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)

Hormones of the thyroid gland (thyroxine, tri-iodothyronine) control the metabolism of cells and tissue of the body, while parathormone and calcitonine are balancing the intra- and extracellular levels of calcium and phosphorus by governing some metabolic functions of bones, kidney and small intestine. Growth, maturation and metabolic homeostasis of the organism depend, among other intrinsic factors, on a normal production and secretory rate of both thyroidal and parathyroidal hormones. Clinical conditions of hyperthyroidism induce 1. increased metabolic turnover of the body with transcutaneous heat loss, 2. disordered growth of hairs and nails, 3. hyperpigmentation of skin, 4. pruritus with or without urticaria. Pretibial (usually symmetrical) myxedema may be associated with conditions of either hyper- or hypothyroidism (e.g., Hashimoto's thyroiditis); if combined with bilateral exophthalmus and acropachyderma of fingers and toes, it is called Diamond syndrome, or E.M.O. syndrome. In hypothyroidism, the skin feels chilly and dry, looks pale, and may present follicular keratoses with or without secondary eczema. The hair appears dull and sparse due to disordered anagen phase. Skin wounds heal with delay. Diffuse myxedema originates in the papillary and periadnexal connective tissue and eventually extends to the dermis as a whole. Clinical conditions of hyperparathyroidism rarely cause secondary calcification of the skin; they may induce severe pruritus, particularly in secondary hyperparathyroidism due to renal failure. Impetigo herpetiformis or generalized pustular psoriasis, resp., may be set off by excessive surgical removal of the goiter. Congenital maldevelopment of both thymus and parathyroid gland leads to cellular immune deficiency with secondary chronic muco-cutaneous candidosis.
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PMID:[The thyroid gland, the parathyroid gland and the skin]. 648 58

Neurological abnormalities are a major cause of the morbidity associated with renal failure. Substantial elevations in parathormone levels have been found to accompany significant increases in brain content of calcium. Two cases of cerebral subcortical calcifications are demonstrated by computed tomography in patients with severe chronic renal failure. To our knowledge this finding has not been described previously.
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PMID:CT demonstration of cerebral subcortical calcifications. 684 11

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

Brain aluminium concentration has been found significantly higher in patients dying with dialysis encephalopathy than in uraemic patients without this syndrome, and it has previously been reported only in haemodialysed patients. We report a case of high brain aluminium concentration in a uraemic boy showing symptoms of severe encephalopathy. He was never dialysed but only treated with aluminium hydroxide orally. Baluarte reported corresponding symptoms in nondialysed uraemic children, but brain aluminium concentrations were not reported. His patients as well as our had very high levels of parathormone which may play a role in the resorption and distribution of aluminium. Aluminium preparations should be avoided in children with renal failure.
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PMID:Dialysis encephalopathy in a non-dialysed uraemic boy treated with aluminium hydroxide orally. 721 65

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

The parathyroids from ten consecutive cases of chronic renal failure coming to operation in a period of seven years were studied by light and electron microscopy. The clinical and biochemical data as well as the levels of immunoreactive parathormone (iPTH) were reviewed. For the sake of comparison adenomata from two cases of primary hyperparathyroidism were studied. In the cases of chronic ;renal failure there were six cases of tertiary hyperparathyroidism with adenoma formation, surrounded by dense fibrous tissue and compression of adjacent parathyroid cell amidst a background of hyperplasia. Two cases showed secondary parathyroid hyperplasia and the remaining two cases were adenomata which clinically affected only one gland. Neither the biochemical data nor levels of iPTH allowed the cases with secondary hyperplasia to be separated from those with tertiary hyperparathyroidism. Similarly electron microscopy showed no distinct differences between these two groups of adenomata from cases of primary hyperparathyroidism. The diagnosis of tertiary hyperparathyroidism is made on a combination of clinical, biochemical and histological features, the histological features being most important. It is concluded that tertiary hyperparathyroidism is part of a histological spectrum in response to chronic renal failure and autonomous glands are related to the mass of parathyroid tissue present.
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PMID:The parathyroid in chronic renal failure-- a light and electron microscopical study. 744 5

Renal osteodystrophy improves after renal transplantation but, after the procedure, other forms of bone disease emerge. We report a male patient that received a renal allograft four years before, who consulted for low back pain secondary to multiple vertebral compression fractures. The patient had good renal function, a parathormone independent hyperphosphaturia, normal 25-OH cholecalciferol, increased urinary hydroxyproline, decreased osteocalcin, reduced bone density and a bone biopsy revealing osteomalacia. The diagnosis of hypophosphatemic osteomalacia was reached and treatment with phosphates and ergocalciferol was started but, despite this, the patient suffered a new fracture two years later. Two mechanisms can produce hypophosphatemia after a renal transplantation: a parathormone excess due to the previous renal failure, that disappears during the first year after the transplantation or a derangement in renal phosphate transport that can be due to a generalized proximal tubule solute transport derangement (Fanconi syndrome), parathormone hypersensitivity or to an "idiopathic" hyperphosphaturia. Despite a good treatment, bone mass is not recovered and there is a high fracture risk. Mineral metabolism must be closely monitored after a renal allograft and its alterations must be quickly treated.
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PMID:[Hypophosphatemic osteomalacia acquired after renal transplantation: a a cause of severe osteoporosis]. 756 51

Predicting the course of parathormone (PTH)-elicited bone turnover in both humans and experimental rat models with moderate chronic uremia, using only standard clinical chemistry analyses, is often difficult. Consequently, rat bone from 1 + 2/3 nephrectomized animals, after 230 days of progressive renal failure, was examined for PTH-stimulated adenylate cyclase (AC) and phospholipase C (PL-C) activities. Correlations to biological parameters related to the function of bone and kidney were made. Reduced renal function was demonstrated by increased serum creatinine; circulating 1,25 dihydroxyvitamin D3 below detection level; diminished renal PTH-elicited AC activity; and decreased urinary cAMP excretion. PTH-activated renal PL-C was also reduced. However, no significant differences were seen in urine creatinine, calcium, phosphate, and hydroxyproline, nor in serum PTH, alkaline phosphatase, calcium, and phosphate. Notwithstanding, renal osteodystrophy developed as estimated by increased plasticity of the long bones, as well as reduction of the diaphyseal (Dd) and inner femoral mid-shaft (Di) diameters. Femoral cancellous bone exhibited a substantial elevation of both eroded surface (ES) and osteoid surface (OS) as well as a marked reduction in trabecular bone volume (TBV). Calvarial PTH-activated AC was enhanced, whereas corresponding PL-C was markedly reduced. PTH-enhanced AC correlated positively with ES and negatively with Di, respectively. PTH-enhanced PL-C, however, correlated positively with bone calcium content and negatively with ES. Our results indicate that bone modeling and remodeling are to a large extent related to PTH-elicited signaling systems, and cannot easily be predicted by standard clinical chemistry analyses.
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PMID:Surgically induced uremia in rats. II: Osseous PTH-susceptible signaling systems as predictors of bone resorption. 782 Jul 79

Calcium and gla-protein content are increased in the calcifications of cardiac bioprostheses. Such calcifications are more frequent during growth, pregnancy and renal failure when bone gla-protein levels are elevated. We investigated whether bone gla-protein and other markers of calcium metabolism play a role in bioprostheses calcifications. Forty-seven patients were separated into 2 groups according to the presence (group A, n = 9) or absence (group B, n = 38) of bioprostheses calcifications, as assessed by echo-doppler and surgery. Plasma levels of calcium, phosphorus, magnesium, creatinine and alkaline phosphatases were measured by standard laboratory methods, parathormone and those of bone gla-protein by specific radioimmunoassays. Results (mean +/- SEM) were compared (group A versus group B, P < 0.01) using Student's test and one-factor variance analysis (ANOVA). Age was similar in both group (53 +/- 12.9 vs 50 +/- 12.3 yrs), whereas duration of implant was greater in group A (104 +/- 12.4 vs 66 +/- 6.5 months, P < 0.01). No statistically significant difference was found between group A and B concerning biochemical and/or hormonal markers of calcium metabolism. These negative results merit to be discussed, and further studies will be needed to explore the potential role of circulating bone gla-protein in bioprostheses calcifications.
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PMID:[Phosphocalcium metabolism in patients with calcified valvular bioprosthesis]. 851 Nov 13

Tertiary hyperparathyroidism developed after a 30-year treatment of low phosphorus osteomalacia with phosphorus supplementation. Parathormone stimulation by exogenous phosphorus would result from sequestration of calcium leading to low plasma levels of both ionized and total calcium. In this case, decreased calcium level was favoured by renal failure. Addition of calcitriol (1.25 hydroxyvitamin D3) to the phosphorus supplementation could avoid secondary hyperparathyroidism in patients with low phosphorus osteomalacia by increasing intestinal absorption of phosphorus and inhibiting, though not totally, parathyroid stimulation. Tertiary hyperparathyroidism is thus a potential complication of long-term phosphorus supplementation in vitamin D-resistant osteomalacia. Parathormone and phosphorus should be measured regularly in order to diagnose induced hyperparathyroidism early since this state is reversible with calcitriol and reduced doses of phosphorus.
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PMID:[Tertiary hyperparathyroidism induced by the treatment of hypophosphatemic osteomalacia]. 894 17


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