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)

From June 1986 to October 1989, ten children suffering from end stage renal disease (ESRD) were treated with continuous ambulatory peritoneal dialysis (CAPD). Their ages ranged from 4 to 16 years; 3 were boys and 7 were girls. IgM mesangial nephropathy (IgMN) (three cases) were the most common causes of renal failure in the patients. All patients were trained in the hospital. After CAPD treatment, serum BUN and creatinine dropped significantly. Serum levels of potassium, phosphorus, and alkaline phosphatase dropped and serum sodium and calcium rose significantly after treatment. Improvement of anemic state and control of hypertension were also noted. Hypercholesterolemia and hypertriglyceridemia developed after CAPD treatment. Despite protein loss through the peritoneal cavity, there was no evidence of protein malnutrition. Total serum protein and albumin increased significantly after treatment. The most common complication was peritonitis. Three of these 10 patients developed an episode of peritonitis, or an incidence of 1 episode per 17.2 patient months. To the present, seven patients are still doing well on CAPD. Three patients have received renal transplantation. The majority of the patients experienced an increased sense of well-being, easier diet and fluid management, freedom for travel and daily activities. Physical development also improved, with body length and body weight gaining steadily. It can be concluded that CAPD is a good modality of long-term therapy for ESRD children.
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PMID:Continuous ambulatory peritoneal dialysis for children with end stage renal disease. 226 Apr 64

Soft tissue calcification is a recognized complication of uremia in adult patients and has been implicated as a cause of ischemic necrosis, cardiac arrhythmias, and respiratory failure. However, soft tissue calcification has been regarded as rare in pediatric renal patients. Following a sudden death due to pulmonary calcinosis in an adolescent after renal transplantation, we retrospectively reviewed clinical, biochemical and autopsy data of 120 patients with uremia, on dialysis, or following renal transplantation cared for at Childrens Hospital of Los Angeles from 1960 to 1983. Soft tissue calcification was found in 72 of 120 patients (60 percent). Forty-three patients (36 percent) had systemic calcinosis (Group A): the most frequent sites of mineral deposition were blood vessels, lung, kidney, myocardium, coronary artery, central nervous system, and gastric mucosa. Vascular calcification was uniformly accompanied by deposits in other organs. Twenty-nine patients had small amounts of focal calcification (Group B) and 48 patients had no soft tissue calcification (Group C). By multiple logistic regression analysis, the use of vitamin D or its analogues, the form of vitamin D medication prescribed, the peak calcium x phosphorus product, the age at onset of renal failure, and male sex were jointly associated with calcinosis (Group A). Vitamin D therapy showed the strongest independent association with calcinosis and the probability of calcinosis was greater in patients receiving calcitriol when compared with dihydrotachysterol and vitamin D2 or D3. The duration of renal failure, peak serum calcium, serum calcium at death, serum phosphorus at death, and primary renal diagnosis, were not statistically associated with calcinosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Soft tissue calcification in pediatric patients with end-stage renal disease. 226 78

Metabolic clearance rate (MCR) and production rate (PR) of calcitriol is decreased in experimental renal failure. In this experiment, we studied uremia and secondary hyperparathyroidism as possible causes of the abnormal calcitriol metabolism. Normal rats were made uremic by infusing phosphorus-free urine for 24 hours. Both the MCR (0.22 +/- 0.01 ml/min/kg, N = 6 P less than 0.001) and the PR (16.6 +/- 1.97 ng/kg/day, P less than 0.01) of calcitriol were significantly suppressed in normal rats following urine infusion when compared to saline infused rats (MCR, 0.30 +/- 0.01; PR, 32.9 +/- 4.1, N = 6). Different levels of protein intake by rats with renal failure produced by subtotal nephrectomy also alter the PR but not the MCR of calcitriol. Thus, the synthesis of calcitriol was significantly lower in rats with renal failure fed a high protein (50% protein) diet (17.6 +/- 0.7 ng/kg/day, N = 8, P less than 0.001) than in rats with renal failure fed a normal protein (20% protein) diet (22.2 +/- 1.4, N = 7). Thyroparathyroidectomy (TPTX) did not alter the MCR of calcitriol in renal failure, even though parathyroid hormone, which may suppress the degradation enzyme, could be elevated in this model of renal failure. The MCR of TPTXed rats with renal failure (0.15 +/- 0.01 ml/min/kg, N = 7) remained lower than that of the TPTXed control rats (0.19 +/- 0.01, N = 7, P less than 0.001), and chronic infusion of PTH to TPTXed rats with renal failure did not change the MCR of calcitriol (0.15 +/- 0.01, vs. control, 0.24 +/- 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Factors influencing calcitriol metabolism in renal failure. 229 8

Phosphorus is a well-known modulator of renal 1 alpha-hydroxylase activity. In early and moderate renal failure it is proposed that dietary Pi reduction ameliorates secondary hyperparathyroidism through increased circulating levels of calcitriol (i.e, 1 alpha, 25-dihydroxycholecalciferol). To gain further insight into the mechanisms by which a low-Pi diet ameliorates secondary hyperparathyroidism in advanced renal insufficiency, studies were performed in five dogs before and 6 mo after the induction of uremia by 5/6 nephrectomy. Glomerular filtration rate decreased from 69.0 +/- 2.3 to 10.5 +/- 0.5 ml/min, immunoreactive parathyroid hormone (irPTH) increased from 66.0 +/- 8.8 to 321.0 +/- 46 pg/ml, and calcitriol decreased from 39.0 +/- 10.4 to 27.0 +/- 6.2 pg/ml. Thereafter, dietary Pi was decreased gradually every 2 wk from 0.95% to 0.6, 0.45, and 0.3%, respectively. Dietary Ca was reduced from 1.6 to 0.6% to prevent development of hypercalcemia. Ionized Ca (ICa) decreased from 5.4 +/- 0.04 to 5.2 +/- 0.05 mg/dl (P less than 0.02), and plasma Pi decreased from 6.3 +/- 0.7 to 4.7 +/- 0.2 mg/dl (P less than 0.05). Calcitriol remained low (23.3 +/- 4.7 pg/ml). However, irPTH gradually decreased from 321.0 +/- 46.0 to 94.7 +/- 22.9 pg/ml (P less than 0.005). These studies indicate that a decrease in dietary Pi from 0.95 to 0.3% suppressed irPTH by approximately 70%. Reduction of irPTH was observed in the absence of a concomitant increase in levels of ICa or calcitriol. These studies suggest that reduction in dietary Pi in advanced renal insufficiency improves secondary hyperparathyroidism by a mechanism that is independent of the levels of calcitriol or plasma ICa.
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PMID:Phosphorus restriction reverses hyperparathyroidism in uremia independent of changes in calcium and calcitriol. 239 69

Hyperphosphatemia and secondary hyperparathyroidism are regular complications in patients suffering from end-stage renal failure. Aluminum-containing drugs are widely used to control serum phosphate, but this therapy carries the well-known risk of aluminum toxicity. Previously we demonstrated that a mixture of ketoacids is very effective in lowering increased serum phosphate and serum PTH levels. Recent studies to clarify the underlying mechanisms whereby these compounds lower serum phosphate revealed that ketoacids act as intestinal phosphate binders. In balance studies we demonstrated that intestinal phosphorus uptake decreased in normal subjects (decrease of absorption during ingestion: 0.7-3.14 mmol/day). Additional in vitro studies not only confirmed the in vivo results but also showed that ketoacids are as efficient as calcium carbonate although they provide less calcium. It is of further interest that ketoacids reached their greatest binding efficiency when the pH is 7.0, whereas calcium carbonate binds phosphate predominantly when the pH is 2.0 or 5.0. Ketoacids represent a further therapy to lower serum phosphate in uremia. As they provide less calcium than calcium carbonate, they could be considered as an advantageous, less dangerous alternative.
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PMID:Calcium salts of ketoacids as a new treatment strategy for uremic hyperphosphatemia. 263 49

Animals with renal failure have a number of fairly predictable metabolic abnormalities. They are commonly presented to the veterinarian in a state of negative water balance, although prior fluid therapy in an oliguric patient may result in overhydration. Animals with oliguric ARF have sodium retention; those with polyuric ARF have increased urinary sodium loss. Chronic renal failure does not necessarily affect the ability of the renal tubule to conserve or excrete sodium, although the response to changes in sodium load is much slower than in the normal animal. Potassium retention occurs in oliguric ARF and potassium wasting in polyuric ARF; potassium balance is approximately normal in animals with CRF. Both ARF and CRF cause metabolic acidosis, although the acid-base status in a given animal will be affected by respiratory compensation, as well as other problems such as vomiting. Calcium levels are usually normal to slightly decreased in renal failure, whereas phosphorus levels are generally increased. The basic principles of fluid therapy should be used when constructing a plan for such therapy in an animal with renal failure. Intravenous administration of fluids is almost always necessary. The choice of the type of fluid, solutes, and electrolytes to be administered is based on the predicted abnormalities associated with renal failure as well as the laboratory abnormalities in the animal. Careful monitoring of the patient and periodic assessment of various laboratory parameters are necessary in order to make appropriate adjustments in fluid therapy.
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PMID:Fluid therapy for acute and chronic renal failure. 264 69

This study represents the first randomized prospective, double-blind, placebo-controlled trial of the efficacy of 1,25(OH)2D3 on bone histology and serum biochemistry in patients with mild to moderate renal failure. Sixteen patients with chronic renal impairment (creatinine clearance 20 to 59 ml per min) received either 1,25(OH)2D3, at a dose of 0.25 to 0.5 microgram daily (eight patients), or placebo. Transiliac crest bone biopsies were performed before entrance into the study and after 12 months of experimental observation. None of the patients were symptomatic or had radiological evidence of bone disease. Of the thirteen patients who completed the study, initial serum 1,25(OH)2D levels were low in seven patients and parathyroid hormone levels were elevated in seven patients. Bone histology was abnormal in all patients. 1,25(OH)2D3 treatment was associated with a significant fall in serum phosphorus and alkaline phosphatase concentrations as well as with histological evidence of an amelioration of hyperparathyroid changes. In contrast to previous reports, no deterioration of renal function attributable to the treatment occurred, perhaps because a modest dose of 1,25(OH)2D3 was employed combined with meticulous monitoring. Further investigation is required to determine whether alternative therapeutic strategies (smaller doses or intermittent therapy) may avoid the potential for suppressing bone turnover to abnormally low levels in the long term.
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PMID:1,25(OH)2D3 administration in moderate renal failure: a prospective double-blind trial. 265 58

Nutritional therapy is the mainstay of management of chronic renal failure in dogs and cats. Diets designed for use in renal failure are typically reduced in protein, phosphorus, and sodium content. These and other dietary modifications are designed to prevent or ameliorate clinical signs of uremia, minimize disturbances associated with excesses or losses of electrolytes and minerals, arrest or retard progression of renal failure, and maintain adequate nutrition.
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PMID:Dietary management of canine and feline chronic renal failure. 265 90

Phosphorus-31 (31P) magnetic resonance spectroscopy of the kidneys promises to provide metabolic information leading to better assessment of renal physiology. However, the problems of studying the metabolism of the heterogeneous renal architecture by precisely localizing the origin of the signal obtained from small voxels and eliminating motion artifacts have not been solved as yet. The normal 31P MRS spectra show a characteristic fingerprint of six peaks including phosphomonoesters, phosphodiesters, inorganic phosphorus, and gamma, alpha, beta adenosine triphosphate (ATP). Renal failure, regardless of its etiology and mechanism of inducement (hypoxia, ischemia, acidosis, or obstruction) produces a loss of ATP with a progressive increase of inorganic phosphorus and a decline in intracellular pH. The severity of renal failure correlates with the severity of the metabolic disturbance. The potential use of 31P MRS in the assessment of renal viability has been applied to the study of renal preservation methods and prediction of renal function following transplantation.
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PMID:Phosphorus-31 MRS of the kidney. 269 45

Phosphorus binders are given to patients with renal failure to increase gastrointestinal excretion of phosphorus. To determine the relative importance of the binding of dietary as compared with endogenous phosphorus and to determine the optimal dose schedule, we gave either 4.4 g of calcium acetate (25 mmol of calcium) or a placebo to six normal subjects on each of seven different schedules in a randomized sequence. The net gastrointestinal balance of phosphorus and calcium was determined by a one-day lavage technique. After a meal containing approximately 12 mmol of phosphorus, the mean phosphorus absorption (+/- SE) measured 9.17 +/- 0.36 mmol (78 percent) with placebo but decreased to 3.81 +/- 0.58 mmol (31 percent) when calcium acetate was given immediately before the meal (representing binding of 5.36 +/- 0.77 mmol of phosphorus). Similar binding was observed when calcium acetate was given immediately after the meal and when half the dose was given before and half after the meal. In contrast, when calcium acetate was given two hours after the meal or while the subject was fasting, phosphorus binding was reduced to 2.00 +/- 0.52 mmol and 1.81 +/- 0.84 mmol, respectively. Calcium absorption from calcium acetate averaged 21 +/- 1 percent when the binder was given with a meal; absorption from calcium acetate averaged 40 +/- 4 percent when the binder was given while the subject was fasting. We conclude that calcium acetate increases fecal excretion of phosphorus by binding both dietary and endogenous phosphorus, but the binding of dietary phosphorus is quantitatively much more important. For the most efficient phosphorus binding, calcium (and presumably other phosphorus-binding cations) should be given with meals.
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PMID:Effect of the time of administration of calcium acetate on phosphorus binding. 260 75


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