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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperglycemia and impaired glucose tolerance are well known phenomena occurring in patients with renal failure. In contrast to true diabetic subjects, an elevated ratio of insulin to glucose during the glucose tolerance test is consistently observed indicating a peripheral insulin insensitivity. Among the possible reasons, a disturbance at the cellular level seems to be most likely. There is some evidence of reduced peripheral glucose utilization on the one hand and increased hepatic glucose output--probably by stimulation of gluconeogenesis--on the other. Agents that have been suggested to be involved in these alterations of carbohydrate metabolism in uremia are hormones, electrolytes, pH, and "toxic" metabolic intermediates or end-products. Of these, an increase in insulin antagonistic hormones; among them growth hormone, catecholamines, and glucagon, seems to be of most significance. Although for the individual hormones no equivocal correlation with glucose intolerance has been proved, the interaction of all of them may result in a preponderance of insulin antagonism thus leading to an apparent insulin resistance.
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PMID:Carbohydrate metabolism in renal failure. 2 64

A high incidence of bacterial infections in patients with fulminant hepatic failure (F.H.F.) has led to an investigation of polymorpho-nuclear-leucocyte (P.M.N.) function. No intrinsic leucocyte abnormality was demonstrable but a factor present in F.H.F. serum was shown to inhibit the metabolic activity of the leucocyte hexose-monophosphate shunt. This effect was due neither to low serum-complement nor to associated renal failure. The inhibitory factor, however, was removed either by pre-incubation with activated charcoal or by in-vitro dialysis, raising the possiblity that charcoal haemoperfusion or other forms of artificial liver support may improve P.M.N. function in this condition.
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PMID:Metabolic inhibition of polymorphonuclear leucocytes in fulminant hepatic failure. 5 4

Metabolic studies were performed on 19 patients with acute renal failure. Therapy included intravenous hyperalimentation using 15 to 20 g of essential amino acids or 20 to 40 g of essential plus nonessential amino acids and hypertonic glucose (37 to 50%). The effect of this parenteral feeding appears to be primarily pharmacological. Hypertonic glucose promotes the hyperinsulinemia important to be membrane function, the operation of the sodium pump, and cell metabolism. Administration of high biological value crystalline amino acdis potentiates the effect of insulin by inhibiting protein breakdown and promoting protein synthesis, particularly in muscle. This reduces tissue catabolism and urea formation, and promotes potassium, magnesium, and phosphate homeostasis. The branched-chain ketogenic amino acids valine, leucine, and isoleucine may be of particular importance. When indicated, administration of renal failure hyperalimentation and peritoneal or hemodialysis can be expected to complement each other and accelerate recovery. This intravenous fluid therapy, in turn, must be coordinated with proper hemodynamics, usually requiring a colloidal solution to maintain intravascular volume, and cardiotrophic agents such as digitalis and dopamine. Early use of renal failure can be expected to demonstrate the most striking response in terms of survival, early recovery from acute renal failure, and the preservation of physiological homeostasis.
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PMID:Criteria for choosing amino acid therapy in acute renal failure. 10 Oct 72

An analysis is made of two groups each of 20 patients with toxic septic states and hypercatabolic renal failure, who were given parenteral nutrition for at least 3 days. Each group was divided into two subgroups, given glucose, 13--20 and 20--27 kcal. 24 h--1 kg--1 body weight; the second subgroup was also given nitrogen-containing infusions of 0.05--0.12 or 0.12--0.17 g of N 24--1/kg--1 body weight, the total calorie intake amounting to 23--28 and 28--33 kcal. 24 h--1 kg--1 respectively, with nitrogen amounting to 150--400 kcal./g. A mean daily decrease of blood urea of 9.2 mg/100 ml was recorded, together with a positive catabolism in the series given nitrogen, and a rise of 0.8 mg/100 ml with negative catabolic index in the series fed with glucose (P less than 0.01); there were similar nitrogen losses in both the series, corrected by catabolism formula. The results demonstrated a decreased rate of catabolism in patients fed with a diet containing nitrogenous compounds.
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PMID:Parenteral nutrition in toxic septic states. 10 85

Two comparative lots were established, of 48 and 44 patients respectively with toxico-septic syndromes, renal failure of the hypercatabolic type, that had received parenteral food for a period of between 3 and 11 days. The first group received only glucose while the second also had injectable aminoacids. In the first group was noted a daily rate of blood urea variation (r) of 1,65 mg% and a good nitrogen elimination. In the second group was noted an r of --8,13mg% (pless than 0,001) and a more rapid improvement of the clinical condition. Next to the fall in the absolute nitrogen elimination (p greater than 0,05), the nitrogen balance, computed at 36% incorporation of the administered nitrogen, was significantly improved in the second group (p greater than 0,01), demonstrating the lowering of the metabolic rate under perfusion with aminoacids.
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PMID:[Decreased catabolism after toxico-septic aggression by administration of injectable amino acids]. 11 51

Chronic renal failure results in a variety of metabolic derangements that perturb glucose homeostasis. These may in part result from the fact that the kidney plays a prominent role in the metabolism of insulin as well as a number of other low-molecular-weight peptide hormones that affect carbohydrate metabolism. Specific abnormalities in glucose utilization that appear to be related to alterations in membrane receptors, resulting in increased glucagon sensitivity and decreased insulin action, are a newly recognized factor in intolerance to oral glucose. Glucose production and utilization are both abnormally increased in patients with chronic uremia, and these disturbances are only partially corrected by hemodialysis treatment. The mechanism(s) contributing to these changes is unclear, but seems to involve a combination of humoral and cellular factors. These include some degree of insulin resistance, probably inadequately modulated proteolytic responses to glucagon and parathyroid hormone, and a basic defect in energy production that alters intracellular concentrations of high-energy phosphate-containing nucleotides. It is unclear whether these changes in carbohydrate tolerance pose an increased risk for the premature development of cardiovascular disease in patients with renal failure, as they appear to do in the nonuremic population. The occasional patient with renal failure may develop clinical hypoglycemia when glucose utilization continues in a setting in which the hepatic capacity to produce glucose is reduced, probably as a consequence of altered substrate delivery and/or inhibition of one or more key gluconeogenic enzymes.
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PMID:Disorders of glucose metabolism in uremia. 11 52

Combined renal and pancreatic transplantation in patients with juvenile diabetes mellitus, diabetic nephropathy and renal insufficiency is designed to improve the poor prognosis observed with hemodialysis or renal transplantation alone. Interest has recently shifted from pancreatic organ to islet transplantation, in view of the absence of complications with the latter. However, no permanent success with islet transplants in diabetic patients has so far been reported. In the series presented, one patient with juvenile diabetes and subsequent renal failure was successfully treated with simultaneous kidney and intrasplenic pancreatic islet allotransplants. One year after the operation the patient has normal blood glucose levels without exogenous insulin, despite treatment with prednisone.
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PMID:[Successful allotransplantation of an island of Langerhans]. 11 44

In glycogenosis type 1 (GT1), glucose synthesis is deficient due to absence of glucose-6-phosphatase. Development of renal failure in such a patient provided the opportunity to test whether or not this metabolic defect could be reversed by a renal allograft, which contains the missing enzyme and has potential for glucose synthesis. Despite normalization of renal function and both glucocorticoid therapy and the infusion of amino-acid precursors of glucose, fasting hypoglycemia persisted unabated. We conclude that a funtioning renal allograft is incapable of meeting the metabolic demands of a patient with glucose-6-phosphatase deficiency.
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PMID:Renal tranplantation in type 1 glycogenosis. Failure to improve glucose metabolism. 20 6

Infectious hematopoietic necrosis (IHN) is a rhabdoviral disease of rainbow trout (Salmo gairdneri). Trout were injected with IHNV, and various hematological and biochemical measurements of clinically ill fish were compared to uninfected controls. Infected fish had reduced corpuscular counts, hemoglobin, and packed cell volume, but normal mean corpuscular volume, mean corpuscular hemoglobulin, and mean corpuscular hemoglobin concentration. The percentage of immature erythrocytes was increased, but the percentage of leukocytes was unchanged. Differential leukocyte counts showed a significant decrease in neutrophils, increase in lymphocytes, but no change in monocytes. Unidentifiable necrobiotic cells were prevelant in blood smears and hematopoietic tissue imprints. Plasma bicarbonate, chloride, calcium, phosphorus, bilirubin, and osmolality were signigicantly reduced, but plasma glucose and anterior kidney ascorbate were unchanged. Plasma pH increased and the alpha fractions of the serum proteins were altered. No change was found in plasma enzymes, except that a LDH isozyme was significantly increased. The alkali reserve was diminished and alterations in acid-base and fluid balance occurred. Death probably resulted from a severe electrolyte and fluid imbalance caused by renal failure.
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PMID:Pathophysiology of infectious hematopoietic necrosis virus disease in rainbow trout: hematological and blood chemical changes in moribund fish. 23 12

Mice challenged intravenously with 10(6) viable Candida albicans died between 1 and 16 days after infection. Near the time of death, over 98% of the recoverable fungi came from the kidneys. Physiologically, animals were in renal failure near the time of death as evidenced by elevated blood urea nitrogen (BUN) and blood creatinine levels and a creatinine clearance rate which was about one-half normal. No abnormalities in liver glucogen and blood glucose levels were detectable. When mice were challenged with 4.5 X 10(6) viable C. albicans, they all died within 12 h. Near the time of death they had normal BUN values and were hyperglycemic. In mice receiving 4.5 X 10(6) heat-killed C. albicans, no deaths occurred and liver glycogen, blood glucose, and BUN levels all remained within a normal range and were different from responses to bacterial endotoxin. Cumulatively, the results demonstrate two distinct syndromes for the pathogenesis of experimental C. albicans infections. At the lower dose, mice were in renal failure associated with progressive renal infection. At the higher dose, renal failure was not observed. If a toxin was associated with death from the latter dose, it was not similar to bacterial endotoxin.
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PMID:Physiological and metabolic alterations accompanying systemic candidiasis in mice. 39 27


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