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

A 23-year-old man presented with a massive fecal impaction, and was subsequently found to be in renal failure along with the presence of intraperitoneal free air on x-ray. Following disimpaction, the renal failure rapidly resolved and exploratory laporotomy revealed no colonic perforations. Obstructive renal failure resulting from fecal impaction is a rare but reported complication. In this report acute renal failure is attributed to severe fecal impaction.
Ala Med 1991 Mar
PMID:Acute renal failure secondary to fecal impaction. 204 47

The effect of metabolic acidosis (MA) on amino acid and keto acid metabolism was studied in fourteen patients with chronic renal failure (CRF) under the low protein diet (0.6-0.8 g/kgBW). The comparative study of five patients with renal tubular acidosis was carried out. Each patient was investigated before [MA(+)period] and after correction with sodium bicarbonate administration lasting 10 days [MA(-)period]. The correction of MA improved nitrogen balance and elevated plasma branched-chain amino acids (BCAA), keto acids (BCKA), glutamine and alanine concentrations. No effect was however, observed in change of plasma insulin and glucagon. Oral administration of the keto-analogues of BCKA [0.1 g/kgBW of alpha-ketoisovalerates (KIV) and alpha-keto-isocaproic acid (KIC)] is made for the purpose of investigating the change in the metabolic conversion rate to amino acids. As a result, MA (+) suppressed an increase in plasma KIV and KIC concentrations. Moreover, an increase in plasma valine and leucine concentrations were suppressed by MA (+). These results suggested that MA stimulates BCKA oxidation and suppresses the protein sparing effect of leucine and KIC, and accelerates the catabolism in CRF under the low protein diet. The correction of MA is ineffective in severe renal failure (serum creatinine above 10.0 mg/dl), because the other uremic factors appear to be affecting protein and amino acid metabolism. Therefore, it might be concluded that MA should be corrected at an earlier stage of CRF.
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PMID:[The effect of metabolic acidosis on amino acid and keto acid metabolism in chronic renal failure]. 205 49

The concentration of 18 alpha-amino acids (AAs) in plasma and renal cortical cell water were measured 3 or 24 hr after 1 hr of unilateral renal artery clamping or 24 or 48 hr after 15 mg/kg body weight HgCl2 injection sc as a test of epithelial integrity. Cellular glycine (Gly), hydroxyproline (Hpr), ornithine (Orn), phenylalanine (Phe), serine (Ser), and tryptophan (Trp) concentrations were depressed 24 hr after HgCl2 (p less than 0.05), but the remaining 12 AAs were not distinguishable from control despite the presence of severe renal failure. ARginine (Arg), glutamic acid (Glu), and valine (Val) also were decreased (P less than 0.05) 24 hr later, but concentrations of half of all measured AAs were still normal. Cellular alanine (Ala), Arg, Glu, Gly, Phe, and Ser concentrations were decreased 3 hr after ischemia, p less than 0.05, but 12 AAs were unchanged and only Arg, Phe, Ser, and threonine (Thr) were reduced 24 hr after ischemia was reversed. Concentrations of even the most affected AAs remained notably higher than in plasma in both forms of acute renal failure (ARF). Total loss of AAs from a small proportion of tubular cells would be hidden by essentially normal concentrations in the rest, and such losses may well have occurred. Unless cellular AAs in ARF are almost completely bound, however, the well-maintained cell:plasma AA concentration ratios indicate that cellular energetics were adequate for AA uptake and that epithelial permeability to AAs in the vast majority of cells was not greatly disturbed. Such findings suggest that most of the epithelium, although seriously damaged, had remained viable.
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PMID:Renal epithelial amino acid concentrations in mercury-induced and postischemic acute renal failure. 221 14

Subtotally nephrectomized rabbits were compared with sham-operated controls. The isolated soleus muscle of one leg was exercised using controlled stimulus parameters at 1 Hz until the contraction tension (amplitude) was reduced by one half. The muscle was then quickly frozen in liquid nitrogen and analyzed for lactate, pyruvate, glycogen, alanine, glutamine and alpha-ketoglutarate. The resting leg was used as a control and similarly frozen and analyzed. The difference between resting and exercised muscle lactate and pyruvate concentration was significantly greater in experimental animals while muscle alanine and alpha-ketoglutarate concentrations were lower in the experimental animals. There was no difference in the time required to reach one half of the muscle contraction amplitude between experimental and control animals. Blood lactate levels rose in the experimental animals to a greater degree than in control animals, similar to that seen in human subjects with renal failure.
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PMID:Carbohydrate utilization in exercising muscle in subtotally nephrectomized rabbits. 236 34

The appearance of jaundice during a septic process is usually associated to multiple organ failure and a high mortality rate. Among 17 septic patients followed prospectively, we found 11 with hepatic dysfunction. Abnormal levels of bilirubin and alanine-aminotransferase were found. Glutamine concentration in spinal fluid was 26 +/- 19.4 mg/dl vs 9.43 +/- 2.41 in patients without liver failure (p less than 0.05). Significant correlations were found among levels of bilirubin and glutamine (r = 0.83), creatinine (r = 0.708), number of platelets (r = 0.778) and between glutamine and creatinine (r = 0.708). Patients with liver failure presented a higher rate of renal failure and thrombocytopenia (p less than 0.01) and a higher mortality rate. These findings confirm that liver failure is associated to multiple organ failure and thrombocytopenia. It may be related to small vessel occlusion.
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PMID:[Role of the liver in septic encephalopathy. A disorder associated with multiple organ failure caused by sepsis]. 251 91

Hypoglycemia associated with renal failure is more common than generally thought. Its occurrence is often a marker of multisystem failure and has an ominous prognostic implication. Its pathogenesis is frequently complex and involves one or several mechanisms. In the evaluation of uremic hypoglycemia, the first step should be the exclusion of obvious causes such as insulin, oral hypoglycemic agent therapy, and the use of drugs known to cause hypoglycemia. Propranolol, salicylates, and disopyramide are among the most commonly implicated agents. Additional triggering events are alcohol consumption, sepsis, chronic malnutrition, acute caloric deprivation, concomitant liver disease, congestive heart failure, and an associated endocrine deficiency. When no obvious cause can be demonstrated, the hypoglycemia is referred to as spontaneous. Spontaneous uremic hypoglycemia has been attributed to deficiency of precursors of gluconeogenesis, that is, alanine, deficient gluconeogenesis, impaired glycogenolysis, diminished renal gluconeogenesis and impaired renal insulin degradation and clearance, poor nutrition, and, in a few cases, deficiency in an immediate counterregulatory hormone such as catecholamine and glucagon. However, the mechanism(s) seems to differ from one patient to the other. Dialysis also predisposes to hypoglycemia in uremia, possibly because of the chronic state of malnutrition. Postdialysis hypoglycemia is secondary to glucose-induced hyperinsulinemia, which is caused by the high glucose content in the dialysate. In uremic hypoglycemia, neuroglycopenic manifestations predominate because of frequent autonomic nervous system dysfunction and lack of catecholamine release in response to hypoglycemia. Its severity and duration are variable. Hypoglycemia should be suspected in any patient with renal failure who exhibits any change in mental or neurologic status. Detection of hypoglycemia should rely on frequent and careful glucose determinations in any patient with uremia.
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PMID:Hypoglycemia associated with renal failure. 264 22

Primary hyperoxaluria is a recessive hereditary disturbance of glyoxylate metabolism caused by deficiency of the liver enzyme, alanine glyoxylate transaminase. The main symptoms are recurrent renal stones, nephrocalcinosis and renal failure. In the advanced state, the disease is frequently complicated by osseous disease, vascular insufficiency and cardiac arrhytmias caused by deposits of calcium oxalate in the tissue. The prognosis is poor. No specific medical treatment exists. Dialysis is not effective and the results of renal transplantation is poor. Combined liver and renal transplantation correct the metabolic defect and the excretion of oxalate is normalised. Combined transplantation must be regarded as the optimal treatment of renal failure caused by PHO. The transplantation should be undertaken preferably before the creatinine clearance falls below 10-20 ml/min in order to avoid tissue deposits of calcium oxalate and excessive urinary excretion of oxalate during immediate post-transplantation period.
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PMID:[Primary hyperoxaluria]. 267 87

An in vivo model of liver hyperplastic noduligenesis was induced in rats by long-term administration of thioacetamide (TAM) (50 mg/kg/day i.p.). Three doses of 50 mg/kg of an antitumoral Rh(III) complex were administered at 14, 9 and 5 days before the end of TAM treatment. Plasma and urine were obtained from either TAM or Rh(III) complex or TAM plus Rh(III) complex treated rats to determine the interactions of both substances with the biochemical parameters related to liver function. The rise in alkaline phosphatase (ALP), leucine aminopeptidase (LAP), gamma-glutamyl transferase (GGT) and the unchanged activities in the aspartate and alanine aminotransferases (AST, ALT) in plasma of TAM-treated rats indicated that the disease induced by this substance can be considered as a chronic obstructive biliary disease with indices of cell proliferation and tumors. The increased concentration of bilirubin both in the plasma and urine of TAM-treated rats suggested liver cholestasis and hepatobiliary obstruction. The very low values of creatinine clearance indicated that there was some degree of kidney failure due to the effect of TAM. The increased concentration of ammonia both in plasma and urine were probably a consequence of the decreased flux in the urea cycle in the liver. The Rh(III) complex alone did not produce significant changes in the plasma enzyme activities. The only significant changes were found in the concentrations of uric acid and ammonia in the urine. When the Rh(III) complex was administered to TAM-treated rats, significant restoration of the following parameters were observed: plasma enzymatic activities, blood bilirubin and ammonia, uric acid and creatinine in the urine and the creatinine clearance. These results suggest that the altered liver function induced by TAM can be restored by Rh(III) complex. The mechanisms by which this complex acts to counteract the TAM-induced changes are not yet established.
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PMID:Effect of a rhodium complex on alterations of hepatic function in thioacetamide-induced hyperplastic noduligenesis in rats. 288 38

Infantile oxalosis is the most severe form of primary hyperoxaluria type I (PH I). Only 28 patients have been reported in detail; it was found that diagnosis was usually delayed, and most patients presented before the age of 4 months in renal failure and died within the 1st year of life. This report comprises two infants in whom diagnosis of PH I was made in the first few weeks of life before renal function was impaired. Case 1, whose brother had died of infantile oxalosis, already had greatly increased urinary oxalate and glycolate excretion at 7 days of age. In Case 2, PH I was diagnosed early because of the finding of increased renal echogenicity at 3 weeks of age; this patient had numerous episodes of stone formation despite continuous treatment with pyridoxine, but maintained renal function with normal serum creatinine levels at the age of 28 months. Prenatal diagnosis was attempted in case 1; however, amniotic fluid oxalate and glycolate concentrations were normal, suggesting that these acids pass the placenta and are not retained. The recent discovery of a transamination defect (deficiency of the peroxisomal enzyme alanine: glyoxylate aminotransferase) explains why some patients respond to pyridoxine treatment. Differences in onset and severity of PH I and in response to pyridoxine suggest that this disorder is biochemically and genetically heterogeneous.
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PMID:New aspects of infantile oxalosis. 315 28

Chronic renal failure is associated with many abnormalities in plasma amino acids. Since patients with renal failure are frequently deficient in vitamin B-6, this study examined whether vitamin B-6 deficiency may be a cause of any of the abnormal plasma amino acid concentrations observed in chronic renal failure. Sham-operated and chronically azotemic rats were pair-fed diets deficient in or replete with vitamin B-6 for 21 d. By the end of 21 d, the EGOT index rose significantly in the B-6-deficient rats but not in the B-6-replete animals. There were several differences in plasma amino acid concentrations between azotemic and control rats. Azotemia and B-6 deficiency each lowered the plasma serine concentration and raised the glycine-to-serine ratio. Plasma glycine was affected by a two-way interaction between azotemia and vitamin B-6 deficiency whereby the highest values were found in the sham-operated vitamin B-6-deficient animals. Plasma alanine and asparagine were reduced by B-6 deficiency and unchanged by azotemia. These results suggest that vitamin B-6 deficiency may contribute to several of the abnormalities in the plasma aminograms observed in chronic renal failure.
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PMID:Effect of vitamin B-6 deficiency on plasma amino acid levels in chronically azotemic rats. 377 16


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