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)

It has recently been documented that a small amount of aluminum is absorbed from a variety of different orally administered aluminum compounds. A variety of factors including gastric acidity, fluoride ingestion, parathyroid hormone, vitamin D and the quantity of aluminum ingested could theoretically modulate aluminum absorption from the gastrointestinal tract. However, partially because of the unavailability of an aluminum isotope, knowledge regarding factors which modify aluminum absorption is quite limited. In healthy individuals the absorbed aluminum is largely eliminated from the body by the kidneys. However, with renal failure the absorbed aluminum is retained and can markedly alter the body aluminum burden with resulting toxicity. In view of this finding, it is suggested that uremic patients receive the smallest amount possible of aluminum-containing, phosphate-binding gels consistent with the control of serum phosphorus levels and that alternate methods for the control of the serum phosphorus should be sought.
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PMID:Gastrointestinal absorption of aluminum. 391 61

The first study compared two groups on dialysis: 25 patients with diabetes mellitus and 25 matched non-diabetic patients, in relation to the presence of signs of hyperparathyroidism, to assess the reported low incidence of hyperparathyroidism in these patients. The diabetic group showed significantly lower values of PTH, Alk phosphatase, percentage of patients requiring vitamin D treatment, and less evidence of hyperparathyroidism on X-ray and in bone histomorphometry. In the second study 16 patients with chronic renal failure due to diabetic nephropathy were compared to 27 patients with the same degree of renal failure of other origin, the diabetic nephropathy group showed no increase in PTH, with falling creatinine clearance. Despite this low PTH, the phosphaturia was higher in the diabetic nephropathy group (Tm PO4/C Cr: 1.94 +/- 0.43 vs 2.5 +/- 0.68). In conclusion, patients with diabetes mellitus are less prone to develop hyperparathyroidism in progressive renal failure. This could be due to a relative increase in phosphaturia during declining function.
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PMID:Low incidence of hyperparathyroidism in diabetic renal failure. 399 89

In normal subjects and patients with endstage renal disease, osteoclast cell volumes were constructed using serial 2-micron thick plastic embedded sections from iliac crest bone biopsy specimens. Four cells randomly selected from each of the subjects were analyzed to give both the cell volume from the cumulative areas and thickness of each cell slice and also the cell axes taking the vector along the bone face as width or Y, thickness from the bone surface as breadth or X and vertical dimension length or Z. The mean cell volume was 6,230 microns3 in the control subjects and was significantly larger being 11,730 microns3 and 13,680 microns3 in the two patient groups. The cells showed polarity with the largest axes, Y and Z, being those in apposition to the bone surface. Howship's lacunae were enlarged in the patients and the cross-sectional area of an individual lacuna corresponded to the area of the contiguous osteoclast, r = 0.62, P less than 0.001. All patients had secondary hyperparathyroidism and osteoclast numbers were increased. There was no correlation between osteoclast size and duration of renal failure, previous vitamin D intake, or aluminum exposure. It is suggested that in ESRD, osteoclasts undergo both an increase in number and size and that these cells, being larger, remove more bone than the smaller cells in normal subjects.
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PMID:Osteoclast enlargement in endstage renal disease. 399 45

Seven patients with advanced renal failure, six of whom were dialysed, received a cation exchange resin in the calcium cycle because of severe hyperkalemia, together with their usual preventive treatment of renal osteodystrophy, including 25 hydroxycholecalciferol. Hypercalcemia developed in four subjects within less than thirty days and disappeared within four days following the withdrawal of the resin. Patients who exhibited hypercalcemia had higher calcium intake, lower predialysis blood calcium and higher PTH values before introduction of the treatment. Three of the four hypercalcemic patients were diabetics. It is therefore advised to frequently monitor blood calcium when using calcium exchange resin in patients treated with vitamin D analogs.
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PMID:Hypercalcemia in 25 OH D3 treated patients receiving a calcium exchange resin. 401 32

Parathyroid allotransplantation was performed in a 25-year-old woman with idiopathic hypoparathyroidism that had been diagnosed at age 4 years. Long-term medical management of the primary condition with vitamin D and oral calcium supplementation was complicated by multiorgan calcinosis and renal failure. At the age of 21 years she received a successful cadaver renal allograft. Four years later she developed calcinosis cutis with widespread skin necrosis. Medical control of calcium and phosphate metabolism was unsatisfactory and the skin necrosis became progressive and life threatening. A parathyroid allograft that was performed with tissue from a parathyroid adenoma resulted in normalization of the serum calcium and phosphorus levels with arrest and subsequent healing of the skin necrosis. Later failure of the parathyroid allograft was followed by successful retransplantation of normal parathyroid tissue from a cadaver organ donor.
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PMID:Parathyroid allotransplantation in the treatment of complicated idiopathic primary hypoparathyroidism. 407 84

The development of a vitamin D-resistant state in the course of renal failure may be responsible for reduced intestinal absorption of calcium and an impaired response of skeletal tissue. Moreover, the kidney has been shown to carry out the conversion of 25-hydroxycholecalciferol (25-OH-CC) to a highly biologically active metabolite, 1,25-dihydroxycholecalciferol (1,25-diOH-CC). In the present studies, vitamin D-deficient rats, made acutely uremic by either bilateral nephrectomy or urethral ligation, received physiological doses of cholecalciferol (vitamin D(3)) (CC), 25-OH-CC or 1,25-diOH-CC; 24 hr later intestinal calcium transport, in vitro, and bone calcium mobilization, in vivo, were assessed. Whereas CC and 25-OH-CC stimulated calcium transport in sham-operated controls, they were without effect in the uremic animals. In contrast, administration of 1,25-diOH-CC stimulated calcium transport in both groups of uremic animals. Administration of 1,25-diOH-CC also stimulated calcium mobilization from bone in each group of animals. However, CC and 25-OH-CC were only effective in the sham controls and the uremic group produced by urethral ligation and had little or no effect in animals without kidneys. These results indicate that renal conversion of calciferol to a more biologically active form is necessary for the stimulation of intestinal calcium absorption and calcium mobilization from bone, and that 1,25-diOH-CC may bypass a possible defect in vitamin D metabolism in uremia. From these studies it is likely that uremia, per se, may also impair intestinal calcium transport.
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PMID:Biologic effects of 1,25-dihydroxycholecalciferol (a highly active vitamin D metabolite) in acutely uremic rats. 434 3

Metabolic bone disease occurring in renal or intestinal disorders has been reviewed with particular reference to etiological factors. Hyperparathyroidism is seen as a recurring cycle of renal damage-hyperphosphatemia-hypocalcemia-parathyroid stimulation-mobilization of bone calcium and phosphate-renal tubular phosphate rejection. In intestinal cases, the initial stimulus is presumably hypocalcemia. Osteomalacia is seen as resulting from phosphate depletion for the following reasons:1. Experimentally, rickets results from dietary phosphate restriction in rats.2. Such rickets is not prevented by the presence of normally adequate amounts of dietary vitamin D, and may therefore be termed "resistant" in the clinical sense.3. Osteomalacia or rickets in intestinal malabsorption and renal tubular disorders is associated with hypophosphatemia due to excessive fecal or urinary loss.4. Renal tubular rickets has been healed by oral phosphate loading in some studies.5. Acidosis may induce osteomalacic changes, experimentally and clinically (for example, in uretero-sigmoidostomy). Reversal of systemic acidosis with oral bicarbonate has resulted in phosphate retention and a rising serum phosphate in one such case.6. Preliminary data from analysis of full-thickness bone biopsy in two osteomalacic patients shows a significant reduction in calcium and phosphate content.7. Despite the hyperphosphatemia of azotemic renal failure, over-all phosphate depletion may be present in this situation also due to: * Diminished dietary phosphate in low protein diets * Nausea and vomiting * Occasional diarrhea * The use of oral phosphatebinding antacids * Perpetuation of urinary phosphate losses by reduction in proportion of tubular reabsorbed phosphate (secondary hyperparathyroidism) and possibly high filtered load per nephron * Repeated losses of phosphate to bath fluid during dialysis.
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PMID:Metabolic bone disease secondary to renal and intestinal disorders. 489 May 32

The possibility to achieve and maintain normal plasma levels of 25-hydroxyvitamin D3 (25OHD3), with long-term vitamin D replacement therapy, has been evaluated in 9 patients with nephrotic syndrome. Plasma levels of 25OHD3 rose from 10.8 +/- 5.0 (SD) nmol/l to 29.5 +/- 11.1 (p less than 0.001) with a daily dose of 25 micrograms of vitamin D3 per os. Plasma levels of 1,25-dihydroxyvitamin D3 were low before treatment (39.5 +/- 22.7 pmol/l) and returned to the normal range under therapy in the patients without renal failure. Low levels of vitamin D metabolites in nephrotic syndrome can be normalized with long-term oral vitamin D replacement therapy.
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PMID:Vitamin D replacement therapy in patients with the nephrotic syndrome. 630 12

Two patients with moderate renal failure sustained spontaneous bilateral hip fractures during treatment with fluoride, calcium, and vitamin D for osteoporosis. They had been taking sodium fluoride (40-60 mg/day) for 11 and 21 months, respectively. Histological examination of a specimen of the bone showed severe fluorosis in the first case, and quantitative analysis of bone showed osteomalacia and skeletal fluorosis in the other case. These abnormalities were considered to be the consequence of excessive retention of fluoride due to renal insufficiency. As bilateral femoral neck fractures are very rare these data suggest a causal link between fractures and fluoride in patients with renal failure. Thus fluoride should be given at a lower dosage, if at all, to patients with even mild renal failure.
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PMID:Bilateral fractures of femoral neck in patients with moderate renal failure receiving fluoride for spinal osteoporosis. 631 15

A simple method for extraction, purification and separation of the principal vitamin D metabolites from a single serum sample is described. The method involved extraction of serum with acetonitrile followed by a first purification employing C-18 Sep-pak cartridges eluted with methanol/water and acetonitrile. Final separation before assay was carried out by high pressure liquid chromatography. 1.25-dihydroxy-vitamin D was measured with radioimmunoassay using an antiserum (S11) with high selectivity for 1 alpha-OH function of the hormone at a final dilution of 1:100,000. 24.25-dihydroxy-vitamin D and 25-hydroxy-vitamin D were measured employing a competitive binding assay with normal rat serum at a final dilution of 1:10,000 as source of binding protein. The mean (+/- SD) serum 1.25-dihydroxy-vitamin D, 24.25-dihydroxy-vitamin D and 25-hydroxy-vitamin D concentrations for a group of healthy subjects were 50.4 +/- 17.3 pg/ml, 2.3 +/- 2.6 ng/ml and 20.8 +/- 12.3 ng/ml, respectively. 1.25-dihydroxy-vitamin D concentrations were low or undetectable in patients on dialysis or with mild renal failure. High 1.25-dihydroxy-vitamin D levels were found in 2 out of 17 patients with primary hyperparathyroidism. In 4 normal subjects treated for two weeks with large doses of 25-hydroxy-vitamin D, serum 25-hydroxy-vitamin D rose from 12.5 ng/ml to 119 ng/ml and from 0.89 ng/ml to 15 ng/ml, respectively; no changes in the 1.25-dihydroxy-vitamin D assay were found.
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PMID:Simultaneous measurement of 1.25-dihydroxy-vitamin D, 24.25-dihydroxy-vitamin D and 25-hydroxy-vitamin D from a single two milliliters serum specimen. Preliminary clinical application. 633 15


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