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)

Acute renal failure was diagnosed by clinical, necropsy and histological criteria in 39 flocks (20 low ground, 13 hill and six marginal upland) in areas served by six veterinary investigation centres. Forty-eight lambs of 12 different breeds or crosses were investigated. The mean age of affected lambs was 38 days (range seven to 84 days); 21 lambs (44 per cent) were aged seven to 28 days, while only eight (17 per cent) were older than two months. Mortality in clinically affected lambs was almost 100 per cent, with no response to various treatments. Histological examination showed that 40 lambs (83 per cent) had nephrosis, while the rest had toxic tubular necrosis, interstitial nephritis or tubular damage associated with oxalate crystal deposits. Only about half of the lambs had any evidence of enteric infections or enteropathy. Acutely ill lambs had azotaemia, haemoconcentration and proteinuria; some lambs had glycosuria or haematuria. Samples of plasma from 22 lambs with nephrosis were compared with similar samples from 82 incontact but asymptomatic lambs. The clinically affected group had significantly elevated plasma urea, creatinine, total protein, globulin, phosphorus and chloride concentrations and significantly reduced plasma calcium concentrations compared with healthy lambs. Affected lambs had a significant reduction also in the calcium:phosphorus ratio. No significant differences between groups was found in plasma concentrations of albumin, glucose, lactate, glycerol, creatine kinase, alkaline phosphatase, sodium, potassium or magnesium.
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PMID:Acute nephropathy in young lambs. 291 11

Daily blood and 24-hour urine samples from 6 runners were studied for 2 days before and for 5 days after a 42.2 km. marathon footrace run in cool environmental conditions. Although the race caused muscle damage as shown by the increased post-race serum creatine kinase activity and C-reactive protein levels, renal function measured by urine flow rates, creatinine clearance and protein excretion was normal during the race. Sodium and fractional sodium excretion decreased during the race despite a maintained osmolar clearance, and remained low for the next 48 hours, whereas osmolar clearance decreased sharply for the remainder of the race day but it was significantly elevated on days 2 to 4 after the race. Creatinine clearance was increased significantly 24 hours after the race, and reached its peak 3 days after the race, while urine flow rates were elevated from days 2 to 5 after the race. Urea excretion was significantly decreased 3 to 5 days after the race, while creatinine excretion was increased significantly on day 3 after the race. Glomerular proteinuria occurred 24 hours after the race with no associated reduction in tubular reabsorption of the low molecular weight protein beta-2-microglobulin. This study shows previously unrecognized substantial delayed effects of prolonged exercise on renal function. The nature of these changes may reflect catabolic followed by anabolic processes in muscle as well as changes consequent on excess sodium retention and related fluid compartment shifts.
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PMID:The immediate and delayed effects of marathon running on renal function. 377 85

Six male and 6 female Beagles, 6 to 7 months old, were allotted to 2 groups: group I--inoculated subcutaneously with 30 Dipetalonema reconditum infective larvae/dog, and group II--noninoculated controls. Group comparisons were made in regard to hematologic values, Knott test results, body weights, blood urea nitrogen, total serum protein, serum albumin and alanine aminotransferase and creatine kinase activities. Routine urinalysis data were compared at 1 week before and at 28 weeks after the inoculations. Mean total leukocyte counts were significantly (P less than 0.05) greater in group I dogs than in group II dogs at postinoculation weeks (PIW) 4, 5, and 7 to 12, and mean eosinophil counts were significantly greater in group I dogs at PIW 3 to 11, 13 to 15, 20, and 23 to 24. Microfilariae were detected as early as the 10th week and sporadically thereafter. Only 1 D reconditum adult worm was recovered from all of the inoculated dogs. Five other dogs (group III) with chronic, patient experimentally induced dipetalonemiasis, were evaluated with the same tests at PIW 70 to 89. Eosinophilia (greater than 750 cells/microliter) was present in 4 of 5 dogs; lymphocytosis (greater than 4,800 cells/microliter) was evident in 1 dog. Proteinuria (greater than or equal to 30 mg/dl) was detected in 3 of 4 dogs with chronic dipetalonemiasis.
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PMID:Clinical responses of dogs to experimentally induced Dipetalonema reconditum infection. 668 83

Abnormal myoglobinemia (above 77 microgram/l) and free hemoglobin in plasma were found in 16 runners and in nine non runners immediately following distance running. The same abnormalities were found iun six elite rowers following rowing. In parallel with the rise in myoglobin and free hemoglobin a rise was found in serum concentrations of cellular enzymes (LDH, CK, ASAT, alkaline phosphatase) and of various metabolites. We found no proteinuria nor casts in the urine. Non runners had a higher rise in serum myoglobin than runners. Competitive running caused a rise in the serum concentration of the heart specific fraction of creatine kinase in seven of the nine (healthy) elite runners. The abnormal findings are only explainable on the basis of leakage of proteins from muscle cells to the circulation in otherwise healthy, well trained persons. Myoglobinemia and a transient rhabdomyolysis is a common phenomenon in long distance running, but evidently also occurs in distance rowing. Three months of running training prevented most of the muscle damage from relaxed jogging in the nine previous non runners. Neither the observed myoglobinemia nor the hemoglobinemia resulted in any significant loss of iron in the urine.
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PMID:Muscle cell leakage due to long distance training. 720 6

A 25-year-old man was admitted with complaints of fever and macrohematuria. Laboratory tests showed a substantial increase in serum creatine phosphokinase and creatinine in association with myoglobinuria and proteinuria. Blood culture grew Streptococcus salivarius and Streptococcus oralis. Findings of renal biopsy were compatible with IgA nephropathy. The glomeruli had a mild mesangial proliferation without crescentic lesions. Changes of the interstitium and tubules were not evident. The clinical course and laboratory results strongly suggested a possible link between Streptococcus salivarius/oralis infection, and rhabdomyolysis. Rhabdomyolysis is rarely seen as a complication of bacterial infection, and the present case emphasizes the importance of suspecting bacteremia due to Streptococcus salivarius/oralis in the presence of rhabdomyolysis.
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PMID:Rhabdomyolysis associated with bacteremia due to Streptococcus viridans. 856 22

The purpose of this study were: (1) to establish the prevalence of exercise-induced hematuria in a group of otherwise healthy male runners (n = 70), and (2) to investigate the role of exercise intensity in those runners who exhibited exercise-related hematuria (n = 10) by evaluating the effect of running and cycling at high and low intensities. The identified and recruited subjects participated in four different exercise protocols: (1) a 60-min treadmill run (RUN) at 90% of anaerobic threshold (Th(ae)), (2) a 60-min leg cycle ergometer ride (BIKE) at 90% of Th(ae), (3) a 3x400-m sprint (SPRINT), each followed by 4 min of rest or light walking, and (4) 3x60-Wingate leg cycle ergometry tests, each followed by 4 min of rest or light cycling. The study employed a 3x4 (time by protocol) within-subjects design and dependent variables were measured before exercise, 4 min after, and 1 h after exercise, and included measurements of hematuria, proteinuria, urinary pH, serum haptoglobin concentration, serum creatine phosphokinase activity, plasma lactate concentration, and hemoglobin. The 400-m sprint at maximal effort significantly increased both hematuria and proteinuria (P<0.01). Post-exercise hematuria for the SPRINT protocol was significantly different than that for the BIKE (P<0.01) and RUN (P<0.01) protocols. Due to the significant increase in hematuria and proteinuria following the SPRINT protocol, it was concluded that exercise-related changes in renal function were associated with weight-bearing exercise intensity rather than non-weight-bearing exercise duration.
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PMID:The effect of exercise intensity on hematuria in healthy male runners. 1005 68

Two girls with mixed connective tissue disease (MCTD) were treated in our hospital in the past 5 years. Patient 1, a 10-year-old girl presenting with migratory arthralgia, had an initial diagnosis of juvenile rheumatoid arthritis. Muscle weakness with elevated levels of creatine kinase and liver enzymes, sclerodactyly, Raynaud's phenomenon and heliotrope sign developed subsequently in the following 3 years. Patient 2, a 13-year-old girl, had been treated for suspected systemic lupus erythematosus since 9 years of age. She presented with lymphadenopathy, arthralgia, pericardial effusion, and paralytic ileus. The symptoms waxed and waned. Sclerodactyly, Raynaud's phenomenon, proteinuria, and hypertension were also noted. Both patients had high serum titers of antinuclear antibody (speckled pattern, 1:5120) and were seropositive for antiribonuclear protein antibody. Intravenous immunoglobulin, prednisolone, cyclosporine A, and nonsteroidal anti-inflammatory drugs (NSAIDs) were given to patient 1. Patient 2 received cyclosporine A, prednisolone, and methylprednisolone pulse therapy. The disease has been well controlled for 2 years by low-dose immunosuppressants and NSAIDs. MCTD is a rare juvenile rheumatic disease: early identification and appropriate treatment can improve the disease outcome.
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PMID:Childhood mixed connective tissue disease. 1077 31

The activities of the enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LD), creatine kinase (CK), amylase (AMS) and angiotensin converting enzyme (ACE) have been used to assess the toxic effects of xenobiotics that have hypoglycaemic action in hepatic, pancreatic, renal and muscle tissue. Using a validated experimental model of diabetes mellitus in rats, we ascertained whether this syndrome itself affected the serum activities of these enzymes over a 53-day period. Levels of hepatic enzymes AST, ALT and ALP were higher in the streptozotocin (STZ)-diabetic rats (group D), but were controlled by insulin therapy (group DI). AMS was reduced in group D and unchanged in group DI rats. Proteinuria was detected 1 day after STZ administration and partially controlled by insulin (group DI); its early presence in group D rats, and the lack of any change in serum ACE in this group, indicates that proteinuria is the better marker for microangiopathy. Microscopic examination of liver, kidney, heart and skeletal muscles (soleus and extensor digitorum longus) revealed various alterations in group D rat tissues, which were less pronounced in group DI. The liver, pancreas and kidney tissue-damage was consistent with the altered serum levels of AST, ALT, ALP and AMS and proteinuria. We conclude that: (i) rigorous control is required when these serum-enzyme levels are used as indicators of tissue toxicity in experimental diabetes, and (ii) LD, CK and bilirubin serum levels, which are unaffected by diabetes, can be used when testing effects of xenobiotics on tissues.
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PMID:Temporal response pattern of biochemical analytes in experimental diabetes. 1282 18

We present four adult cases of acute renal failure associated with hypothyroidism. All patients presented with symptoms suggestive of moderate to severe hypothyroidism, such as cold intolerance, constipation, muscle weakness, and lower extremity oedema. Initial serum creatinine levels ranged between 115 and 203 micromol/L (1.3 and 2.3 mg/dL), with creatinine clearances (CrCl) ranging between 0.58 and 0.97 mL/s (34.5 and 58 mL/min). After 6-12 weeks of treatment with levothyroxin, serum creatinine levels decreased to the range of 80 and 124 micromol/L (0.9 and 1.4 mg/dL) and CrCl increased to 0.74-1.64 mL/s (44-98 mL/min). One patient had proteinuria of 800 mg/day, which decreased to the normal range (<200 mg/day) after levothyroxin treatment. One patient developed acute gouty arthritis before normalization of thyroid-stimulating hormone (TSH), which was successfully managed with prednisone therapy. All of our patients had increased creatine kinase (CK), ranging between 1000 and 2360 U/L (normal range, 22-165 U/L), which normalized after 6 weeks of levothyroxin treatment.
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PMID:Reversible acute renal failure associated with hypothyroidism: report of four cases with a brief review of literature. 1501 34

The combined dyslipidaemia that accompanies the nephrotic syndrome increases the cardiovascular risk and appears to worsen long-term renal function. Our aim was to determine the efficacy and safety of 10 mg atorvastatin in the control of dyslipidaemia in these patients. We carried out a prospective, open, 6 month study of 10 patients with primary or secondary nephrotic syndrome (proteinuria >3.5 g/day, hypoalbuminaemia, oedema and hyperlipidaemia). The changes in lipids and plasma lipoproteins were measured, as well as the safety profile (transaminases, creatine phosphokinase, fibrinogen and antithrombin III activity) and parameters of renal function. The addition of 10 mg atorvastatin daily for 6 months resulted in a 41% reduction in low density lipoprotein (LDL) cholesterol and 31% in triglycerides (both P < 0.05), and a 15% increase in high density lipoprotein (HDL) cholesterol (NS). The drug was well tolerated and there was no change in the safety profile or deterioration in renal function. In fact, the levels of proteinuria fell in all but one patient (6.2 +/- 2.6 vs 4.8 +/- 2.5 g/24 h; P < 0.05). Atorvastatin, at the above dose, and for the time used proved to be a safe drug that effectively reduced dyslipidaemia in patients with nephrotic syndrome.
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PMID:Atorvastatin in dyslipidaemia of the nephrotic syndrome. 1501 35


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