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)

Serial prospective observations were made on 40 patients with end-stage renal failure who transferred voluntarily from long-term maintenance hemodialysis (MHD) to continuous ambulatory peritoneal dialysis (CAPD). Adequate data were available through 6 months on CAPD in 26 participants, whereas 20 completed the study (1 year on CAPD). There were 12 (30%) treatment failures, including two deaths. Standard CAPD (four 2-L exchanges per day) proved to be inadequate therapy in large, young males with low total urea clearances (Ktu) on MHD. There was a large variation in Ktu within MHD and CAPD therapies that employed apparently similar or identical dialysis prescriptions; this underscores the need to quantify dialysis by a measure such as Ktu. Hematocrit, white blood cell (WBC) and platelet counts, and serum bicarbonate levels were significantly higher, whereas blood urea nitrogen (BUN) and serum potassium levels were significantly lower on CAPD than on MHD. While body weight, blood pressure, bone disease, parathyroid hormone (PTH) levels, and lipid profile did not change significantly, nutritional indices tended to decline with time on CAPD. Urea generation rate (Gu) decreased significantly after transfer to CAPD and correlated with Ktu regardless of treatment modality. Central nervous system (CNS) function reflecting uremic symptomatology and as indexed by average quantified electroencephalogram (EEG) discriminant scores did not change significantly. Hospitalization rates and stays were similar during equal time intervals on both therapies. Sufficiently diverse responses followed the MHD to CAPD therapy change to warrant more extended observations on larger numbers of patients.
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PMID:Multicenter study of change in dialysis therapy-maintenance hemodialysis to continuous ambulatory peritoneal dialysis. 155 69

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.
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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)
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PMID:Pulse oral calcitriol for the treatment of hyperparathyroidism in patients on continuous ambulatory peritoneal dialysis: preliminary observations. 159 2

Recent advances in renal osteodystrophy deal with the pathogenesis of the disease, in particular in early renal failure, with the mechanisms of skeletal resistance to parathyroid hormone, with the potential role of iron, and with increased knowledge of adynamic bone disease. For the control of phosphatemia, aluminum-containing phosphate binders are more and more avoided, whereas calcium acetate or carbonate are more and more prescribed. X-linked hyphophosphatemia continue to cause great interest as well as the various iatrogenic osteomalacias.
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PMID:Renal osteodystrophy, disorders of vitamin D metabolism, and hypophosphatasia. 159 20

Calcitonin secretion is stimulated by acute hypercalcemia. Furthermore, in the rat, the calcemic response to parathyroid hormone (PTH) is decreased by calcitonin stimulation. However, in renal failure, it is not known if an increase in the serum calcium concentration within the physiologic range of serum calcium stimulates calcitonin and whether the increased calcitonin decreases the calcemic response to PTH. In the present study, four groups of pair-fed rats were evaluated: normals (N); parathyroidectomy (PTX); and two groups with renal failure (RF)--basal serum calcium less than 8.5 mg/dl (RFa) and basal serum calcium greater than 8.5 mg/dl (RFb). Hypocalcemia was induced by parathyroidectomy or in the RFa group, by a high phosphate diet. Increases in the serum calcium were produced by a 48 hour infusion of rat 1-34 PTH. In the RFa and PTX groups, stimulation of calcitonin was observed as the serum calcium increased from hypocalcemia to normal levels of calcium (P less than 0.01). In all four groups, increasing the serum calcium from normal levels to hypercalcemia increased the serum calcitonin level (P less than 0.05). The relationship between serum calcitonin and calcium was best expressed as a sigmoidal curve. In the two groups with basal hypocalcemia, PTX and RFa, the calcitonin-calcium curve was shifted to the left of the N and RFb groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sigmoidal relationship between calcitonin and calcium: studies in normal, parathyroidectomized, and azotemic rats. 174 20

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)
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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)
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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.
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PMID:Effects of recombinant human growth hormone in adults receiving maintenance hemodialysis. 177 93

Renal osteodystrophy is a metabolic bone disease resulted from chronic renal failure. The long-standing alterations in a mineral metabolism generated by renal failure have a profound effect on the skeleton and induce severe systemic metabolic bone disease. Iliac crest biopsies of 194 patients of chronic renal failure were taken and among them 10 cases were examined for Calcium(Ca), phosphorus (p), parathyroid hormone (PTH), 1,25(OH)2D3 and aluminium (Al). The histological bone changes are characterized by development of osteitis fibrosa, increase of bone resorption and the number of osteoclast, increase of osteoid volume (osteoblastic osteoid and acellular osteoid), active remodelling of bone and aluminum deposition in the bone. According to histological appearance, advanced renal bone disease could be subdivided into three groups namely: Secondary hyperparathyroid bone disease (high turnover uremic osteodystrophy), osteomalacia (low turnover uremic osteodystrophy) and mixed uremic osteodystrophy consisting of mild to moderate hyperparathyroid bone disease and defective mineralization. Aluminum-related bone changes might be obtained in various extent in all these groups. Although this classification does not fully represent all the separated entities, and there is also transformation from one form to another, it seems no less significant as a reference for clinical considerations.
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PMID:[Pathological analysis of renal osteodystrophy in 194 cases]. 181 63

Prevention of bone disease associated with impairment of the renal function is desirable. Attempts at such prevention inevitably also embrace prevention of the extraosseous consequences of autonomous hyperparathyroidism, such as the effects of hypercalcaemia, need for parathyroid surgery, and, perhaps, toxic effects of the parathyroid hormone. Strategies for prevention in early, moderate, and end-stage renal failure are reviewed and discussed with particular reference to dietary phosphorus restriction, use of gut phosphorus binders, control of acidosis, calcium supplementation, use of oral and intravenous calcitriol, and use of synthetic analogues of 1,25-dihydroxyvitamin D3. The onset of severe renal osteodystrophy can be delayed. Early attempts at prevention are logical, but we do not know whether these will reduce the need for parathyroid surgery or will make patients feel better or live longer. The costs of prophylaxis--both financial and in terms of incidence and severity of complications--remain to be defined. An individual approach to each patient with renal impairment seems at present appropriate.
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PMID:Prevention of renal osteodystrophy. 181 86


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