Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In view of the known toxicity of aluminum, we studied the effects of CaCO3 as an alternative phosphate binder in 12 chronic renal failure (CRF) children during 152 patient-months. Mean (+/- SD) serum creatinine concentration rose during that period from 3.7 +/- 1.8 to 5.1 +/- 3.0 mg/dl. 8 patients received CaCO3 from the start, and 4 were switched from A1(OH)3 after 2 months of interruption. In addition to CaCO3 (0.1-0.3 mg/kg BW) all patients received NaHCO3, and all but two received 1 alpha-hydroxyvitamin D3 [1 alpha(OH)D3] or dihydrotachysterol (DHT). Urine and blood variables were checked every 4-6 weeks and medication dosages were adjusted accordingly, aiming to keep serum Ca at 10.4-10.8 mg/dl, serum Pi at 3.5-5.5 mg/dl, and serum HCO-3 above 18 mEq/l. Bone X-rays were obtained every 6-9 months. With treatment, mean serum Ca increased from 8.9 +/- 0.7 to 10.3 +/- 0.4 mg/dl (p less than 0.01), serum Pi decreased from 6.3 +/- 0.9 to 4.2 +/- 0.5 mg/dl (p less than 0.01), and the mean Ca X P product decreased slightly and insignificantly. Mean serum alkaline phosphatase levels decreased significantly from 486 +/- 251 to 168 +/- 28 IU (p less than 0.01). Bone X-rays at the end of the study showed either healing of renal osteodystrophy or its prevention. Only one episode of mild hypercalcemia (serum Ca 11.7 mg/dl) was observed in 1 patient, but his Ca X P product remained low.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oral calcium carbonate as phosphate-binder in infants and children with chronic renal failure. 380 30

We evaluated the effectiveness of calcium carbonate as a phosphate binder in 19 children with chronic renal failure; ten children were undergoing dialysis therapy (eight maintained by CAPD and two by hemodialysis). Twelve children had previously received aluminum hydroxide, while calcium carbonate was the primary phosphate binder used in seven children. Among all the children, the serum phosphorus level on no phosphate binder was 7.4 +/- 0.9 mg/dL, which decreased significantly (P less than .001) to 5.9 +/- 0.8 mg/dL during calcium carbonate therapy, while the serum calcium, bicarbonate, and creatinine were unchanged. The reduction in the serum phosphorus level occurred while dietary intake of calcium and phosphorus were unchanged, as demonstrated by three-day dietary records. The dose of calcium carbonate required to maintain the serum phosphorus in the normal range varied from 600 mg to 15 g/d (mean 7.4 g/d). Among the 12 children and four others who had received aluminum hydroxide, serum aluminum levels fell from 108.8 +/- 121.8 ng/mL to 36.1 +/- 29.1 ng/mL after aluminum hydroxide was stopped (P less than .05). Serum alkaline phosphatase and parathyroid hormone (PTH) levels during aluminum hydroxide therapy were similar to levels obtained during calcium carbonate therapy, while PTH levels fell in children treated initially with calcium carbonate. All the children have been observed for a mean of 12.0 months (range 4 months to 3 1/2 years). Hypercalcemia occurred in seven children, usually when vitamin D therapy was initiated or the dose changed. Hypercalcemia resolved with adjustment of the vitamin D or calcium carbonate dose in all but one patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium carbonate is an effective phosphorus binder in children with chronic renal failure. 382 69

Quantitative bone histology, biochemistry and height velocities were studied in 18 children suffering from chronic renal failure. Eight received calcitriol, 7 ergocalciferol and 3, though alloted to a treatment group, failed to comply with therapy. A histochemical stain for aluminum showed heavy deposition at the calcification front in 3 patients; 2, in the calcitriol group had severe osteomalacia which worsened during treatment, and 1 in the ergocalciferol group had osteomalacia which did not improve. One had never undergone hemodialysis. Bone histology improved markedly in the remaining 12 patients, whichever vitamin D preparation was used; it was unchanged in 3 non-compliant children. Plasma calcium levels rose while parathyroid hormone and alkaline phosphatase levels fell following both treatments, and were unchanged in non-compliant children. Hypercalcemia occurred more frequently following calcitriol therapy (11 episodes) than following ergocalciferol therapy (3 episodes). Height velocities, studied in 11 children, increased in 5 (3 on ergocalciferol and 2 on calcitriol) and were unchanged in 6 (1 on ergocalciferol, 5 on calcitriol). Improved bone histology did not correlate with increase in height velocity. As ergocalciferol and calcitriol had similar therapeutic effects and as side-effects were more common with calcitriol, it is concluded that calcitriol provides no advantage over ergocalciferol in the treatment of renal bone disease in children.
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PMID:Treatment of childhood renal osteodystrophy with calcitriol or ergocalciferol. 387 85

In patients with severe chronic renal failure (SCRF), especially in those undergoing chronic dialysis, aluminium may accumulate in the body. The aluminium is derived from the dialysate and/or from orally-administered, aluminium-containing phosphate binders. Accumulation preferentially occurs in the bone causing aluminium-induced osteomalacia. The physiopathological mechanisms of the disease still have to be elucidated. It has been suggested that aluminium accumulates at the osteoid/calcified-bone boundary (OCBB) inhibiting the influx of calcium there, and also that aluminium directly suppresses the secretion of parathyroid hormone (PTH). A third factor inducing the mineralization defect may be the presence of aluminium within the mitochondria of the osteoblast. In accordance with these hypotheses, hypercalcemia and relatively low iPTH levels are frequently found in aluminium-induced osteomalacia. Histologic methods are essential for demonstrating the actual existence of aluminium-induced osteomalacia. A large bone biopsy is desirable. When the biopsy is not decalcified and embedded in plastic, excellent histologic pictures are obtained wherein mineralized and non-mineralized bone (i.e. osteoid) can be distinguished clearly. Furthermore, the un-decalcified sections can be stained for aluminium, iron or both, and they are suitable for evaluation of the bone marrow status. Several features, like irregularly distributed osteoid with variable thickness, a relatively low number of cubic osteoblasts, and the absence of marrow fibrosis, are suggestive of aluminium-induced osteomalacia. However, the latter can only be proven by histochemical methods, e.g. by the aluminon staining. The treatment of aluminium-induced osteomalacia is quite different from that of other types of renal bone disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aluminium-induced osteomalacia in severe chronic renal failure (SCRF). 391 58

The milk-alkali syndrome is the association of hypercalcaemia and renal failure, with or without alkalosis, in the presence of absorption of excessive quantities of calcium, alkali, or both. Two patients with the milk-alkali syndrome are described, one representing an acute, reversible disorder and the other demonstrating a chronic syndrome with only partially reversible renal disease. Differential diagnosis is not difficult and is usually aided by the initial clinical evaluation as well as rapid response to conservative therapy. Because the initial stages of renal insufficiency are often fully reversible, the early identification and treatment of the milk-alkali syndrome can prevent progression to irreversible, chronic renal failure. Although non-absorbable antacids, H2 blockers, and sucralphate are the basis of modern treatment of peptic ulcer disease, the syndrome may still occur, especially in patients who self-treat symptoms of dyspepsia.
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PMID:The 'milk-alkali' syndrome: two case reports with discussion of pathogenesis. 400 10

Aluminum intoxication is an increasingly frequent complication of chronic renal failure. Because hypercalcemia, elevated parathyroid hormone levels, and radiologic changes said to be typical of osteitis fibrosa commonly occur with aluminum intoxication, it is frequently confused with hyperparathyroidism. In this report, examples of this dilemma are described. The pathophysiology leading to the confusing clinical picture is discussed, with a suggested approach to the problem.
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PMID:Pseudohyperparathyroidism. Syndrome associated with aluminum intoxication in patients with renal failure. 401 98

A study is reported of the estimation of plasma calcium fractions and the calcium-binding affinity of plasma proteins in a total sample of 59 people, which included 29 normal subjects and 30 patients with either hypercalcaemia or hypocalcaemia. It was demonstrated that when the sample was considered as a whole there was a significant correlation between the total plasma calcium concentration and the ultrafiltrable, ionized, and protein-bound calcium fractions and between the ultrafiltrable and ionized fractions. We have also demonstrated that in patients with either hypercalcaemia or hypocalcaemia, including acidotic uraemics, the calcium-binding affinity of the plasma proteins did not differ significantly from that in normal subjects. A significant correlation was also found between the total plasma calcium concentration and the ultrafiltrable, ionized and protein-bound calcium fractions when the normal subjects and the groups of patients with hypercalcaemia and hypocalcaemia due to chronic renal failure were considered as separate groups. The group of patients with hypercalcaemia included patients both with hyperparathyroidism and with hypercalcaemia due to other causes.
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PMID:Plasma calcium fractions and the protein-binding of calcium in normal subjects and in patients with hypercalcaemia and hypocalcaemia. 513 91

In 16 patients with chronic renal failure and osteomalacia resistant to vitamin-D therapy, aluminium was demonstrated in bone biopsy specimens at the interface between thickened osteoid and calcified bone by means of both X-ray microanalysis and a specific histochemical stain. 14 patients also had hypercalcemia. It is suggested that this is due to the blocking by aluminium of additional calcium uptake into bone coupled with the availability of additional calcium from dialysis fluid and vitamin-D therapy. This study provides more aetiological evidence linking aluminium and the development of osteomalacia in chronic renal failure. Further, if hypercalcaemia develops in such patients it is important that aluminium toxicity be excluded as the cause to prevent unnecessary parathyroidectomy.
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PMID:Hypercalcaemic osteomalacia due to aluminium toxicity. 612 1

Four patients under maintenance dialysis for chronic renal failure were suffering from aluminium toxicity. One showed evidence of encephalopathy, two presented with fractures and one was asymptomatic. Hypercalcaemia was constant, whereas high serum aluminium levels were present in only 2 patients. In all cases, iliac bone biopsy specimens, non-decalcified and stained with Aluminium , were found to contain aluminium deposits along the mineralization fronts, thus confirming the diagnosis of aluminium overload. In addition, biopsies revealed an excess of osteoid tissue with morphological and dynamic signs of osteomalacia (2 cases) or strongly depressed bone formation (2 cases). Histomorphometric bone biopsy appears to be the best mean of diagnosing aluminium intoxication and analyzing its effects on bone remodeling and mineralization. It is also very useful to monitor the treatment.
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PMID:[Aluminum poisoning in renal dialysis patients: bone histology. Value of quantitative bone biopsy]. 623 88

Elucidation of the vitamin D endocrine system and the availability of potent metabolites have led to new approaches to vitamin D therapy. The traditional management of exogenous (sunlight) or endogenous (malabsorption) vitamin D deficiency without evidence of disordered vitamin D metabolism has not changed, since it consists of treatment with vitamin D itself--a therapy which preserves the normal intrinsic mechanisms for regulating the rate of production of 1,25-dihydroxycholecalciferol. 1,25-DHCC and the analogue compound 1 alpha-CC should be reserved for treatment of hypocalcemia consequent on chronic renal failure or hypoparathyroidism, where 1-hydroxylation is lacking or impaired. Hypophosphatemic rickets has been treated with 1-hydroxylated compounds, with promising results; this use of the latter metabolites warrants further investigation. The use of vitamin D metabolites and of pharmacological doses of vitamin D itself must be regarded as substitution of a hormone or hormone precursors. Therefore, careful monitoring of serum and urine calcium is required in every patient receiving these compounds, in order to avoid excessive dosage. Special attention must be paid to patients with sarcoidosis since they often develop hypercalcemia after vitamin D or UV-light exposure, as a result of an intrinsic regulation defect in 1,25-DHCC synthesis.
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PMID:[Therapy with vitamin D and D-metabolites]. 626 26


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