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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperparathyroid bone disease is a common complication of end stage renal failure, particularly in patients on maintenance haemodialysis. Several studies have, however, shown a near absence of hyperparathyroid bone disease in diabetic patients who have been receiving haemodialysis for periods of up to 4 years. We have studied biochemical indices of mineral metabolism in 54 consecutive pre-dialysis patients with moderate to severe renal impairment. Deteriorating renal function was associated with developing hypocalcaemia and hyperphosphataemia. Hypocalcaemia was strongly related to increased severe alkaline phosphatase activity (p less than 0.001), suggesting the development of hyperparathyroidism. Five patients with hypocalcaemia and increased alkaline phosphatase were studied in detail. All had elevated serum concentrations of parathyroid hormone and histological signs of hyperparathyroidism on bone biopsy. Three of the patients had low serum 25 hydroxyvitamin D levels with associated osteomalacia, the other 2 patients were notable for their long duration of renal failure. In the long-term (greater than 4 years) we also observed the development of hyperparathyroidism in a small group of diabetic patients maintained on haemodialysis. We conclude that diabetic patients are not uniquely protected against renal osteodystrophy. Although the prevalence of hyperparathyroidism may be lower in diabetic patients than in those with other types of renal disease, the same factors which predispose to bone disease in non-diabetic patients (long duration of renal failure, low serum 25 hydroxyvitamin D and long periods on haemodialysis) also operate in the diabetic population.
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PMID:Hyperparathyroid bone disease in diabetic renal failure. 213 93

Renal excretion is the major route of magnesium elimination from the body and a positive magnesium balance would be expected under conditions of renal insufficiency. However, a compensatory decrease in tubular reabsorption is operating to maintain an adequate urinary magnesium excretion even when glomerular filtration rates are very low. Nevertheless, in end-stage renal disease, the limited ability of the kidney to excrete an increased magnesium load may result in toxic concentrations of the ion in serum. While magnesium intoxication is a real hazard when magnesium-containing drugs are given, magnesium balance may be normal or even decreased in uraemic patients. This is usually due to decreased dietary intake combined with the impaired intestinal magnesium absorption which characterizes chronic renal failure. Impairment of magnesium absorption seems to be related to deficient synthesis of the active metabolite of vitamin D by the non-functioning kidney. Following the institution of chronic haemodialysis or continuous ambulatory peritoneal dialysis (CAPD) treatment, the major determinant of magnesium balance is the concentration of magnesium in the dialysate. Changes in the dialysate magnesium have been used to reduce the incidence of renal osteodystrophy, to alleviate uraemic pruritus, or to retard the development of arterial calcification in chronic renal disease. However, uncertainty about magnesium, calcium and parathyroid hormone relationships in renal failure makes a reasoned approach to such manipulations extremely difficult.
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PMID:Magnesium metabolism in chronic renal failure. 213 26

Until recently, the measurement of circulating parathyroid hormone (PTH) has been unsatisfactory due to poor analytical performance of immunological assays and due to interference in such assays by circulating biologically inactive fragments of PTH. The development of a two-site immunometric assay with the use of acridinium ester as label has solved these problems. This immunochemiluminometric assay (ICMA) measures the intact molecule and is capable of detecting PTH levels in normal subjects as well as suppression of PTH after oral administration of calcium. The ICMA PTH assay has been shown to be adequate in the diagnosis of primary hyperparathyroidism and it could prove useful in monitoring renal failure patients and investigating other bone diseases such as osteoporosis.
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PMID:The measurement of circulating parathyroid hormone. 218 52

Uremic myopathy seems unfrequently studied although it can be really inconvenient in daily activities for some patients. Its is a proximal and non specific myopathy that should be discriminated from uremic neuropathy. Several disturbances from renal insufficiency have been incriminated but they only play an adjuvant role in regard with renal osteodystrophy. Indeed the presence of myopathy in cases of severe osteodystrophy and its close similarity with myopathies accompanying the different forms of osteomalacia and/or hyperparathyroidism without renal failure suggest that the most important pathogenic factors come from calcium metabolic disorders: excessive parathyroid hormone, vitamin D deficiency, and/or impaired calcium transport. The treatment is subject to the predominant bone lesions: secondary hyperparathyroidism or osteomalacia; but the best attitude remains their prevention.
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PMID:[Myopathy in uremic patients]. 218 33

Renal osteodystrophy is a complex disorder which can be divided into five distinct bone histologic subtypes: mild bone disease, hyperparathyroid bone disease, mixed bone disease, osteomalacia, and low-turnover bone disease. Hyperparathyroidism develops in renal failure due to two principal abnormalities: 1,25(OH)2D3 deficiency and hyperphosphatemia. Treatment of these problems is important in order to prevent hyperparathyroidism. Most cases of osteomalacia, mixed bone disease, and low-turnover bone disease are influenced by aluminum status and parathyroid hormone. Aluminum-associated bone disease can be treated with termination of aluminum exposure and/or deferoxamine therapy. Numerous diagnostic pitfalls exist in the evaluation of renal osteodystrophy, and the bone biopsy is extremely important to avoid these problems and plan proper therapy.
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PMID:Renal osteodystrophy. 219 69

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

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

To clarify the mechanisms of hypocalcemia with renal insufficiency and to gain more insight into the mechanisms of secondary hyperparathyroidism in these patients, an 85-day study was conducted to examine the effect of dietary phosphate restriction on divalent ion metabolism in patients with early renal insufficiency. The study was conducted on four male patients with stable mild renal insufficiency who had creatinine clearances of 55 to 60 mL/min. Our results correspond with those of other studies that indicate that phosphate restriction is adequate to reverse and correct secondary hyperparathyroidism as well as other abnormalities in divalent ion metabolism. Because dietary phosphate restriction appears to exert its effect through the increased production of 1,25(OH)2D, an alternative therapeutic approach would be supplementation of 1,25(OH)2D3 (calcitriol). To test this, another study was conducted evaluating the effect of 1-year therapy with 1,25(OH)2D3 on blood levels of parathyroid hormone (PTH) and on various parameters of bone pathology in patients with creatinine clearances of 15 to 55 mL/min. Our results showed that the use of calcitriol is safe and effective in the management of secondary hyperparathyroidism and bone disease in patients with moderate renal failure.
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PMID:Role of 1,25(OH)2D in the genesis of secondary hyperparathyroidism of early renal failure and its use in the prevention of this abnormality. 232 65

A myopathy basically involving proximal respiratory muscles can develop in uremia. To evaluate respiratory muscle force in uremia, maximal inspiratory pressure (MIP) was measured in 27 patients with renal failure. MIP was very limited in patients with a creatinine clearance (Crc) lower than 10/ml/min 1.73 m2 not treated with hemodialysis (HD) and in patients on HD who were not treated with 1.25 (OH)2D3 (45 +/- 9 and 43 +/- 5 cm H2O, respectively), moderately reduced in patients on HD treated with 1.25 (OH)2D3 (58 +/- 5 cmH2O) and normal in patients with Crc higher than 10 ml/min 1.73 m2 (86 +/- 6 cmH2O). The treatment with 1.25 (OH)2D3 during 3 months promoted a significant increase in MIP and serum calcium level and a reduction in parathyroid hormone in patients with Crc lower than 10 ml/min. It was concluded that, in uremia, a respiratory muscle weakness partially reversible with vitamin D therapy may be found.
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PMID:[Chronic kidney insufficiency and respiratory muscle function. Changes induced by treatment with 1,25(OH)2D3]. 232 53

The cardiorespiratory and metabolic response to exercise was evaluated in children with end-stage renal failure maintained on haemodialysis. Eight patients (haemodialysis group), 4 boys and 4 girls, with a mean age of 13.4 +/- 3.6 years (range 9.4-18.6 years) and haemoglobin levels ranging from 5.3 to 7.6 g/dl and 16 healthy children (control group) performed a progressive exercise testing on a treadmill. Gas exchange was simultaneously monitored. The mean ventilatory anaerobic threshold of the haemodialysis group, expressed as a percentage of the reference values, was 59.1 +/- 18.2%, and their maximum work load (29.9 +/- 19 W) was about one fourth of that reached by the control group (113.3 +/- 51.6 W). Ventilatory anaerobic threshold values in the haemodialysis group significantly correlated with blood haemoglobin levels, but not with creatinine and parathyroid hormone concentrations. We, therefore, conclude (1) that children maintained on chronic haemodialysis have a marked reduction in aerobic working capacity and (2) that the major cause for this limitation appears to be the reduced haemoglobin concentration.
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PMID:Exercise tolerance in end-stage renal disease. 235 65


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