Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Affected male (AM) Samoyed dogs with X-linked hereditary nephritis (HN) demonstrate splitting of all of their glomerular basement membranes (GBM) and rapidly develop renal failure within the first year of life, features reminiscent of those seen in male patients with X-linked HN. In contrast, carrier female (CF) dogs with X-linked HN show only isolated foci of splitting of GBM, and renal failure is never seen at such an early age. In the present study, we assessed whether a diet designed for dogs in renal failure could modify the changes seen in GBM of AM and CF dogs and improve the clinical outcome in the AM dogs. Beginning at 35 days of age, one group of dogs (unaffected, AM, and CF) was fed a regular diet, while a second group was fed a modified diet (i.e., restricted in protein, lipid, calcium, and phosphorus). AM dogs fed the modified diet showed less of a reduction in glomerular filtration rate than AM dogs fed the regular diet, indicative of a delay in the onset and a decrease in the severity of renal damage. Nevertheless, all of the AM dogs eventually died of renal failure regardless of diet. However, the onset and progression of renal failure were delayed and the severity of splitting of GBM was reduced in the AM dogs fed the modified diet; these dogs lived 53% longer than AM dogs fed the regular diet. CF dogs fed the modified diet also showed a reduced severity of splitting of GBM. In addition, when two CF dogs on the modified diet were switched to the regular diet, splitting of their GBM increased, indicating that continual administration of the modified diet was required to maintain the reduced rate of splitting. These studies indicate that dietary modification is beneficial in canine X-linked HN, and suggest that similar benefits (i.e., reduction in severity of splitting of GBM and delay in development of renal failure) might be observed in patients with HN who are treated with an appropriately modified diet.
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PMID:Dietary modification reduces splitting of glomerular basement membranes and delays death due to renal failure in canine X-linked hereditary nephritis. 207 66

Home parenteral nutrition has prevented malnutrition in patients who cannot maintain adequate nutrition by enteral feedings alone. The risk of bone and mineral abnormalities in these patients is significant for several reasons. Pre-existing skeletal disease can occur from factors known to affect the population at large as well as from malnutrition, malabsorption, and corticosteroid use related to the underlying disease process. Long-term use of infused nutrients and potential toxins can further alter bone turnover. Hypercalciuria is frequently present during HPN, yet its etiology is poorly defined. Parenteral nutrition admixture concentrations of calcium, phosphorus, protein, sodium, and dextrose may all play a role. Any development of acidosis can certainly aggravate hypercalciuria, which may be an indirect marker of abnormal bone turnover. Although increased protein intake can promote the development of acidosis-induced calciuresis, infused phosphorus and acetate can help reduce calcium excretion. Parenteral nutrition contamination by aluminum can cause a spectrum of osteomalacic bone disease similar to aluminum-associated changes seen in renal failure patients. Even with recent attempts to remove aluminum from the parenteral admixture, low-turnover bone disease can still occur. At present, HPN-related bone disease is a poorly understood entity because of its multifaceted nature. Patients receiving long-term parenteral nutrition should be considered to have an increased risk for the development of metabolic bone disease. Early monitoring for and treatment of bone disease should be considered in all patients receiving HPN.
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PMID:Long-term parenteral nutrition and metabolic bone disease. 211 69

A clinical trial, to evaluate the effects of a Chinese herbal drug, Rheum E and angiotensin converting enzyme inhibitor, Captopril on chronic renal failure (CRF), was conducted. Thirty cases with initial serum creatinine (Scr) levels of 344.8 +/- 114.0 mumol/L were allocated randomly to 3 groups: Rheum E treated group, Captopril treated group and Rheum E + Captopril group. A control group of 12 cases were on dietary therapy alone. During the 6-22 months of treatment, all the patients were kept on low-protein (0.6g/kg/d), and low-phosphorus (10mg/kg/d) diet. The results showed that the progression rate of renal failure, calculated by regression analysis of 1/Scr vs time, was found to be retarded after treatment with the increased regression coefficient (b value). Scr levels and blood urea nitrogen were kept stable or fell slightly. Albumin rose during the follow-up period (P less than 0.05) in the treated patients, being more marked in both Rheum E and Rheum E + Captopril groups. Uremic symptoms of nausea, anorexia improved in most of the treated patients. It is concluded that long-term low-dose Rheum E taken orally is beneficial to CRF. Its effect is better than that of Captopril. The regime of Rheum E and Captopril is a preferable choice in the long-term treatment for preventing progression of CRF.
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PMID:Clinical effects of rheum and captopril on preventing progression of chronic renal failure. 212 52

We evaluated the results of essential amino acids supplementation added to a protein restricted diet (0.6 g/kg/day) in patients with advanced renal failure (creatinine clearance under 20 ml/min). A diet containing food with high biologic value was used as control. Diets were tested during 7 months. Anthropometric and nutritional (serum albumin and transferrin) values were normal in both groups both at the beginning and at the end of the treatment period. A slight increase in weight in the natural diet group and in serum phosphorus level in the amino acid supplemented group was observed. Two patients in each group required chronic dialysis, renal function remaining stable in the rest. We conclude that both forms of diet supplementation were effective in preserving nutritional status possibly in delaying deterioration of renal function in patients with advanced renal failure.
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PMID:[Treatment of chronic renal failure: effects of a supplemented diet with essential amino acids]. 213 4

Horses suffering from trauma, sepsis, and severe burns need 12% to 16% of protein (dry matter basis) in their diet. Since reduced appetite may be a problem, relatively energy dense (greater than 2 Mcal DE/kg) feeds should be offered. In hepatic failure, maintenance protein requirements (8% on a dry matter basis for adult horses) should be met with feeds that are high in short branched-chain amino acids and arginine but low in aromatic amino acids and tryptophan (for example, milo, corn, soybean, or linseed meal) in addition to grass hay. Vitamins A, C, and E should also be supplemented. In cases with renal failure, protein, calcium, and phosphorus should be restricted to maintenance or lower levels. Grass hay and corn are the best feeds for horses with reduced renal function. Do not offer free-choice salt to horses with dependent edema from uncompensated chronic heart failure. Following gastrointestinal resection, legume hay and grain mixtures are the feeds of choice. Horses with diarrhea should not be deprived or oral or enteral alimentation for prolonged periods of time. Liquid formulas may be used if bulk or gastrointestinal motility are a problem. Apple cider vinegar and a high grain diet may reduce the incidence of enteroliths in horses prone to this problem. Pelleted feeds will reduce fecal volume and produce softer feces for horses that have had rectovaginal lacerations or surgery. Horses with small intestinal dysfunction or resection should be offered low residue diets initially, but long-term maintenance requires diets that promote large intestinal digestion (alfalfa hay, vegetable oil, restricted grain). Geriatric horses (greater than 20 years old need diets similar to those recommended for horses 6 to 18 months old.
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PMID:Clinical nutrition of adult horses. 220 96

Three infants with irreversible renal failure and treated with continuous ambulatory peritoneal dialysis (CAPD) developed hypophosphatemia. In one of them rachitic lesions were observed on X-ray and bone biopsy showed osteomalacic osteodystrophy. Different mechanisms may have been at the origin of the hypophosphatemia: high doses of phosphate binders, low phosphorus intake, phosphate loss with the dialysate and possibly nutritional repletion. Dietary phosphorus restriction and use of phosphate binders should be applied with caution and serum phosphate should be monitored regularly in infants treated with CAPD.
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PMID:Hypophosphatemia in infants on continuous ambulatory peritoneal dialysis. 222 64

Certain data support the notion that chronic exposure to excess parathyroid hormone (PTH) is associated with decreased motor nerve conduction velocity, while other studies failed to confirm such an effect. Also, chronic renal failure of 4 months duration in dogs did not elicit changes in MNCV or calcium content of nerve. These discrepancies may be due to differences in other metabolic parameters, such as degree of uremia, serum levels of calcium, phosphorus, or magnesium, and acid-base parameters, or in duration of chronic renal failure. To examine the effect of PTH on peripheral nerve function in renal failure in a more defined biochemical setting, we studied the changes in MNCV and nerve calcium content in dogs with and without excess PTH and with prolonged and similar duration of chronic renal failure (57 +/- 1.7 weeks) and comparable biochemical parameters. Dogs with chronic renal failure displayed a significant (P less than 0.01) decrease in MNCV (before renal failure, 65 +/- 1.5 m/sec; after renal failure, 49 +/- 3.5 m/sec) and marked elevation in calcium content of peripheral nerve (444 +/- 45 mg/kg dry wt). These derangements were not observed in parathyroidectomized chronic renal failure animals; MNCV before renal failure was 66 +/- 1.5 m/sec and after renal failure was 65 +/- 1.5 m/sec, and nerve calcium content after renal failure was 229 +/- 3 mg/kg dry wt. Also, parathyroidectomy of three dogs with preexisting chronic renal failure of 52 weeks was associated with reversal of the abnormalities in MNCV and calcium content of nerve despite an additional period of renal failure of 52 weeks in two of the dogs and 40 weeks in the third. Our data are consistent with the proposition that excess PTH plays a major role in the genesis of peripheral nerve dysfunction in chronic renal failure. This adverse effect of the hormone is most likely mediated by the PTH-induced accumulation of calcium in peripheral nerve.
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PMID:Role of parathyroid hormone in the decreased motor nerve conduction velocity of chronic renal failure. 223 3

Little notice has been paid in the surgical literature to problems with psychoeffective lithium, which by interfering with adenylate cyclase affects thyroid and parathyroid function, causing hypercalcemia, hyperparathyroidism, and hypothyroidism. Seven patients with lithiumogenic hyperparathyroidism occurring after years of lithium therapy underwent treatment and manifested osteoporosis (n = 2), hypertension (n = 2), nephrolithiasis (n = 1), coma (n = 1), rising hypercalcemia (n = 1), goitrous myxedema (n = 4), nephrogenic diabetes insipidus (n = 2), renal failure (n = 2), and hyperlipidemia (n = 1). Disease-directed parathyroidectomy (without morbidity) was curative. Unique laboratory findings included normal serum phosphorus and reduced urinary calcium and cyclic adenosine monophosphate values. Three separate cases of thyroid carcinoma after long-term lithium therapy were also treated, being preceded by myxedema (n = 2) and concurrent with hyperparathyroidism (n = 1). There has been only one previous report of lithium-associated thyroid carcinoma. All patients taking lithium should undergo surveillance for thyroid and parathyroid dysfunction and neoplasia, and appropriate surgical and medical treatment should be considered in each situation. Although hyperparathyroidism may be reversible with lithium discontinuance, such therapy may be obligatory for patient well-being, thus dictating parathyroidectomy.
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PMID:Lithiumogenic disorders of the thyroid and parathyroid glands as surgical disease. 224 24

In six patients with terminal renal failure the effectiveness was assessed of intermittent peritoneal dialyses (IPD) using the dialysing fluid of modernised composition. On the basis of the obtained results the values were calculated of the total sodium (TMTNa) and potassium (TMTK) elimination glomerular filtration rate, and the sodium elimination index. The values were calculated of the dialysing clearance of urea, creatinine, potassium, and inorganic phosphorus. The correlations were analysed between the dialysing clearance of studied substances and the body area of patients, the duration of dialysis, and glomerular filtration rate. The results were compared with the effectiveness of peritoneal dialysis carried out with the dialysing fluids of formerly used electrolyte composition.
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PMID:[Effectiveness of peritoneal dialysis using dialysis fluid of modernized composition]. 226 Mar 11

Disorders of phosphorus, calcium, and vitamin D are common in patients with renal failure. Medical management, including dietary phosphorus restriction, administration of phosphate binding agents, and calcium and vitamin D sterol supplementation, must be instituted to control serum concentrations of these substances because of the loss of normal homeostatic mechanisms. If these measures are not employed, soft tissue calcification and hyperparathyroidism may result. We report the case of a 22-year-old woman with endstage renal disease treated with continuous ambulatory peritoneal dialysis who developed secondary hyperparathyroidism and tumorous calcinosis as a result of noncompliance with dietary phosphorus restriction and phosphate-binding agent therapy. The etiology and treatment of soft tissue calcification in patients with renal disease are discussed. Compliance with dietary restrictions and phosphate binding agents is frequently problematic in this population. Pharmacists should play an active role in educating patients with renal disease on the consequences of noncompliance with dietary and drug therapy.
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PMID:Soft tissue calcification in renal failure. 226 Mar 46


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