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)

End-stage renal disease (ESRD) patients, whether they are treated with hemodialysis or continuous ambulatory peritoneal dialysis, frequently suffer from protein-energy malnutrition, which is associated with increased morbidity and mortality. The protein requirements in dialysis patients are increased compared to those of healthy individuals and nondialyzed patients with chronic renal failure. The intake of protein and energy is frequently reduced because of the underlying disease, comorbidity, psychosocial factors, and uremic anorexia (underdialysis). There are several factors in ESRD patients that may enhance protein catabolism and increase protein requirements, such as low energy intake, amino acid abnormalities, metabolic acidosis, endocrine abnormalities (insulin resistance, hyperglucagonemia, hyperparathyroidism, insensitivity to growth hormone and insulin-like growth factor-1, cardiac failure, infection and inflammation, anemia, and physical inactivity. The dialytic procedures per se may enhance protein catabolism due to dialytic losses of protein and amino acids and, in hemodialysis, an inflammatory response to blood-dialyzer interaction. The relative importance of the various factors which cause anorexia and stimulate protein catabolism is still not well understood.
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PMID:Factors contributing to catabolism in end-stage renal disease patients. 939 22

Some genetic conditions, as cystinosis, familial hypophosphataemic rickets, type-I vitamin D-resistant rickets and renal tubular acidosis have an impact on growth and growth failure is one of the major problem in children with chronic renal failure (CRF). In early childhood, anorexia and malnutrition, electrolyte disturbances and metabolic acidosis are the main contributing factors for reduced growth, whereas renal osteodystrophy, anemia and hormonal disturbances are responsible for growth impairment later and during puberty. During infancy, loss of growth potential can be prevented by adequate nutrition. Later in life, catch-up growth cannot be induced by nutritional intervention or dialysis and renal transplantation allows catch-up growth in only a small percentage of patients. There is evidence for a state of resistance to growth hormone (GH) and insulin-like growth factor-I (IGF-I) in CRF. GH secretion is normal, but GH half-life is prolonged and the binding activity of the GH-binding protein is reduced, which points to a low receptor expression. IGF-I production may be diminished and the serum concentration of IGF-binding proteins (IGFBP-1 and 3) is increased. The imbalance between normal IGF-I and excessive IGFBP serum levels results in decreased IGF bioactivity that plays a pathogenic role in the growth failure. This insensitivity seems to be overcome by supraphysiological doses of recombinant human GH (rhGH). Many clinical studies have confirmed that rhGH increases growth velocity in children with CRF with and without dialysis and after renal transplant, without significant side-effects. The improvement of growth is more marked in prepubertal patients and during the first year of rhGH treatment. Long-term rhGH treatment in children with CRF improves the growth potential of children, achieving target adult height. The Authors discuss the recent studies employing rhGH in renal diseases and attempt to give some guide lines to rhGH treatment in these illnesses.
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PMID:[Growth and renal function]. 949 25

Loss of lean body mass is common in patients with acute or chronic renal failure but the mechanisms causing this loss are only beginning to be understood. One mechanism involves an inability of uremic patients to activate the critical metabolic responses that maintain protein balance when dietary protein is limited. Metabolic responses to dietary protein restriction include a sharp reduction in the degradation of essential amino acids and protein; changes in protein synthesis are less reliable. If uremia prevents suppression of essential amino acid or protein degradation when dietary protein is reduced by anorexia, negative nitrogen balance and loss of lean body mass will ensue. One complication of uremia, metabolic acidosis, stimulates the degradation of branched-chain amino acids and proteins and therefore blocks the ability of the patient to respond to a low-protein diet. The mechanisms require glucocorticoids and involve increased activity of branched-chain keto acid dehydrogenase and the ubiquitin-proteasome proteolytic pathway; there also is increased transcription of genes encoding components of enzymes involved in the pathways. Besides acidosis, a low insulin concentration and cytokines activate the ubiquitin-proteasome proteolytic pathway. Understanding how proteolysis is activated, including how these genes are stimulated, is important because the same pathways are activated in diabetes, cancer, sepsis, burns, starvation, and muscle denervation. Activation of the ubiquitin-proteasome pathway leads to reduced lean body mass.
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PMID:Robert H Herman Memorial Award in Clinical Nutrition Lecture, 1997. Mechanisms causing loss of lean body mass in kidney disease. 949 77

A 14-year-old Arabian gelding had weight loss and anorexia of 3 weeks' duration. Results of repeated laboratory tests revealed persistent hypercalcemia and serum phosphorus concentration that was within or less than the reference range. Parathyroid hormone concentration was high. Histologic examination of specimens obtained at necropsy revealed parathyroid adenoma. A diagnosis of primary hyperparathyroidism attributable to a functional parathyroid adenoma was made. Abnormalities in calcium and phosphorus concentrations were similar to those seen with primary hyperparathyroidism in dogs, in which this syndrome is best described. Primary hyperparathyroidism should be considered to be a potential cause of hypercalcemia in horses in which other more common causes of hypercalcemia, such as humoral hypercalcemia of malignancy, nutritional secondary hyperparathyroidism, chronic renal failure, vitamin D toxicosis, and bony or granulomatous disease, are ruled out.
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PMID:Primary hyperparathyroidism caused by a functional parathyroid adenoma in a horse. 963 93

The anorexia of chronic renal failure (CRF) is frequently managed with enteral feeds using combinations of commercial preparations, glucose polymers and fat emulsions. Such feeds might predispose to atherogenic blood lipid profiles. Our aim, therefore, was to compare the blood lipid profiles of enterally fed and non-enterally fed children. Plasma lipid subfractions were measured in 37 children with CRF managed conservatively and 10 managed with peritoneal dialysis (PD); 10 of the children were tube fed, 5 of whom were on PD. Results were compared between these groups. Overall, triglycerides (TGs, mean +/- SD) were high (2.3 +/- 1.4 mmol/l) and total cholesterol (TC) was at the upper limit of normal (5.2 +/- 1.5 mmol/l). Low-density lipoprotein (LDL), high-density lipoprotein (HDL), apoprotein A1 (apo A1), A2 (apo A2) and B (apo B), and lipoprotein (a) [Lp(a)] were within the normal range. There was an inverse correlation between TGs and glomerular filtration rate (P = 0.0001). There were no differences in the levels of TC, TG, LDL, HDL, apo A1, apo A2 or Lp(a) between tube-fed and non-tube-fed children. We conclude that enteral feeding does not enhance hyperlipidaemia.
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PMID:Effect of enteral feeding on lipid subfractions in children with chronic renal failure. 968 60

The low-protein diet (LPD) is used in patients with advanced chronic renal failure (CRF) to improve their symptoms and decrease the progression of CRF. LPD entails the risk for caloric malnutrition, which increases protein catabolism. Two groups were obtained from a total of 33 patients with CRF with LPD (0.6 g protein/kg/day): control group (group C), which went on with the same diet, and a group S, in which a portion of proteins and calories were provided through a low-protein and hypercaloric supplement (Suplena). During 6 months the protein intake and the evolution of the nutritional status and renal function were studied and compared between both groups. Additionally, tolerance and secondary effects of the supplement were studied in group S. Twenty-two patients (eleven in each group) completed the six month follow-up. At the end of the study, group S had the nutritional parameters better preserved, came closer to the low-protein diet objective, had a better compliance with therapy and had a less marked decrease in renal function--as measured by creatinine clearance--than group C. Tolerance to supplement was good in more than 70% of patients and secondary effects--nausea, vomiting and loss of appetite--occurred in 18% of patients at the end of the 6 months. We conclude that the use of this supplement in an LPD is usually well tolerated, enhances the compliance with the diet and can be of benefit for the mebacolic-nutritional status.
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PMID:[Treatment with low-protein diet and caloric supplements in patients with chronic kidney failure in predialysis. Comparative study]. 1111 1

There is abundant evidence that patients with chronic renal failure (CRF), including those treated by hemodialysis or peritoneal dialysis, have evidence of malnutrition with decreased body weight and subnormal values of serum proteins (suggesting a loss of visceral protein stores). Potential causes of an abnormal nutritional status that have been identified include an inadequate intake of protein or calories, an inability to activate the metabolic responses that are needed to achieve nitrogen and protein balance, or the presence of a disease that prevents activation of these metabolic responses or acts to stimulate the breakdown of body protein stores. Three critical metabolic responses to a limited protein intake have been identified: a reduction in the irreversible degradation of amino acids and the degradation of protein breakdown and an increase in protein synthesis in response to a meal. Metabolic acidosis blocks the first two responses and hence contributes to malnutrition in patients with chronic uremia. Other factors that could contribute to malnutrition include an inadequate intake because of anorexia or hormonal imbalances that impair protein turnover. In evaluating CRF patients with malnutrition, the first task is to ensure an adequate intake and to eliminate factors that impair the ability to achieve nitrogen balance.
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PMID:Factors causing malnutrition in patients with chronic uremia. 991 87

Malnutrition is frequently observed in patients with end-stage renal disease. Studies indicate that poor nutritional status plays a major role among factors adversely affecting patients outcome. Therefore prevention and treatment of malnutrition in renal patients is a major issue. In this article the potential mechanisms for alterations in muscle protein metabolism in uremia are explored. Malnutrition has been mainly attributed to inadequate intake of nutrients, superimposed illnesses, or both. However, both clinical and experimental evidence show that uremia per se may adversely affect the control of muscle protein and amino acid metabolism. Available evidence suggests that catabolic factors appear to be distinct for patients at different stages of chronic renal failure and require different modalities of treatments. Both nutritional requirements and the prevalence of malnutrition increase as end-stage renal disease progresses. Muscle protein degradation is increased by metabolic acidosis, which is often found in uremic patients. Another relevant, but less proven cause for increased protein degradation is insulin resistance. Furthermore, specific defects in muscle amino acid metabolism, resistance to growth hormone, insulin-like growth factor 1, or a very low protein intake can reduce muscle protein synthesis. Finally, the hemodialytic procedure per se can stimulate protein breakdown or reduce protein synthesis. All these factors may potentiate the effects of concurrent catabolic illnesses, anorexia, and physical inactivity often found in uremic patients.
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PMID:Muscle amino acid metabolism and the control of muscle protein turnover in patients with chronic renal failure. 999 May 80

Food intake is regulated by short-term satiety factors (gastric distension, amino acids, peptide hormones), as well as factors involved in long-term appetite regulation (leptin, insulin). Integration of the various signals takes place in the central nervous system (CNS). Appetite suppression in uremia is multifactorial and may include effects of uremia per se and of various comorbidity and psychosocial factors. Uremic anorexia is associated with elevated levels in plasma and CNS of short-term satiety factors (cholecystokinine, glucagon, serotonin, middle molecules) and factors that influence long-range regulation of appetite (leptin, insulin), but it is still unsettled to what extent these factors cause or contribute to appetite loss in uremic patients. Proinflammatory cytokines most probably also have a role in appetite suppression and malnutrition in patients with chronic renal failure.
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PMID:Mechanisms of uremic suppression of appetite. 1043 Oct 31

In this paper, the experience in the treatment of complications due to continuous ambulatory peritoneal dialysis for chronic renal failure with traditional Chinese medicine (TCM) is reported. Modified Renshen Yangrong Tang (Ginseng Nutrition Decoction) was used for anorexia and hypoproteinemia; modified Xiangsha Liujunzi Tang (Decoction of Cyperus and Amomum with Six Noble Ingredients) for abdominal pain and distension; modified Da Chaihu Tang (Major Bupleurum Decoction) for peritonitis; modified Shenling Baizhu San (Powder of Ginseng, Poria and Atractylodes) for diarrhea due to insufficiency of the spleen with abundance of dampness; Lizhong Tang (Decoction for Regulating the Function of Middle-jiao) and modified Sishen Wan (Pills of Four Miraculous Drugs) for insufficiency of both the spleen and the kidney; Siwu Tang (Decoction of Four Ingredients) added with other drugs for cutaneous pruritus, and Guishao Sijunzi Tang (Decoction of Four Noble Drugs added with Chinese Angelica Root and white Peony Root) for renal anemia. The therapeutic principles of invigorating the liver and kidney, strengthening the bones and muscles, and promoting blood circulation to eliminate blood stasis were adopted in the treatment of renal osteopathy, and the therapeutic principles of invigorating the liver and kidney, expelling phlegm and resolving dampness, and promoting blood circulation to eliminate blood stasis in the treatment of hyperlipemia. Shen Tekang capsules (capsules for improving the renal function) was administered to patients for strengthening the viability and improving the nutrition state, and the recipe for treating renal function failure (both formulated by the authors) for improving the renal function so as to decrease the frequency and duration of dialysis.
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PMID:Treatment of complications due to peritoneal dialysis for chronic renal failure with traditional Chinese medicine. 1045 76


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