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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the effect of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) in both hypercalcemic and hypocalcemic rat models and the effect of exogenous 25-hydroxyvitamin D3 (25(OH)D3) on serum and tissue aluminum (Al) burdens. Rats fed a 0.2% Al diet received daily subcutaneous injections of either 1,25(OH)2D3 (80.9 ng/kg, n = 5 and 809 ng/kg, n = 8), 25 (OH)D3 (809 ng/kg, n = 4, and 8090 ng/kg, n = 8) or propylene glycol vehicle for 18 days. Rats given 809 ng/kg of 1,25(OH)2D3 were hypercalcemic and when compared with pair-fed controls had higher serum (33.1 vs. 14.3 micrograms/L, P less than 0.01), bone (21.2 vs. 13.2 micrograms/gm, P less than 0.01), and kidney (6.5 vs. 2.0 micrograms/gm, P less than 0.01) but not brain (1.2 vs. 1.5 micrograms/gm) or liver (0.9 vs. 0.8 micrograms/gm dry tissue) Al concentration. The lower dose of 1,25(OH)2D3 had no effect on serum or tissue Al. Treatment with 25(OH)D3 did not increase serum Ca and Al or tissue Al concentration. To dissociate a specific effect of exogenous 1,25(OH)2D3 from the concurrent hypercalcemia, endogenous production of 1,25(OH)2D3 was stimulated. Animals were fed a low Ca diet until hypocalcemia developed and were then divided into four groups: one given low Ca (n = 7) for 21 days, one given low Ca plus 0.2% Al (n = 7) for 21 days, one returned to a normal Ca diet (n = 4) for 30 days, and one returned to a normal Ca diet for 9 days and continued with a normal diet plus 0.2% Al (n = 5) for 21 days. Hypocalcemic rats fed the Al diet, when compared with hypocalcemic controls, had higher serum (143.6 vs. 31.8 micrograms/L, P less than 0.01), bone (16.0 vs. 2.9 micrograms/gm, P less than 0.01), and kidney (8.2 vs. 2.8 micrograms/gm, P less than 0.005) but not brain (3.4 vs. 2.3 micrograms/gm) or liver (3.8 vs. 2.3 micrograms/gm) Al concentrations. Serum, bone, and kidney Al concentration was also significantly higher than that in normocalcemic rats fed the Al diet. These results indicate that pharmacologic doses of 1,25(OH)2D3 and dietary hypocalcemia enhance gastrointestinal Al absorption and serum, kidney, and bone Al concentration.
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PMID:1,25-Dihydroxyvitamin D3 increases serum and tissue accumulation of aluminum in rats. 375 57

Aluminum-containing phosphate (Al-binders) employed to control serum phosphorus in patients with chronic renal failure can be associated with the development of aluminum toxicity. To obviate the need for Al-binders, we examined the effectiveness of CaCO3 as a phosphate binder in 31 hemodialysis and 8 CAPD patients followed for 2 months while receiving Al-binders, and then, for 3-14 months while receiving CaCO3 (5.8 +/- 0.4 g/day). Monthly serum phosphorus averaged 5.4 +/- 0.2 mg/dl with Al-binders and 5.1 +/- 0.3 to 5.7 +/- 0.4 mg/dl with CaCO3 (p = NS). There were 25.2 episodes of hyperphosphatemia (serum phosphorus greater than 6.5 mg/dl) per 100 treatment months with Al-binders and 19.2 episodes/100 treatment months with CaCO3 (p = NS). Plasma aluminum levels, 105 +/- 21 micrograms/l during ingestion of Al-binders, fell to 34 +/- 11 micrograms/l after 8 months of therapy with CaCO3 (p less than 0.01). Monthly serum Ca averaged 9.5 +/- 0.1 mg/dl during Al administration and was 8.9 +/- 0.8 to 10.0 +/- 0.2 mg/dl with CaCO3 (p = NS). Thirty-four episodes of hypercalcemia (serum Ca greater than 11.0 mg/dl) occurred in 14 patients ingesting CaCO3, but hypercalcemia did not occur with ingestion of Al-binders. Al-related bone disease was found on bone biopsy in 11 of 13 patients who developed hypercalcemia, compared to only 5 of the 11 biopsied patients who remained normocalcemic (p less than 0.01 by chi 2 analysis). Other side effects included diarrhea in 1 patient and constipation in 3 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of calcium carbonate as a phosphate binder in dialysis patients. 380 29

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

The physiopathology of metabolic bone disease described during long term total parenteral nutrition is poorly understood. We therefore prospectively assessed bone status of seven adult patients [mean age, 42 +/- 16 (SD) yr] treated with cyclic total parenteral nutrition for a period of 7 +/- 2 (SD) months. All patients had hypercalciuria (381 +/- 96 mg/day) associated with negative calcium balance in six of seven patients (-49 +/- 120 mg/day). A correlation was found (r = +0.74, P less than 0.01) between protein intake and calciuria. Two patients developed slight transient hypercalcemia. Serum magnesium and phosphate levels remained within the normal range. A high aluminum load due to the added phosphate solution (253 +/- 84 micrograms/day) was associated with increased serum aluminum levels (52 +/- 38 micrograms/liter). Normal serum levels of 25 hydroxyvitamin D (12 +/- 7 ng/ml) and low normal 1,25 dihydroxyvitamin D levels (21 +/- 8 pg/ml) were found. Serum PTH was normal in five and increased in two of the seven patients. However, in these two patients skeletal unresponsiveness to the action of PTH was found. A new histomorphometric picture of bone was observed; it consisted of a markedly reduced bone formation with subnormal osteoclastic activity leading to a low trabecular bone volume. No osteomalacia was found. The aluminum load may have played a role in these bone defects. The hypercalciuria with negative calcium balance was attributed to the cyclic amino-acid delivery during TPN.
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PMID:Multifactorial low remodeling bone disease during cyclic total parenteral nutrition. 391 65

Ten dialysis-treated patients with hypercalcemia (11.5 +/- 0.3 mg/dl, mean +/- SE) due to renal osteodystrophy were compared with 30 control dialysis-treated patients who were not hypercalcemic (9.5 +/- 0.1 mg/dl). The hypercalcemic patients were more disabled than the control patients. Fifty percent of the hypercalcemic patients and 37 percent of the control patients had a mineralization defect (p greater than 0.6). In the control group, intact parathyroid hormone level was significantly higher in patients with osteitis fibrosa than in those with osteomalacia (247 +/- 39 pg/ml versus 60 +/- 20 pg/ml, respectively, p less than 0.005) whereas in the hypercalcemic patients, parathyroid hormone measurements did not discriminate between these two types of bone disease. Osteomalacia was more severe and bone aluminum staining was stronger in the hypercalcemic patients than in the control patients (2.02 +/- 0.47 versus 0.35 +/- 0.11 mm/mm2 tissue area, p less than 0.001). The mean serum calcium level fell from 11.2 +/- 0.2 mg/dl to 10.5 +/- 0.3 mg/dl (p less than 0.01) in eight hypercalcemic patients treated with 24,25-dihydroxyvitamin D. It is concluded that hypercalcemia in patients undergoing dialysis is associated with an increase in bone aluminum level, and with more severe osteomalacia. Intact parathyroid hormone levels are useful for predicting bone histomorphometric parameters but only when hypercalcemia is not present. The drug, 24,25-dihydroxyvitamin D, was effective in lowering the serum calcium level.
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PMID:Spontaneous hypercalcemia in patients undergoing dialysis. Etiologic and therapeutic considerations. 396 41

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

The effect of high doses of CaCO3 on serum phosphorus and calcium (sPi,sCa) and the changes in serum aluminum (sAl) induced by Al(OH)3 interruption were investigated in patients on regular hemodialysis treatment. Some patients were administered Al(OH)3 and CaCO3, others only the former or the latter and others nothing. Al(OH)3 was stopped in all but one in whom it was only reduced, and CaCO3 was started or increased in all patients. A better control of sPi and serum Ca-Pi product was observed during high Ca supplementation, despite Al(OH)3 discontinuation, and was associated with a significant decrease of sAl. As expected, taking into account the dialysate Ca level of 4 mEq/l, a significant hypercalcemia occurred in some patients, especially in those who had a normal predialytic sPi without Al(OH)3 supplementation. Therefore, lowering the dialysate Ca concentration according to individual need and increasing interdialytic oral Ca supplements can be recommended with the dual purpose of keeping a positive Ca balance and correcting hyperphosphatemia.
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PMID:Effects of high CaCO3 supplements on serum calcium and phosphorus in patients on regular hemodialysis treatment. 404 44

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


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