological data are within normal range without using any drug. A trial seems justified to confirm the value of this mode of therapy.
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PMID:[Thrombotic thrombocytopenic pupura (TTP)--remission following treatment with high-dose immunoglobulin]. 177 57


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