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)

We studied the effect of converting 100 established CAPD patients from aluminium- to calcium-based phosphate binders. After a follow-up of 1 year only 60% of patients remained on calcium carbonate. Hypercalcaemia was the major problem, with more than 40% of patients having a serum calcium in excess of 3.0 mmol/l. Several patients required hospitalization for symptomatic hypercalcaemia. Hypercalcaemia was more common in patients with normal serum parathyroid hormone concentrations (65 versus 25%, P less than 0.01). Serum phosphate control was better prior to commencing calcium carbonate when patients were treated with aluminium phosphate binders mean 1.71 +/- 0.15 mmol/l (SEM) than at the time of maximum serum calcium concentration, 1.81 +/- 0.25, P less than 0.05. This study does not confirm the findings of others, which have suggested that calcium carbonate is a safe and effective phosphate binder for patients with end-stage renal failure.
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PMID:Audit of the use of calcium carbonate as a phosphate binder in 100 patients treated with continuous ambulatory peritoneal dialysis. 838 46

Total and regional bone mineral densities (BMD) of ten male haemodialysis (HD) patients and ten male patients on continuous ambulatory peritoneal dialysis (CAPD) were measured using dual-energy X-ray absorptiometry (DEXA), and compared with that of age- and sex-matched controls. Our data showed that patients with renal failure on dialysis had reduced bone densities as manifested by a reduction in total body BMD, femoral neck BMD, and Ward's triangle BMD. In addition, head BMD and femoral trochanter BMD were also reduced in HD patients. Among HD patients, the length of the period of dialysis correlated with serum level of parathyroid hormone and the reductions in total body BMD and head BMD. Furthermore, there was a strong negative correlation between bone density of the skull and serum parathyroid hormone. Our results demonstrated regional variations in the reduction of bone density in patients with asymptomatic renal bone disease. DEXA bone scan is a useful adjunct in the early assessment of renal osteodystrophy and bone density of the skull can be used as a monitor in hyperparathyroid bone disease.
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PMID:Total and regional bone densities in dialysis patients. 132 17

Glucose-induced insulin secretion is impaired in chronic renal failure (CRF), and this abnormality is due to the elevation of cytosolic calcium [Ca2+]i and other derangements in pancreatic islet metabolism. Verapamil given to rats from day 1 of CRF prevented the rise in [Ca2+]i of islets and the impairment in insulin secretion. However, it is not known whether verapamil can reverse the abnormalities of islet function and metabolism in animals with preexisting renal failure. Such a documentation has important clinical implications for the treatment of carbohydrate intolerance in patients with CRF. The present study examined this question. After 6 weeks of CRF, rats were randomized into two subgroups and maintained for additional 6 weeks. One subgroup received intraperitoneal injections of verapamil (0.1 micrograms/kg body weight twice daily) and the other received vehicle only. At the time of randomization, there were no significant differences between the two subgroups in their body weight, plasma levels of calcium, phosphorus and creatinine, serum parathyroid hormone and creatinine clearance. Similarly, at the time of sacrifice (12 weeks), there were no significant differences in these parameters except for a modestly lower plasma level of creatinine and modestly higher creatinine clearance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Verapamil reverses glucose intolerance in preexisting chronic renal failure: studies on mechanisms. 132 12

We evaluated the degree of secondary hyperparathyroidism (SHPT) in the patients undergoing long-term hemodialysis treatment. Most patients showed improvement of SHPT by administration of the active vitamin D3 analogue. However, some patients developed overt SHPT even under intensive treatment. Pulse therapy with large dose of vitamin D3 for those who suffered from overt SHPT was an effective treatment modality at the initial stage, however, hypercalcemia which developed in the majority of the patients at the later stage of this treatment became an obstacle for the continuation of this treatment. Therefore, early detection of the hypersecretion state of parathyroid hormone (PTH) as well as earlier initiation of intensive therapy are important factors in preventing overt SHPT. Establishment of a suitable assay system for early detection of SHPT is an important task and the high sensitivity-PTH assay system may be the most desirable. Though diabetic patients were not likely to develop overt SHPT, this system could detect even the mild chronological increase of serum PTH level in diabetic patients. On the other hand, relatively earlier initiation of vitamin D3 therapy to the predialysis patients from the conservative treatment stage caused aggravation of deterioration of renal function. Therefore, we should be prudent to initiate vitamin D3 therapy on predialysis patients suffering from renal failure. Strict management of the patients by vitamin D3 as well as calcium supplement therapy along with evaluation of the serum PTH level is still an important measure to avoid overt SHPT.
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PMID:[Evaluation of secondary hyperparathyroidism in the patients undergoing hemodialysis--focused on parathyroid hormone assay system]. 133 62

Much interest is currently centered on the use of calcium acetate as a phosphorus binder in patients with renal failure. Therefore, this compound in subjects previously stable on calcium carbonate and undergoing high-efficiency hemodialysis with a dialysate calcium of 2.5 mEq/L was evaluated. Twenty subjects were switched from generic calcium carbonate to a single calcium carbonate preparation for a period of 2 months. This was followed by a phase (1 month) in which calcium acetate was substituted for calcium carbonate at a dose containing half the amount of elemental calcium. Subjects then continued calcium acetate for 6 months. It was found that calcium acetate allowed comparable control of immunoreactive parathyroid hormone, calcium, and phosphorus levels compared with calcium carbonate. This occurred with half the amount of elemental calcium ingested in the form of calcium acetate (349 +/- 25 versus 699 +/- 75 mmol/day; P less than 0.001). With this lower dose, the overall incidence of hypercalcemia was the same with each formulation. In the eight subjects concurrently receiving i.v. calcitriol, the incidence of hypercalcemia was significantly higher during the first month of calcium acetate compared with that in those not receiving this compound (P less than 0.05). Of those four subjects receiving the high dose of calcitriol (2 micrograms thrice weekly), all required either reduction in the dose or discontinuation of the drug. Thus, mineral metabolism could be controlled adequately with calcium acetate despite using half as much elemental calcium compared with calcium carbonate. This, however, did not result in a lower incidence of hypercalcemia, particularly in those receiving i.v. calcitriol.
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PMID:Calcium acetate as a phosphorus binder in hemodialysis patients. 139 13

Nephrocalcinosis is accepted to contribute to the progression of renal failure. We have reviewed evidence that nephrocalcinosis is caused directly by the excess parathyroid hormone produced in renal disease. Evidence that hyperparathyroidism in uremic patients results from calcitriol deficiency and the mechanisms by which this comes about have been discussed. We have shown that renal secondary hyperparathyroidism can be eliminated or substantially reduced without increasing blood calcium using a low-dosage regimen of calcitriol. Decreasing PTH concentrations to or near normal alleviates this hormone's toxicity to many organs, including the kidneys. Potential benefits for the uremic patient include an increase in the quality and length of life. Calcitriol treatment provides a powerful means to reduce PTH concentration in uremic patients that may not be achieved with other methods. Further prospective clinical studies of uremic dogs and cats are warranted to document preservation of renal function and histology during calcitriol treatments.
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PMID:Nephrocalcinosis caused by hyperparathyroidism in progression of renal failure: treatment with calcitriol. 141 Aug 53

Uremic hyperlipidemia was recently suggested to contribute to progression of chronic renal failure (CRF). To investigate the relationship between lipoprotein abnormalities and decline of renal function, plasma lipids with apoproteins A1, B, E, CII, CIII, CII/CIII and E/CIII ratios, parathyroid hormone (PTH), insulin and glucose levels were examined in 72 patients with different degrees of CRF and compared to 28 patients of a reference group. A significant decrease of CII/CIII ratio was already evident below a Ccr of 60 ml/min, while increased apo-CIII and triglycerides (TG) with reduced HDL-cholesterol (HDL-C) levels occurred below a Ccr of 30 ml/min. Both TG and apo-CIII showed a positive correlation with creatinine levels. On the contrary, apo-CII/apo-CIII and HDL-C inversely correlated with the progression of renal failure. PTH and insulin showed a positive correlation with TG, the former being also inversely related to apo-CII/apo-CIII ratio. Our results point to early apolipoprotein changes in the course of CRF. Elevated apo-CIII and reduced apo-CII/apo-CIII ratio may be considered the most typical features of uremic hyperlipidemia and likely account for the impaired TG removal and the hypertriglyceridemia (HTG). Secondary hyperparathyroidism may contribute to reduce peripheral lipolytic activity and cause HTG. A contributory role of hyperlipidemia in the progression of renal disease is also supported.
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PMID:Lipids and apolipoproteins change during the progression of chronic renal failure. 145 39

The effects of a very low-protein diet (VLPD) supplemented with amino acids and ketoanalogues (KA) and with 1 g of calcium carbonate and 1000 IU of vitamin D2, were studied in 17 patients with advanced renal failure (GFR < or = 20 ml/min) over a period of one year. The protein intake was 0.3 g protein/kg body wt/day. Daily phosphorus and calcium intake were respectively 1,500 mg and 300 mg. Sequential bone densitometry was performed and bone histomorphometry after double tetracycline labeling was evaluated, before and after one year of diet. Calcium and phosphate metabolism parameters were monitored every two months. In spite of a significant decrease of GFR, phosphorus, parathyroid hormone (1-84) and osteocalcin plasma levels decreased significantly, while low plasma bicarbonate normalized, and calcitriol and calcium levels remained respectively low and normal. Before the diet, histological study disclosed four cases of mixed osteopathy: osteomalacia associated with osteitis fibrosa (OM/OF), nine pure osteitis fibrosa (OF) and four with normal bone remodeling (NB). After one year of diet, the OM component of OM/OF disappeared, as evidenced by a normalization of the mineral apposition rate and osteoid thickness. In the patients presenting pure OF, a significant decrease in osteoblastic and osteoclastic surfaces, in the number of osteoclasts, and in the bone formation rate (BFR) were found. Vertebral mineral density measured by quantitative computerized tomodensitometry did not change significantly. In conclusion, this study not only confirms the beneficial effects of VLPD + KA + calcium on uremic hyperparathyroid bone disease in advanced renal failure assessed using static bone histomorphometry, but also shows a correction of histodynamic bone parameters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ketodiet, physiological calcium intake and native vitamin D improve renal osteodystrophy. 145 6

Secondary hyperparathyroidism occurs in the very early stages of renal failure. In the past, there has been considerable controversy concerning the signal triggering secondary hyperparathyroidism. Recently, it has become clear that secondary hyperparathyroidism is, at least to a major extent, the consequence of the deranged endocrine feedback between calcitriol, the secretory product of renal 1-alpha-hydroxylase, and parathyroid hormone. Another recent insight concerns disturbances of the secretion of hypophyseal hormones. These hormones, e.g. GH, gonadotropins and TSH, are secreted in a pulsatile fashion. For all three hormones, reversible abnormalities of secretory rhythmicity have been demonstrated in renal failure. Disturbed oscillatory patterns of hormone secretion provide a new dimension to our understanding of the genesis of endocrine disturbances.
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PMID:New insights into endocrine disturbances of chronic renal failure. 146 53

Parameters of calcium and phosphate metabolism were measured in 27 patients with mild renal failure [glomerular filtration rate (GFR) 40-90 ml/min], 12 patients with moderate renal failure (GFR 20-39 ml/min) and in 12 healthy subjects. GFR was determined by technetium-99m diethylenetriamine penta-acetic acid clearance. Intact parathyroid hormone (PTH) was measured by a sensitive immunochemiluminometric assay and somatomedin-C was determined by radioimmunoassay. Both 1,25-dihydroxyvitamin D [1,25(OH)2D] and vitamin-D-binding protein were measured allowing calculation of the free 1,25(OH)2D index. By linear regression and multivariate analysis, PTH was negatively and independently correlated with GFR, plasma bicarbonate and 25-hydroxyvitamin D [25(OH)D] while free 1,25(OH)2D was positively correlated with GFR. Increased PTH secretion and reductions in 1,25(OH)2D were present in mild renal failure patients before any changes in plasma calcium, phosphate and bicarbonate were noted. Plasma alkaline phosphatase was significantly higher in mild chronic renal failure patients compared to normal subjects, possibly indicating early effects of the secondary hyperparathyroidism on the skeleton. Somatomedin-C did not correlate with the free 1,25(OH)2D index or a measure of 1,25(OH)2D production. It is concluded that the secondary hyperparathyroidism which occurs very early in the onset of chronic renal failure may be due to a reduction in the circulating concentration of 1,25(OH)2D consequent upon the renal failure. Low plasma bicarbonate and 25(OH)D also appear to be determinants of a raised PTH concentration. The compensatory increase in PTH presumably maintains extracellular calcium and phosphate levels constant but with possible deleterious effects on the skeleton.
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PMID:Determinants of intact parathyroid hormone and free 1,25-dihydroxyvitamin D levels in mild and moderate renal failure. 150 39


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