Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nutrient intake and urinary excretion characteristics of eight young university women were studied over a 4-day period at low altitude (140 m) and subsequently over a 7-day sojourn on Pikes Peak (4,300 m). High-altitude exposure was associated with a transient decrease in the consumption of protein, carbohydrate, fat, sodium, calcium, phosphorus, vitamin A, riboflavin, thiamin, and niacin and a more sustained decrease in the consumption of potassium and ascorbic acid. In most instances minimal values were observed during the first 3 days of exposure. The carbohydrate fraction of energy intake was increased at the expense of fat during this time period. Individual hypophagic responses appeared to be related to severity of acute mountain sickness. Altitude had no effect on water consumption but did lead to an average body weight loss of 1 kg. Urinary measurements revealed a marked oliguria during the entire sojourn. These measurements also showed the first 3 days to be associated with a net loss of body nitrogen and sodium. During this time period body potassium and phosphorus were conserved, and probably increased. The urea fraction of body potassium and phosphorus were conserved, and probably increased. The urea fraction of total urinary nitrogen was not affected by altitude exposure, nor was the daily excretion of uric acid and creatinine. Ammonia excretion, however, was reduced to 50% of the low-altitude value and remained at this level throughout the sojourn. With a few exceptions, the qualitative characteristics of altitude hypophagia in women were similar to those reported for men. Quantitatively, however, the responses were much more transient in women.
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PMID:Nutritional aspects of high-altitude exposure in women. 106 32

The urinary excretion of 3-methylhistidine (3MH), creatinine and total nitrogen was measured during the course of energy balance studies on 20 black Kenyan children. Studies were carried out over 24 h during an acute attack of measles with a second (control) study after recovery, and complete urinary collections were obtained on 14 ill and 18 recovered children. The nutritional status was assessed by anthropometry, and energy intake was determined by duplicate diet analysis. Twelve out of 13 acutely ill and 6 out of 17 recovered children were in negative energy balance. No effect on the rate of excretion of 3MH or of creatinine attributable to differences in nutritional status, of energy intake or to infection was observed. The linear relationship between the excretion rate of all three metabolites and body weight which was observed in recovered children was absent during acute infection. Nitrogen excretion was correlated (P less than 0.05) with the level of energy intake. The linear relationship between the rate of excretion of 3MH and creatinine and of 3MH and nitrogen was significantly closer in recovered than in ill children. The simultaneous effects of infection, underfeeding (and oliguria) on the rate of excretion of protein metabolites may be complex and contradictory. Our results suggest that the excretion of 3MH, creatinine and nitrogen is sustained during infection accompanied by negative energy balance. Disruption during infection of the relationship between the excretion of all three metabolites and body weight, and between 3MH and the other two metabolites suggests perturbation in protein metabolism at this time.
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PMID:Urinary excretion of 3-methylhistidine, creatinine and total nitrogen by Kenyan children during acute measles and after recovery. 274 62

The pathogenetic agents which cause encephalopathy due to fulminant hepatic failure are still under debate. Ammonia and benzodiazepine-like compounds are two of the most important agents considered, so far. Herein, we report the levels of benzodiazepine-like compounds in serum and in urine and of venous ammonia measured during the course of the disease (30 days). The patient rapidly developed stage IV encephalopathy with high levels of ammonia and with only a slight increase of benzodiazepine-like compounds. At that moment, the levels of these compounds were similar to those recorded in the blood when the patient regained full consciousness 28 days later. During the course of the disease, there was a 10-fold increase of benzodiazepine-like compounds in serum which was recorded in parallel with an impaired excretion due to oliguria. This observation seems to indicate that encephalopathy may develop in the absence of significantly increased levels of these compounds and that their episodic increase during fulminant hepatic failure may be an epiphenomenon linked with several factors such as impaired renal function.
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PMID:Changes in endogenous benzodiazepine-like compound levels during the course of fulminant hepatic failure: potential effects of decreased renal function. 949 56