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Query: UMLS:C0162275 (ketonuria)
 553 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A modification of the urine osmolal gap was evaluated as an estimate of urine [NH4+]. We proposed that: Urine [NH4+] = Urine osmolality - [2(Na+ + K+) + urea + glucose]/2 Spot urine samples were collected from normal volunteers and from individuals with ketonuria; the modified urine osmolal gap as well as two other previously described estimates of urine [NH4+] were compared with measured urine [NH4+]. There was a significant positive linear correlation between the urine [NH4+] and the modified urine osmolal gap in normal volunteers (r = 0.81; p less than 0.01) and in individuals with ketonuria (r = 0.93; p less than 0.001). The originally described urine osmolal gap greatly overestimated the urine [NH4+] but also showed a significant correlation. The urine anion gap was not a valid estimate of urine [NH4+] within the range of values measured in our subjects. The modified urine osmolal gap is an improvement over previously described estimates of urine [NH4+] and can be used as a single calculation in place of the other two.
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PMID:A modification of the urine osmolal gap: an improved method for estimating urine ammonium. 208 Jul 86

On a farm where the ration of cows contained 88.0 g of butyric acid, an experimental group of cows (n = 8), producing milk containing 7.9 mg or more acetone per litre, was studied for 14 days for the effect of a 250 g supplement of sodium acetate to the ration (combined with single i.m. administration of vitamins A, D2 and E) on selected metabolism parameters and on milk production. As distinct from the control group of cows (n = 8) from the same farm which produced milk containing 3.9 mg or less acetone per litre and which were fed without sodium acetone supplements, a tendency of increased alkaemia of the organism was suggested in the experimental cows. This tendency manifested itself during the trial in increased pH values, increased base excess (BE) and standard bicarbonate (SB) in the blood, and in an increase in the pH value and net acido basic secretion in urine. A decrease was recorded in the concentration of the acetone + acetacetic acid sum, the same as beta-hydroxybutyric acid in blood and the sum of acetone and acetacetic acid in milk (P less than 0.01). An insignificant increase of the activity of gammaglutamyl transpeptidase (GMT) was recorded in the blood serum of the experimental cows and a significant increase occurred in the content of potassium (up to P less than 0.01) and urea (up to P less than 0.01) in urine. The supplement of sodium acetate to the feed ration did not influence the degree of ketonuria and the finding of urobilinogen in urine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Use of sodium acetate in feed rations in ketotic cows]. 258 30

In the years 1983-1986 in the Department of Infectious Diseases Medical Academy in Cracow 189 adult patients were treated for salmonellosis. A significant rise was noted in the number of cases in recent years. The most frequent pathogen was Salmonella enteritidis. The clinical pattern of salmonellosis was similar to that described in preceding years. The disease was associated with increased urea level and decreased sodium level in serum, appearance of young cell forms in white blood cell count, and acetonuria. Most convalescents were discharged with positive results of stool cultures.
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PMID:[Salmonella food poisoning treated at the Infectious Disease Clinic, Institute of Internal Medicine, Medical Academy, in Cracow 1983-1986]. 261 7

The winter athlete has several potential tactics for sustaining body temperature in the face of severe cold. An increase in the intensity of physical activity may be counter-productive because of increased respiratory heat loss, increased air or water movement over the body surface, and a pumping of air or water beneath the clothing. Shivering can generate heat at a rate of 10 to 15 kJ/min, but it impairs skilled performance, while the resultant glycogen usage hastens the onset of fatigue and mental confusion. Non-shivering thermogenesis could arise in either brown adipose tissue or white fat. Brown adipose tissue generates heat by the action of free fatty acids in uncoupling mitochondrial electron transport, and by noradrenaline-induced membrane depolarisation and sodium pumping. The existence of brown adipose tissue in human adults is controversial, and although there are theoretical mechanisms of heat production in white fat, their contribution to the maintenance of body temperature is small. Acclimatisation to cold develops over the course of about 10 days, and in humans the primary change is an insulative, hypothermic type of response; this reflects the intermittent nature of most occupational and athletic exposures to cold. Nevertheless, with more sustained exposure to cold air or water, humans can apparently develop the humoral type of acclimatisation described in small mammals, with an increased output of noradrenaline and/or thyroxine. The associated mobilisation of free fatty acids suggests the possibility of using winter sport as a pleasant method of treating obesity. In men, a combination of moderate exercise and facial cooling induces a substantial fat loss over a 1- to 2-week period, with an associated ketonuria, proteinuria, and increase of body mass. Possible factors contributing to this fat loss include: (a) a small energy deficit; (b) the energy cost of synthesising new lean tissue; (c) energy loss through the storage and excretion of ketone bodies; (d) catecholamine-induced 'futile' metabolic cycles with increased resting metabolism; and (e) a specific reaction to cold dehydration. Current limitations for the clinical application of such treatment include uncertainty regarding optimal environmental conditions, concern over possible pathological reactions to cold, and suggestions of a less satisfactory fat mobilisation in female patients. Possible interactions between physical fitness and metabolic reactions to cold remain controversial.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adaptation to exercise in the cold. 388 60

Diabetic ketoacidosis is usually associated with marked secondary hyperaldosteronism. Plasma levels of renin, angiotensin II, and aldosterone are markedly raised before treatment in most patients, with values falling rapidly toward normal as metabolic control is restored. In a few patients, mostly those with long-term complications of diabetes, plasma levels of renin, angiotensin II, and aldosterone before treatment remain within the normal range. In moderately hyperglycemic patients who have glycosuria but not ketonuria, plasma levels of all three substances are significantly higher than when control is improved. Occasionally, moderately hyperglycemic patients have mild secondary hyperaldosteronism. Improved metabolic control in such patients causes a rise in plasma volume and a rise in total exchangeable sodium, the latter to levels significantly above normal. Plasma catecholamine levels are markedly elevated in diabetic ketoacidosis, probably as a consequence of the ketoacidotic state. In nonketotic patients with moderate hyperglycemia, basal plasma norepinephrine levels are normal; catecholamine responses to exercise may be exaggerated, however. Epidemiological and animal studies suggest a relationship between blood pressure and blood glucose levels. There are few clinical studies of the effects of altering metabolic control of diabetes on blood pressure, and this is an important area for further study.
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PMID:Diabetic control and the renin-angiotensin system, catecholamines, and blood pressure. 393 82

To delineate the hormonal mechanism of dietary-induced changes in sodium balance, the role of insulin and glucagon in natriuresis of fast was evaluated in obese subjects submitted to a total starvation and given either glucagon or somatostatin infusion on day 4 of fast. While large amounts of glucagon (1 mg over 6 h) stimulated concomitantly ketonaemia, ketonuria and renal sodium losses, the ten-times lower amounts of glucagon induced an increase in renal ketone body and sodium excretion without any significant change in ketonaemia. It was concluded, therefore, that elevated plasma glucagon level may enhance renal sodium loss in ketotic states, through a direct renal effect reducing tubular ketone body reabsorption, hence increased ketonuria and natriuresis. It appears nevertheless that decreased insulin secretion, rather than an increase in plasma glucagon level must be considered as a key hormonal factor responsible for natriuresis attending starvation. Indeed, the concomitant reduction in plasma glucagon and insulin levels, resulting from somatostatin infusion on day 4 of fast, was followed by significant increase in natriuresis. The latter observation supports several previous studies indicating that insulin stimulates sodium reabsorption by the kidney and that the reduction in insulin secretion may induce an increase in renal sodium excretion. It was concluded, therefore, that not only sodium intake but also the carbohydrate content of the diet should be reduced in an attempt to induce a negative sodium balance and to correct hypertension in obese subjects.
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PMID:Influence of insulin and glucagon on sodium balance in obese subjects during fasting and refeeding. 611 18

Interrelations between glucose and electrolyte homeostasis were evaluated in 193 insulin-treated diabetic out-patients. All had normal serum creatinine and were studied during their everyday metabolic control. Although the patients were selected to be without proteinuria and ketonuria, they exhibited wide ranges of blood glucose values (2.5-29.5 mmol/l) and urine glucose excretions (0-301 mmol/mmol creatinine). Patients with blood glucose values within 2.5-10 mmol/l (n = 80) had entirely normal levels of serum sodium (140.6 +/- 2.7 (SD) versus 141.0 +/- 2.6 mmol/l) and potassium (4.35 +/- 0.38 versus 4.40 +/- 0.38 mmol/l) as compared with normals (n = 371). In contrast, diabetics with higher blood glucose concentrations (n = 113) showed hyponatremia (137.7 +/- 2.6 mmol/l, p less than 0.001) and a moderate increase of serum potassium (4.60 +/- 0.39 mmol/l, p less than 0.001). On stratification into classes of blood glucose, serum sodium declined from 142 to 135 mmol/l (r = -0.61, p less than 0.001), whereas serum potassium rose from 4.33 to 4.87 mmol/l (r = 0.37, p less than 0.001). Despite these reciprocal changes the urinary excretion rates relative to creatinine of sodium potassium and water rose with rising degrees of glycosuria (r = 0.24, p less than 0.001; r = 0.28, p less than 0.001; and r = 0.63, p less than 0.001, respectively). The decline in serum sodium represents a well-known osmoregulatory response to hyperglycemia. However, the rising level of serum potassium in virtual absence of renal failure and ketonuria suggests an abnormality in potassium homeostasis. Diabetic dysregulation, or rather insulin deficiency may be its cause.
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PMID:Hyponatremia and hyperkalemia in relation to hyperglycemia in insulin-treated diabetic out-patients. 703 73

Investigations of renal function have been done in healthy ewes in different stages of reproduction, and after food restriction, as well as in ewes sick with ketosis, hypocalcemia, rumen acidosis and different nephropathies. The determination was based on the estimated weight dependent endogenous creatinine excretion (E). A reference population of 56 healthy non or early pregnant ewes (before day 120 of pregnancy) was used as control. Late pregnancy (121.-149. day, n = 14) and lactation (n = 14) lead to higher renal creatinine-clearance (approximately GFR). Food restriction in all stages of pregnancy was followed by lower plasma concentrations of potassium, calcium, magnesium and glucose, and a reduced fractional excretion of potassium, calcium and magnesium. Pregnancy and especially food restriction caused a marked rise of the 3-OH-hydroxybutyrate values in the plasma and a significant acetonuria. After withdrawal of feed in lactating sheep, in opposition to pregnant sheep, the plasma values of phosphate were higher. In ketotic sheep (n = 43) a failure of renal function could not be demonstrated, the pronounced acetonuria could be explained by acetonemia. In hypocalcemia (n = 23) disturbance of creatinine-clearance and tubular reabsorption of sodium, potassium, glucose and 3-OH-butyrate could be seen. Glucosuria and acetonuria were caused by increased plasma concentrations and reduced tubular reabsorption. In rumen acidosis (n = 10) disturbances of low degree of GFR and reabsorption could be seen, glucosuria was mainly due to hyperglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical studies of kidney function in sheep. II. Effect of pregnancy, lactation and feed restriction and metabolic diseases on kidney function]. 772 May 46

A case of adult Reye's syndrome is described. A previously healthy 17-year-old man developed convulsions 2 days after resolution of an upper respiratory infection with parainfluenza virus type 3. During the preceding infection, he took aspirin. On admission, he was drowsy. There was no focal signs. Cranial CT scan was unremarkable. A lumbar puncture revealed an opening pressure of 180 mm H2O; the cerebrospinal fluid was acellular with normal protein level. Serum chemistry showed elevated transaminase activities and normal bilirubin level. Blood ammonia level was high; urea and citrulline levels were abnormally low. These abnormalities disappeared later, suggesting transient cysfunction of mitochondrial urea-cycle enzymes. Free and acyl carnitine levels were unremarkable. Both metabolic acidosis and ketonuria were absent. Thus, a variety of aminoacidurias and organic acidemias are unlikely. All these findings meet diagnostic criteria for Rye's syndrome proposed by the CDC of the USA. Status epilepticus was treated with intravenous infusion of thiamylal sodium. He was treated with hypertonic glucose solution and osmotic diuretic. Three months after the onset of the illness, his convulsions were controlled only with zonisamide, clonazepam, and carbamazepine. He had motor dysfunctions. This case is unique in that a patient with adult Reye's syndrome and status epilepticus favorably recovered.
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PMID:[A case of adult Reye's syndrome with favorable outcome despite status epilepticus]. 904 59

An intriguing problem of diabetes mellitus is the development of generalized angiopathy and concomitant hypertension. However, there is still a controversy whether beta-adrenoceptor antagonists can be used as antihypertensive agents in diabetes. Four groups of rats were investigated: nondiabetic controls, diabetes mellitus, diabetes + celiprolol (250 mg/kg body weight/day), diabetes + metoprolol (125 mg/kg body weight/day) after 6 months. Diabetes was induced by i.v. streptozotocin injection. We examined vascular structure and function histologically and by an in vitro microvideoangiometry of isolated perfused mesenterium. Additionally, we investigated the effects of hyperglycemia and celiprolol on NO release in cultivated aortic endothelial cells and the effect of celiprolol on transendothelial paracellular permeability. Diabetes resulted in endothelial dysfunction, characterized by a reduced response to acetylcholine and L-N(G)-nitro-arginine and an unchanged response to sodium nitroprusside (SNP). These effects were significantly antagonized by celiprolol but were not influenced by metoprolol treatment. This was supported by the finding of typical vascular changes associated with diabetes like media thickening, reduced cardiac capillary/muscle fiber ratio, and glomerulosclerosis, which were significantly reduced by celiprolol but not influenced by metoprolol treatment. Ketonuria improved after celiprolol treatment, whereas blood glucose, lipids, and body weight were not different between the diabetic groups. In cultured cells, celiprolol did not induce direct NO release but reversed the impairment of stimulated NO release caused by hyperglycemia. Furthermore, celiprolol reduced endothelial paracellular permeability. We conclude that celiprolol can exert antiangiopathic effects in diabetic rats and that both beta-adrenoceptor antagonists did not aggravate diabetic angiopathy and metabolic derangement.
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PMID:Different effects of the beta-adrenoceptor antagonists celiprolol and metoprolol on vascular structure and function in long-term type I diabetic rats. 1002 26


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