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 have determined plasma calcitonin levels in 72 chronic dialysis patients and investigated their possible correlations with other parameters of calcium and phosphorus metabolism, including plasma levels of calcium, phosphorus, alkaline phosphatase and parathormone, as well as with the duration of treatment. Forty-one of the patients were being treated with hemodialysis (HD) and thirty-one with continuous ambulatory peritoneal dialysis (CAPD). Increased calcitonin levels were detected in 83% of the HD patients and in 79% of the CAPD group. In the former there was a positive correlation between the levels of calcitonin and the calcium, corrected calcium, alkaline phosphatase and parathormone levels and with the duration of treatment, whereas in the latter the calcitonin levels only correlated with the serum calcium. The patients receiving CAPD also showed significantly lower calcium and calcitonin levels than the HD patients. Our conclusion is that, apart from accumulation due to renal failure, the main factor determining the calcitonin level is the blood calcium level, and that the observed increase might play a role in the physiological protection of bone against the action of parathyroid hormone.
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PMID:Plasma calcitonin concentration in patients treated with chronic dialysis: differences between hemodialysis and CAPD. 685 Dec 65

Nine patients with renal osteodystrophy were tested for 6.5 to 35 months with 1,25-dihydroxycholecalciferol (1,25-DHCC). A close biochemical follow-up was performed during the first 6 months of treatment, including biweekly determinations of serum calcium, phosphorus, magnesium, alkaline phosphatase and creatinine levels. A bone biopsy, radiologic investigations and determinations of plasma levels of immunoreactive parathyroid hormone (IPTH) and intestinal absorption of calcium 47 were performed before and after the 6 months. Although the five patients with osteitis fibrosa showed a significant improvement, the four with predominantly osteomalacic lesions showed no response to treatment. These four had a normal initial plasma iPTH level, higher serum calcium levels than the other five patients, extreme sensitivity to 1,25-DHCC, with frequent episodes of hypercalcemia, and only a slightly increased serum alkaline phosphatase level, which remained unchanged during treatment. All but one of the patients, irrespective of the histologic abnormality, showed a decrease in the uptake of radionuclide by bone after treatment. The renal function of one patient, a man with long-standing stable renal failure who had not undergone dialysis, deteriorated during treatment.
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PMID:Treatment of renal osteodystrophy with 1,25-dihydroxycholecalciferol. 689 3

Patients with end-stage renal failure develop osteodystrophy in part due to defective production of 1,25-dihydroxycholecalciferol by the kidney. We treated eight adults with chronic renal failure and osteodystrophy with 1,25-dihydroxycholecalciferol (calcitriol) for 30-44 months. Seven of these patients were also symptomatic with bone pain and/or muscle weakness. Striking amelioration of muscle weakness occurred, and bone pain was considered to be significantly improved in four of seven patients. Hypercalcemia was noted in all the patients, necessitating a reduction in the daily dose of calcitriol to a range of 0.125 to 0.5 microgram/day. While serum alkaline phosphatase fell during therapy, serum iPTH did not show any significant change. Bone mineral content improved in four patients, though it still remained below normal. Radiographic changes of osteodystrophy showed definite improvement in only three.
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PMID:Long-term therapy of uremic osteodystrophy in adults with calcitriol. 689 93

To confirm and extend previous observations of enhanced linear growth in children with chronic renal disease being treated with 1,25-dihydroxyvitamin-D3 and to characterize further the calcium, phosphorus, magnesium, and zinc disorders in renal failure, 11 children (mean age 8 +/- 5 years) with chronic renal insufficiency (glomerular filtration rate 18% +/- 13% of normal) were evaluated on the basis of their reciprocal serum creatinine concentrations, height-velocity curves, mineral balances, and radiologic findings. Reciprocal serum creatinine concentrations analyzed retrospectively and prospectively during 32 months of 1,25-dihydroxyvitamin-D3 therapy showed progression of renal failure at rates linearly identical with those before treatment, thus suggesting that the treatment did not accelerate the rate of deterioration of glomerular filtration rate in chronic anal insufficiency. Indeed, one patient manifested a lesser decline in renal function (P less than .05). The height velocity of six of the children (75%) less than 12 years of age improved markedly over that expected for chronologic and bone ages after one year of treatment with orally administered 1,25-dihydroxyvitamin-D3, 15 to 35 ng/kg/day. All other medications except vitamin D2 were continued at their pretreatment dosage levels throughout the study. Growth velocity was unimproved in two of three children older than 12 years at the initiation of 1,25-dihydroxyvitamin-D3 therapy. Mineral balance data showed significant retention of calcium, phosphorus, magnesium, and zinc (357 +/- 32 mg/sq m/day, 250 +/- 82 mg/sq m/day, 38 +/- 32 mg/sq m/day, and 1,157 +/- 283 microgram/sq m/day, respectively), after treatment for 12 months. In addition, serum calcium, alkaline phosphatase, and parathyroid hormone concentrations returned toward normal. Finally, healing of renal osteodystrophy was radiologically evident after six months of therapy.
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PMID:Effects of 1,25-dihydroxyvitamin-D3 on renal function, mineral balance, and growth in children with severe chronic renal failure. 689 62

The clinical, biochemical, radiological and histological appearances of the bones of 38 patients with advanced renal failure are presented. Thirty-three patients had histological evidence of hyperparathyroidism and 17 also showed osteomalacia. Of five showing evidence of neither hyperparathyroidism nor osteomalacia, two had borderline osteopenia. There was an inverse correlation between the plasma calcium concentration and trabecular surface covered by osteoid with a tendency for those with the lowest concentrations of plasma calcium to show histological osteomalacia. There was an inverse correlation between extent of calcification front and both volume and surface extent of osteoid. No relation was found between plasma phosphorus concentration and any of the histological measurements made. Patients with radiological hyperparathyroidism had a lower calcium and higher plasma phosphorus than those without. Phalangeal sub-periosteal erosions were as common in those with histological osteomalacia as in those with histological hyperparathyroidism alone. There was no association between plasma alkaline phosphatase activity and type of bone disease. There was no correlation between the radiological second metacarpal index and the histological volume of cancellous iliac bone.
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PMID:Quantitative bone histology in 38 patients with advanced renal failure. 706 5

Clinical, biochemical, radiological and bone biopsy findings were studied in 15 patients with end stage renal disease due to analgesic nephropathy and compared with data from age and sex matched controls who had end stage renal disease from other causes. Patients with analgesic nephropathy had significantly higher osteoid volume (P less than 0.04), reduced calcification fronts (P less than 0.001) and lower percentage mineralization (P less than 0.04). Serum alkaline phosphatase was significantly higher in the analgesic group (P less than 0.005). It is concluded that osteomalacia is more common and severe in the group of patients with end stage renal disease due to analgesic nephropathy. There was no relationship between osteomalacia and the duration of renal failure, acidosis, aluminium deposition or other serum biochemical abnormalities.
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PMID:Bone disease in analgesic nephropathy. 715 45

Calcium (Ca) metabolism was compared in 2 groups of patients with chronic interstitial nephritis: in 21 patients (AAN-group) nephropathy was due to exposure for 5 to 50 years (mean 21.1) to phenacetin containing analgesics, whereas in 21 other patients (controls) it was due to exposure for 1 to 80 years (mean 21.4) (NS) to other causes. Patients were followed for 2.5 +/- 0.6 and 1.6 +/- 0.6 years respectively (mean +/- SEM) (NS). Blood Ca, P, protein, creatinine, alkaline phosphatase, parathyroid hormone (PTH), 25-hydroxyvitamin D (25-OH-D), together with arterial acid-base status and urinary excretion rate of Ca, P and creatinine were measured serially. For each patient the results were averaged for 2 degrees of renal failure, i.e. for creatinine levels below and above 400 mumol/l (logarithmic mean). Results were included only when P was maintained between 0.7 and 1.9 mmol/l. The range of creatinine levels studied was 95 to 1600 mumol/l. No differences were found between the 2 groups with respect to creatinine clearance, blood, P, protein, arterial pH and urinary excretion rates of Ca and P. There was a trend for blood HCO3 to be lower in the AAN group. Mean plasma Ca was significantly lower, and PTH was significantly higher, in the AAN than in the control group at both degrees of renal failure; mean plasma alkaline phosphatase activity was also significantly higher in the AAN group, but at severe degrees of renal failure only. Significant correlations were observed between individual values of both Ca and PTH (r = -0.747) and PTH and alkaline phosphatase (r = 0.603). The degree of hypocalcemia and of hyperparathyroidism was not related to the plasma level of 25-OH-D. It is concluded that at comparable degrees and duration of renal failure patients with AAN, when compared with patients with interstitial nephritis of other origins, have lower blood Ca and consequently higher PTH levels and alkaline phosphatase activities, suggesting more severe osteodystrophy.
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PMID:[Particularly severe calcium metabolic disorder in nephropathy from analgesic abuse]. 717 76

A 68 year old man with prostatic carcinoma and extensive painful osteoblastic metastases was discovered to have hypocalcemia (serum calcium 7.1 mg/dl) without evidence of hypoalbuminemia, renal failure or malabsorption. Baseline studies revealed hypocalciuria (24 hour urine calcium less than 5 mg/day), normal serum phosphate (3.4 mg/dl), low tubular reabsorption of phosphate (68 percent), undetectable serum calcitonin, normal serum 25-hydroxyvitamin D, slightly elevated serum parathyroid hormone level and increased urinary cyclic AMP (8.87 mumol/g creatinine). These studies were compatible with secondary hyperparathyroidism. The intravenous administration of parathyroid extract produced no further change in urinary phosphate but a 25-fold increase in nephrogenous cyclic AMP. Three days administration of intramuscular parathyroid extract slowly and temporarily restored serum calcium to normal levels while increasing urinary cyclic AMP and phosphate. Chemotherapy with cyclophosphamide and 5-fluorouracil rendered the patient free of pain while reducing serum acid and alkaline phosphatase levels and restoring serum total and ionized calcium and urinary cyclic AMP excretion to normal.
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PMID:Hypocalcemia with osteoblastic metastases in patient with prostate carcinoma. A cause of secondary hyperparathyroidism. 724 80

1 The free fraction of azapropazone in the plasma of 37 healthy volunteers ranged from 0.0027 to 0.0070 (0.0044 +/- 0.0009, mean +/- s.d.). The principal binding protein was found to be albumin. 2 In 27 patients with various degrees of renal failure the free fraction values of azapropazone were markedly enhanced (0.0260 +/- 0.0239, mean +/- s.d.) and increased more than tenfold in some patients. There was a weak correlation (r = 0.46, P less than 0.05) between the free fraction and the clearance of endogenous creatinine. Such correlation was not found for serum creatinine, serum albumin, serum uric acid and serum urea nitrogen. 3 In 32 patients with chronic liver disease the free fraction values of azapropazone were also markedly higher (0.0210 +/- 0.0242, mean +/- s.d.) than in healthy subjects. There were statistical significant correlation between free fraction values and the prothrombin complex activity in the plasma (r = 0.40, P less than 0.05) and the total bilirubin concentration in the plasma (r = 0.90, P less than 0.001), respectively. Such correlation was not found for serum albumin, serum glutamic oxalacetic transaminase, serum gamma-glutamyl transpeptidase and serum alkaline phosphatase. 4 In patients with kidney and liver disease the free fraction values of azapropazone correlated well with those of the anticoagulant drug phenprocoumon (r = 0.93, P less than 0.001). However, the binding of the latter drug was less impaired. Bilirubin, when added in vitro, displaced both drugs from plasma proteins but this displacing effect was much smaller than the binding changes observed in patients with liver disease. 5 Kidney and liver disease caused a marked impairment of the plasma protein binding of azapropazone. In patients with kidney disease the degree of impairment of azapropazone binding cannot or only poorly (creatinine clearance) be predicted from the biochemical parameters of kidney function whereas in patients with chronic liver disease the total bilirubin concentration in the plasma may serve as an index of the binding defect.
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PMID:Plasma protein binding of azapropazone in patients with kidney and liver disease. 725 29

Sixty radiological, clinical and biochemical features were simultaneously recorded in a population of 46 patients on maintenance hemodialysis. Radiological signs of bone reabsorption (hands, acromio-clavicular and sacro-iliac joints) were demonstrated in 65% and were quantified as a radiological index of hyperparathyroidism. The index was correlated with the levels of parathormone and of alkaline phosphatase (p less than 0.01) and with the duration of renal failure (p less than 0.01), and inversely related to bone densitometry (p less than 0.05). Discriminant analysis confirmed the redundant value of parathormone and alkaline phosphatases in predicting bone lesions. Factorial analysis showed the existence of 12 classes of patients statistically close to one another. These results demonstrate the heterogeneity of renal osteodystrophy.
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PMID:[Renal osteodystrophy in patients on maintenance hemodialysis: statistical study of clinical, radiological and biochemical features]. 728 Jun 47


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