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

Recombinant human erythropoietin (EPO) was administered to 12 children with terminal renal failure aged 8-17 years subjected to hemodialysis for a mean period of 16 (S.D. = 19.7) month prior to EPO utilisation. The hormone was administered thrice weekly at an intravenous dose of 25-75 u/kg until Hb value of 100 g/l was obtained, and subsequently at maintenance doses for mean period of 7 (S.D. = 4.0) month. The urea kinetic modeling (UKM) algorithms allowed to compute protein catabolic rate (pcr) for each patient in modeling sessions performed once a month. The analysis included the effect of EPO upon: 1. peripheral whole blood count; 2. individual UKM parameters; 3. selected lab data describing the metabolic status of the patient (predialysis potassium, phosphorus, creatinine, total blood protein and albumin--and iron levels), in three randomized groups according to the value of pcr. Group I presented pcr less than 1.0 g protein/kg/day typical for malnutrition; group II--pcr = 1.0-1.4 g protein/kg/day--with appropriate protein catabolism; group III--pcr greater than 1.4 g protein/kg/day--hypercatabolic. The results from 188 pre-EPO modeling sessions and 78 sessions in the course of EPO treatment were compared. All the three groups revealed statistically significant increased Hb, Ht and erythrocyte count after EPO administration, which also resulted an increase of protein catabolism what is manifested in a decrease in the number of sessions by 26.1% in Group I and a corresponding increase by 13.5% and 12.6% in Groups II and III, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Effect of recombinant human erythropoietin--rHu-EPO on the metabolism of children treated by long-term hemodialysis]. 145 8

A retrospective review of 25 patients who underwent orthotopic liver transplantation was performed to relate the prevalence and preferred sites of microscopic calcium deposition seen at autopsy to clinical parameters, namely, hypercalcemia, hypercalcemia, hyperphosphatemia, and renal failure. Microscopic foci of calcification were noted in 84% of patients, and hypercalcemia was noted in 68%. Multiple regression analysis demonstrated that the number of microscopically calcified organs depended in part on the peak total serum calcium level and the duration of hypercalcemia and that the peak total serum calcium level depended in part on the peak phosphorus level and the quantity of calcium administered intraoperatively. Univariate analysis showed that peak phosphorus level was partially dependent on the peak creatinine level. The data suggest that hypercalcemia and postoperative ectopic calcification are common and related occurrences following hepatic transplantation and that intraoperative manipulations of serum calcium levels and renal failure partially, but not entirely, account for this phenomenon.
 ...
PMID:Tissue calcification after orthotopic liver transplantation. An autopsy study. 152 56

Control of phosphorus accumulation in chronic renal insufficiency is crucial to the prevention of secondary hyperparathyroidism and metastatic calcification. In early renal failure, calcitriol levels are normal and parathyroid hormone levels are elevated. The phosphorus levels are maintained in the normal range by the phosphaturia induced by hyperparathyroidism. In this situation, dietary phosphorus restriction increases calcitriol levels and suppresses parathyroid hormone secretion. As renal failure progresses into late stages, hyperphosphatemia is evident along with low levels of calcitriol and worsening hyperparathyroidism. Phosphorus restriction will not affect calcitriol concentrations, yet parathyroid levels may decline. During long-term dialysis, urinary excretion of phosphorus is usually minimal. Therefore, phosphorus balance is determined primarily by the net amount absorbed by the bowel and the quantity removed during dialytic therapy. Given an adequate diet, no form of conventional dialysis is able to fully compensate for the gastrointestinal absorption of phosphorus. Hence, compounds that bind phosphorus in the bowel are often necessary. With the realization that the use of phosphorus binders containing aluminum leads to aluminum accumulation and its sequelae: osteomalacia, dementia, myopathy, and anemia, other phosphorus binders have been evaluated. Calcium carbonate has been investigated the most thoroughly and is in wide use. It is inexpensive and contains a high percent of elemental calcium. However, it is only modestly potent in the binding of phosphorus, and large doses are often necessary to attain satisfactory control of phosphorus. This may lead to hypercalcemia. One approach to this problem is to decrease the concentration of calcium in the dialysate. Alternatively, a more effective phosphorus binder may be used. Calcium acetate has been shown in acute studies to have twice the binding capacity of phosphorus per calcium absorbed than calcium carbonate. Whether use of this compound decreases the incidence of hypercalcemia is unproven. Calcium citrate increases the gastrointestinal absorption of aluminum and offers no advantage over calcium carbonate. Other compounds, such as calcium ketoacids and calcium alginate, have not been extensively studied and are not generally available. The use of phosphorus binders containing magnesium in conjunction with a dialysate low in magnesium may be efficacious. Large doses of magnesium will cause diarrhea and thus limit its use as a single agent. Reasons for failure to control hyperphosphatemia include poor compliance, improper prescription of binders, poor dissolution rates seen with some generic brands of calcium carbonate, and the presence of severe hyperparathyroidism. Optimal control of serum phosphorus in dialysis patients should always be viewed in the context of adequate nutrition and protein intake.
 ...
PMID:Hyperphosphatemia: its consequences and treatment in patients with chronic renal disease. 156 18

A direct effect of calcitriol on the regulation of the secretion of parathyroid hormone (PTH) has been shown in vitro and in vivo. In patients with renal failure on maintenance hemodialysis, it has been shown that intravenous (IV) administration of calcitriol appears to be superior to continuous oral administration. This may be due to the higher levels of calcitriol obtained in blood with consequent improved delivery of calcitriol to peripheral target tissues including the parathyroid glands. However, IV administration of calcitriol, is not practical for patients with end-stage renal disease (ESRD) who are maintained on continuous ambulatory peritoneal dialysis (CAPD). The present studies were designed to investigate whether intermittent administration of large doses of calcitriol orally ("pulse therapy") could mimic the effects of IV calcitriol in hemodialysis patients and achieve suppression of PTH secretion. Studies were performed in five patients who had been maintained on CAPD for more than 6 months. After basal determinations of calcium, phosphorus, and PTH, therapy was begun with calcitriol administered orally in a dose of 5 micrograms given twice per week. Calcium carbonate was continued as a phosphate binder. Dialysate calcium concentration was 1.75 mmol/L (3.5 mEq/L). With this therapy, PTH levels decreased rapidly, and, after 4 to 6 weeks of therapy, reached values 60% lower than pretreatment values. Mean values for serum calcium did not change significantly (2.29 +/- 0.12 mmol/L [9.6 +/- 0.5 mg/dL] before treatment compared with 2.32 +/- 0.08 mmol/L [9.7 +/- 0.25 mg/dL] after therapy). Mean serum phosphorus was also unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Pulse oral calcitriol for the treatment of hyperparathyroidism in patients on continuous ambulatory peritoneal dialysis: preliminary observations. 159 2

Hyperphosphatemia is an electrolyte abnormality that most frequently results from renal insufficiency and the attendant inability to excrete phosphorus (PO4) efficiently. A case is presented in which a young man with hemorrhagic shock developed severe hyperphosphatemia in the absence of renal failure. This is the first such case documented to the authors' knowledge. The prompt correction of the primary cause (ie, hypoperfusion and acidosis) resulted in a rapid return of PO4 levels to normal. This was probably related to the intracellular shift of PO4. Physicians should be aware of this electrolyte disturbance because it is not a well-recognized complication and because, in most cases, proper treatment of shock will also correct the elevated PO4.
 ...
PMID:Severe hyperphosphatemia associated with hemorrhagic shock. 161 21

We examined the effects of ileocystoplasty on renal function and bone mineral content in 160 juvenile male Wistar-Furth rats with and without renal insufficiency induced by 5/6 nephrectomy. At intervals up to 20 weeks blood, bone and kidney samples were obtained with the animals under anesthesia and then they were sacrificed. Serum parameters of renal function and calcium metabolism were measured. Samples of bone were analyzed for calcium, magnesium and phosphorus content. At 20 weeks after 5/6 nephrectomy renal function was decreased by approximately half. The decrease in renal function and the changes in renal histology were identical in animals with and without ileocystoplasty. Bone mineral content in the animals with renal insufficiency with or without ileocystoplasty was not different from sham operated animals or from animals with an ileocystoplasty and normal renal function. These studies demonstrate that ileocystoplasty per se does not hasten the progression to renal failure or produce bone demineralization in rats having moderate renal insufficiency.
 ...
PMID:The effects of ileocystoplasty on the development of renal failure in a rat model 5/6 nephrectomy. 164 May 23

Renal failure in itself generates a state of malnutrition, due to three main causes: inadequate ingestion (anorexia, vomiting or diet insufficiencies), the existence of catabolic factors (proteins, acidosis, PTH) and extrarenal depuration (which provokes a lack of amino acids and vitamins). Artificial nutrition constitutes a series of measures that can be adopted to act upon each of the above causes. Adequate ingestion compared to inadequate ingestion can be performed orally (especially in chronic renal failure) by parenteral administration (preferable in acute renal failure) and enteral administration (complementary in both cases). The quantity and quality of adequate nutrients is non-dependent on the method of administration; 500 ml, of water should be administered plus diuresis, plus loss from other tracts; the mineral intake of sodium, potassium and phosphorus should be restricted; in the case of vitamins, these should be administered, especially the B and D complexes; there should be sufficient calories to constitute a hypercaloric diet (from 30-50 kg/day), at least 50% in the form of carbohydrates (hypertonic glucose, if administered intravenously, and dextrinolmaltose or starch if administered through the digestive tract) and at least 40% in the form of lipids (preferably of vegetable origin, rich in non-saturated fatty acids); proteins are the mainstay of nutrition in renal failure; thus, with a normal renal function or in dialysis, a dose of 1 g/kg/day is recommended; in chronic renal failure, 0.5 g/kg/day; in cases of renal failure not on dialysis, 0.3 g/kg/day, supplemented by essential amino acids or cetoacids (the effectiveness of the latter is still in dispute).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Artificial nutrition in kidney failure]. 176 Apr 78

The calcemic response to parathyroid hormone (PTH) is decreased in renal failure. The reduction of hyperphosphatemia improves the calcemic response to PTH in animals with advanced renal failure. However, since low calcitriol levels in renal failure may also contribute to the decreased calcemic response to PTH, the improved calcemic response observed during the reduction of serum phosphorus may be partially mediated by an increase in serum calcitriol levels. The present study evaluated the calcemic response to PTH in rats with moderate and advanced renal failure and how this response was modified by a high and a low phosphorus diet. In addition, the effect of a change in dietary phosphorus on calcitriol levels was also evaluated. A 48-hour continuous infusion of 1-34 rat PTH increased the serum calcium level to 18.2 +/- 0.4 mg/dl in normal rats, versus 13.7 +/- 0.9 and 12.1 +/- 0.2 mg/dl in rats with moderate and advanced renal failure, respectively. During the PTH infusion, a high phosphorus diet increased the serum phosphorus and resulted in a reduced calcemic response to PTH at each level of renal function; respective serum calcium levels were 13.8 +/- 0.6 mg/dl in normals, 11.2 +/- 0.2 mg/dl in moderate renal failure and 9.6 +/- 0.5 mg/dl in advanced renal failure. In normal rats and in rats with moderate renal failure, dietary phosphorus restriction during the PTH infusion increased serum calcitriol levels. In rats with advanced renal failure, serum calcitriol levels were lower than in the other two groups and were not affected by changes in dietary phosphorus.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Calcemic response to parathyroid hormone in renal failure: role of phosphorus and its effect on calcitriol. 176 6

Hyperparathyroidism due to renal failure begins in the early stages of renal insufficiency and is in part secondary to skeletal resistance to the calcemic action of parathyroid hormone (PTH). Factors which have been reported to reduce the calcemic response to PTH include: decreased calcitriol levels, hyperphosphatemia and down regulation of PTH receptors in bone. While hyperphosphatemia may directly decrease the calcemic response to PTH, it may also act indirectly by a suppression of calcitriol synthesis. In this study, the effect of calcitriol on the calcemic response to PTH was evaluated in normal rats and in rats with moderate and advanced renal failure. To determine the combined effect of calcitriol and phosphorus on the calcemic response to PTH, rats receiving calcitriol were fed either a high (1.0%) or low (0.2%) phosphorus diet during a 48-hour PTH infusion. In advanced renal failure, calcitriol administration increased the calcemic response to PTH independent of the dietary phosphorus intake. During ingestion of a low phosphorus diet, a 48 hour PTH infusion resulted in a serum calcium level of 13.7 +/- 0.5 and 12.1 +/- 0.2 mg/dl (P less than 0.02) with and without calcitriol administration, respectively. In normal rats and in rats with moderate renal failure, calcitriol administration improved the calcemic response only during a high phosphorus intake. After a 48-hour PTH infusion in normal rats, the serum calcium levels with and without calcitriol were 16.1 +/- 0.9 and 14.8 +/- 0.6 mg/dl, P less than 0.01 respectively; in rats with moderate renal failure, calcitriol administration increased serum calcium, 13.2 +/- 0.5 versus 11.2 +/- 0.4 mg/dl, P less than 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Calcemic response to parathyroid hormone in renal failure: role of calcitriol and the effect of parathyroidectomy. 176 7

Administration of recombinant human growth hormone stimulates protein synthesis, decreases urea generation, and improves nitrogen balance in individuals with normal renal function. However, little information is available concerning the effects of growth hormone in patients with renal disease. This pilot study evaluated urea kinetics and clinical/metabolic responses to short-term growth hormone administration in five clinically stable adult patients requiring maintenance hemodialysis for end-stage renal failure. The dialysis prescription, medications, and oral calorie and protein intake of each patient remained constant during an initial control week and a subsequent 2-wk growth hormone treatment period. During treatment, growth hormone (5 or 10 mg) was administered s.c. immediately after each dialysis session. Protein and calorie intake, vital signs, body weight, and other clinical parameters remained stable throughout the 3-wk study. BUN values fell significantly (approximately 20 to 25%) during growth hormone administration compared with control week values. Similarly, urea kinetic modeling demonstrated a significant reduction in urea generation and the protein catabolic rate during each week of growth hormone treatment. Plasma insulin-like growth factor I levels rose significantly, and serum phosphorus and intact parathyroid hormone levels fell significantly during growth hormone administration. Serum glucose and other blood values remained stable. This preliminary study suggests that growth hormone administration reduces urea generation and improves the efficiency of dietary protein utilization in stable adult hemodialysis patients. Growth hormone may be a useful adjunctive therapy to diminish body protein catabolism in this patient population.
 ...
PMID:Effects of recombinant human growth hormone in adults receiving maintenance hemodialysis. 177 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>