Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9BZE4 (chronic renal failure)
 13,583 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical effects of ninzin-to with daiokanso-to were studied on 15 patients with chronic renal failure. The level of urea nitrogen and creatinine in sera was slightly decreased in early days of treatment (about 3 months long), but thereafter these levels were gradually increased in many patients and 2 patients needed hemodialysis treatment. The effects of these drugs against subjective symptoms were found in bowel habits, general malasia and anorexia. The overall effective rate was 80% in early term and 60% in late term. There were no severe adverse reactions.
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PMID:[The effects of ninzin-to with daiokanso-to in patients with chronic renal failure]. 324 30

The experience with chronic renal failure in two institutions, a tertiary care referral hospital with a high prevalence of diabetes mellitus and a Veterans Administration Hospital, was utilized to formulate guidelines for the nutritional assessment and therapy of chronic renal failure. For optimal nutritional support of patients with renal failure, it is important to characterize objectively nutritional deficiencies. Thus, dietary history, anthropometric measurements (weight/height ratio, arm muscle circumference, and triceps skinfold), and serum protein measurements (total protein, albumin, and transferrin, in particular) provide valuable data concerning the nutritional status of the patient. The serum urea nitrogen to serum creatinine ratio and urea nitrogen appearance are useful for selecting optimal protein intake. The serum urea nitrogen/creatinine ratio must be interpreted with respect to the factors which influence it; i.e., the urea clearance and the urea nitrogen appearance. The goal of nutritional therapy is the preservation of body cell mass and function, fluid, electrolyte, and acid-base homeostasis, mineral balances, and with early use of dialysis, the avoidance of uremic toxicity. Nutritional therapy, especially in patients with superimposed illnesses and associated anorexia, may be enhanced by the use of formula feedings, tube feedings, and, if necessary, total parenteral nutrition.
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PMID:Nutritional assessment and treatment of chronic renal failure. 739 79

Protein and calorie malnutrition often starts before initiation of dialysis, and reflects the anorexia and the catabolic state of chronic renal failure. In the face of inadequate dialysis, which perpetuates the uremic state, malnutrition often worsens. Several studies, though not all, suggest that optimal dialysis improves nutritional status of dialysis patients. Such optimal dialysis now must include the use of biocompatible membranes to deliver Kt/V > 1.4 (urea reduction ratio > 65%). Additional interventions can include the use of enteral or intravenous hyperalimentation, and recombinant growth factors such as growth hormone or insulin-like growth factor-1. Importantly, studies to document the improvement in the morbidity and mortality of patients with these interventions are still needed and require large multicenter trials.
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PMID:Interventions to treat malnutrition in dialysis patients: the role of the dose of dialysis, intradialytic parenteral nutrition, and growth hormone. 761 Dec 60

Anemia is an inevitable and potentially serious complication of chronic renal failure and one of the most important limiting factors in patient rehabilitation. Although adequate dialysis can control many of the symptoms of uremia, dialysis does not reverse anemia-associated fatigue, and thus, many patients are not rehabilitated. Human recombinant erythropoietin (epoetin) therapy has proven to be effective in reversing anemia and increasing hematocrit levels in the majority of patients with chronic renal failure. Among this patient population, increases in hematocrit level have resulted in improvements in the symptomatology of organ hypoxia, neurobehavioral indices, anorexia, insomnia, depression, and sexual disinterest and dysfunction, as well as a reduction in cardiomegaly. However, despite the availability of epoetin and the dramatic improvements in the complications associated with the anemic state observed following therapy, it appears that patient rehabilitation remains a challenge. One aspect of the continuing problem of rehabilitation appears to be the reluctance of the medical community to increase hematocrit levels above 30%, despite the fact that higher hematocrit levels are associated with greater improvements and that potential adverse events related to hemodynamic adaptation are manageable. Indeed, a comparison of the results from two Epoetin alfa clinical trials, one in which hematocrit levels were maintained at 35% and a large phase IV study in which the target hematocrit level appears to have been approximately 30%, clearly demonstrate the benefits of optimizing hematocrit levels and thus improving the potential for rehabilitation.
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PMID:In search of an optimal hematocrit level in dialysis patients: rehabilitation and quality-of-life implications. 802 33

Growth retardation commonly complicates chronic renal failure in children. Although the etiology of this growth impairment is multifactorial, inadequate nutrition is considered an important cause in infants and young children. An "aggressive" nutritional approach has been repeatedly suggested in children with early onset chronic renal failure and poor feeding habits, but the possibility of inducing catch-up growth by energy supplementation is still controversial. The nutritional effects of a long-term, home-based enteral feeding program were studied in two infants and three children with moderate to severe chronic renal failure and impaired growth associated with persistent anorexia. In all patients, renal failure had developed during the first year of life due to congenital diseases. Enteral feeding was performed at home, during the night, through a silicone rubber nasogastric tube. The treatment lasted for 1 year. The energy intake ranged between 101% and 116% of the recommended dietary allowance (RDA), and the protein intake between 96% and 113% of the RDA in all patients but one, in whom proteins were restricted to 75% of the RDA. All children showed a substantial improvement in deviation score for both weight (mean increase +1.76), height (mean increase +1.52) and in the general metabolic condition, irrespective of age, severity of osteodystrophy, or degree of renal failure. The treatment was well tolerated and, apart from a few episodes of vomiting, no complications arose during the treatment. Tube feeding may be an effective therapeutic option for overcoming malnutrition when chronic renal failure is associated with persistent anorexia. In infants and young children, growth retardation can be opposed and catch-up growth obtained.
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PMID:Catch-up growth in children with chronic renal failure treated with long-term enteral nutrition. 855 42

Feeding problems, anorexia and vomiting are common in infants and children with chronic renal failure (CRF), and play a major role in the growth failure often found in this condition. However, the gastroenterological and nutritional aspects of CRF in children have received little attention, hence therapeutic interventions are usually empirical and often ineffective. Gastritis, duodenitis and peptic ulcer are often found in adults with CRF on regular haemodialysis and following renal transplantation. Despite persistent hypergastrinaemia, gastric acid secretion is decreased rather than increased in most of these patients, and active peptic disease appears to be promoted by the removal of the acid output inhibition (neutralisation of gastric acid by ammonia) that follows active treatment. Helicobacter pylori, on the other hand, does not seem to play a significant role in the pathogenesis of peptic disease in CRF. Gastro-oesophageal reflux has been found in about 70% of infants and children with CRF suffering from vomiting and feeding problems, and thus appears to be a major problem in these patients. In a number of symptomatic patients with CRF, gastric dysrhythmias and delayed gastric emptying have also been found; hence there appears to be a complex disorder of gastrointestinal motility in CRF. Serum levels of several polypeptide hormones involved in the modulation of gastrointestinal motility [e.g. gastrin, cholecystokinin (CCK), neurotensin] and the regulation of hunger and satiety (e.g. glucagon, CCK) are significantly raised as a consequence of renal insufficiency, and can be reverted to normal by renal transplantation. Furthermore, several other humoral abnormalities (e.g. hypercalcaemia, hypokalaemia, acidosis, etc.) are not uncommon in CRF. By directly affecting the smooth muscle of the gut or stimulating particular areas within the central nervous system, all these humoral alterations may well play a major role in the gastrointestinal dysmotility, anorexia, nausea and vomiting in patients with CRF. Specific pharmacological and nutritional interventions should thus be considered for the treatment of vomiting and feeding problems in CRF.
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PMID:Gastrointestinal function in chronic renal failure. 874 22

It is well established that chronic renal failure is associated with loss of lean body mass. Possible explanations for this problem include an inability to limit essential amino acid oxidation and protein degradation when dietary protein is limited by anorexia or therapeutically. Alternatively, uremia could directly stimulate protein catabolism. In rats, we have uncovered evidence that metabolic acidosis not only blunts the responses to a low-protein diet but also directly stimulates the degradation of muscle protein. In cultured muscle cells as well, acidification of the media stimulates protein degradation. The mechanisms for catabolism involve activation of the ATP-ubiquitin-proteasome-dependent pathway causing muscle protein degradation and stimulation of branched-chain ketoacid dehydrogenase activity causing degradation of branched-chain amino acids. Glucocorticoids are required but are not sufficient for these catabolic responses.
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PMID:Cellular mechanisms of catabolism activated by metabolic acidosis. 882 Dec 2

Leptin, secreted from fat cells, functions as a lipostat mechanism through modulation of satiety signals. The role of leptin in humans has been only partly revealed. However, obese patients have markedly elevated levels of this hormone, and in both normal-weight and obese subjects there is a direct correlation between serum leptin levels and the percentage of body fat. The aim of the present study was to investigate the role of leptin and its relation to body fat content in chronic renal failure (CRF), a disorder associated with decreased appetite. Serum leptin levels and body composition (dual-energy x-ray absorptiometry) were measured in a cohort of 59 patients with terminal CRF (creatinine clearance rate, 8 +/- 1 ml/min). Sixteen of the patients were re-evaluated after 12 mo of peritoneal dialysis treatment, and eight patients were re-evaluated after 12 mo of hemodialysis treatment. The mean serum leptin concentrations were markedly higher (mean +/- SEM) in patients with CRF than in healthy control subjects matched for gender and body mass index (25.7 +/- 5.2 ng/ml versus 8.4 +/- 0.9 ng/ml; P < 0.001). Patients with ongoing signs of inflammation (C-reactive protein > 10 mg/L) demonstrated higher serum leptin levels (41.9 +/- 13.7 ng/ml versus 18.6 +/- 4.2 ng/ml; P < 0.05) than patients with normal C-reactive protein. A strong positive correlation (rho = 0.83; P < 0.0001) was found between serum leptin concentrations and the percentage of body fat. After 12 mo of peritoneal dialysis, the amount of body fat increased markedly (19.0 +/- 1.5 to 25.1 +/- 2.2 kg; P < 0.001), and the changes in serum leptin concentrations correlated significantly (rho = 0.69; P < 0.01) to the changes in the body fat content. In contrast, no significant changes in either body fat content or serum leptin levels were recorded in the eight patients that were re-evaluated after 12 mo of hemodialysis. Serum leptin concentrations are approximately three times higher in patients with CRF compared with healthy control subjects with a similar body mass index. In this study, it is also demonstrated that serum leptin is a good marker for the body fat content in CRF patients and correlates strongly to changes in body fat during 12 mo of peritoneal dialysis. These findings suggest that serum leptin could serve as a valuable clinical marker for the body fat content in patients with CRF. Further studies are needed to verify the hypothesis that increased serum leptin concentrations may contribute to uremic anorexia.
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PMID:Serum immunoreactive leptin concentration and its relation to the body fat content in chronic renal failure. 929 34

The pathogenesis of protein wasting in chronic renal failure is multifactorial. Potential mediators of protein catabolism in chronic uremia include anorexia, low protein-energy intake, increased cortisol and parathyroid hormone secretion, insulin resistance, metabolic acidosis and unidentified uremic toxins. In non-acidotic uremic patients the rate of protein turnover (that is, synthesis and degradation) has often been found to be decreased. Malnutrition also decreases both protein synthesis and degradation. In contrast, during acidosis protein degradation is primarily accelerated and results in rapid loss of body proteins. Cytokine concentrations have often been found increased in both dialyzed and undialyzed chronically uremic patients. Our study determined the circulating levels of TNF-alpha and of type I (60 kDa) and type II (80 kDa) soluble TNF-alpha receptors in undialyzed uremic patients, and found that their plasma levels were greatly increased. Serum creatinine correlated with TNF-alpha soluble receptors but not with the TNF-alpha. Thus, TNF-alpha is potentially an important mediator of protein wasting in chronically uremic patients. Pharmacological therapy of protein catabolism in chronic uremia may include the administration of pentoxifylline, which has been shown to decrease protein degradation by interfering with the TNF-alpha system (that is, TNF-alpha and its soluble receptors) in experimental models. Growth hormone and insulin-like growth factor-1 administration may also be beneficial in these patients, but further evaluation of the hormone effects on glucose and glutamine metabolism is called for.
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PMID:Mechanisms of malnutrition in uremia. 935 Jun 78

Many factors are involved in inducing muscle wasting and derangements of protein metabolism in chronic renal failure. Anorexia, low protein intake, hormonal abnormalities (increased cortisol and parathyroid hormone secretion, and insulin resistance), acidosis, abnormalities of the cytokine system, and other unidentified uremic toxins create a negative nitrogen balance and stimulate protein catabolism. The protein turnover rate (i.e., synthesis and degradation) is generally decreased in non-acidotic uremic patients. However, in uncorrected acidosis, protein degradation is accelerated and a rapid loss of body proteins supervenes. Nutrition can be improved in chronically uremic patients through pharmacological therapy that can control protein catabolism. Administration of growth hormone and insulin-like growth factor-1 has been shown to be effective. These hormones influence both glucose and glutamine metabolism. Another approach is the administration of pentoxifylline, which may have an anticatabolic effect by interfering with the tumor necrosis factor-alpha system.
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PMID:Modulation of protein kinetics in chronic renal failure. 938 20


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