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

Current concepts concerning the mechanisms, diagnosis and means of treatment of a number of the major causes of hypercalcemia and hypocalcemia are reviewed. In particular, the role of abnormalities in metabolism of vitamin D including (1) excessive hepatic production of 25-hydroxyvitamin D (vitamin D intoxication), (2) increased production of 1 alpha, 25-dihydroxyvitamin D (hyperparathyroidism and sarcoidosis), (3) impaired production of 1 alpha, 25-dihydroxyvitamin D (hypoparathyroidism, renal failure, vitamin-D-dependent rickets type I, pseudohypoparathyroidism) and (4) resistance to 1 alpha, 25-dihydroxyvitamin D; the use of vitamin D and its metabolites therapeutically is discussed.
Nephron 1979
PMID:Hypercalcemic and hypocalcemic disorders: diagnosis and treatment. 44 May 8

Parathyroid hormone (PTH), creatinine, calcium and phosphate blood levels were repeatedly measured in 5 patients with acute renal failure. 1 patient developed hypercalcemia during the recovery phase of the illness. PTH was elevated in all cases before starting hemodialysis treatment and returned to normal when renal function recovered. Calcium and PTH were inversely correlated in 3 patients including the patient with transient hypercalcemia. These data show that parathyroid function in acute renal failure is closely related to changes in renal function and the hypercalcemia, when occurring, is not necessarily due to parathyroid hyperactivity.
Nephron 1978
PMID:Parathyroid hormone and calcium blood levels in acute renal failure. With special reference to one patient developing transient hypercalcemia. 63 17

Parathormone levels were determined in 17 patients with functioning renal transplants. In 8 patients recently transplanted, very high serum levels of parathormone were found without obvious relation to the glomerular filtration rate. Hypophosphatemia was also present in these cases. In 9 other patients studied 2-7 years after transplantation the mean level of parathormone was lower than in the previous group but levels above normal were noted in half of the patients, some of which had perfect renal function and normal serum phosphorus. The response to induced hypercalcemia was used as a sensitive test to reveal abnormal responses even in cases which initially had normal peripheral levels of parathormone. From these results, tertiary hyperparathyroidism would appear to be rare although hyperfunctioning parathyroid glands can be demonstrated long after kidney transplantation, even when renal function is close to normal.
Nephron 1976
PMID:Evolution of secondary hyperparathyroidism after renal transplantation. 77 58

76 kidney transplant recipients who were up to 4 years post transplant, were studied to assess the incidence of secondary hyperparathyroidism. All patients had good renal function with a mean serum creatinine of 1.4 mg/100 ml. Secondary hyperparathyroidism, as evidenced by increased serum parathyroid hormone levels, was present in 53 of the 76 patients (66%) and radiologic bone disease in 26 of the 76 patients (34%), while hypercalcemia (serum calcium greater than 11.0 mg/100 ml) occurred in only 6 patients (8.5%). The incidence of secondary hyperparathyroidism decreased slightly with time following transplantation, but the degree of secondary hyperparathyroidism as indicated by the levels of serum parathyroid hormone at various times following renal transplantation was essentially similar. The causes for the persistence of this condition are not totally known, but it was found that its incidence was related to the duration of dialysis prior to transplantation.
Nephron 1976
PMID:Secondary hyperparathyroidism in human kidney transplant recipients. 78 18

Hypercalcemia was induced in 5/6 nephrectomized rats fed a low calcium diet by administering pharmacologic doses of vitamin D. The degree of hypercalcemia was greater in uremic rats than in sham-operated rats both of which were given vitamin D. Bone resorption was marked in both groups but differed in distribution. Increased osteoclasis in uremic rats was limited to diaphyseal cortical bone while metaphyseal trabeculae were relatively unaffected compared to sham-operated rats administered vitamin D. Ultrastructurally thyroid C cells were degranulated and in an active stage in both groups of rats receiving vitamin D. Urinary calcium excretion was greater in sham-operated rats given vitamin D than in uremic rats. The greater renal retention of calcium in uremic rats given vitamin D was felt to contribute to the development of hypercalcemia. These studies suggest that although trabecular bone was resistant to pharmacologic levels of vitamin D in renal failure, hypercalcemia developed due to selective resorption of cortical bone and impairment of renal calcium excretion.
Nephron 1977
PMID:Vitamin D-induced hypercalcemia in experimental renal failure. 84 25

Deficiencies in acid excretion during hypercalcemia have been reported, and this defect has been ascribed to a deficiency in ammonia excretion. Because no changes in urine pH and urine flow occurred to explain decreased ammonia excretion, this suggested to us that decreased excretion was secondary to decreased renal ammonia production. To test this hypothesis, we investigated the ability of kidney slices from rats to produce ammonia and glucose and to consume oxygen when incubated in varying concentrations of calcium. High medium concentrations of calcium (3 and 4 mM) decreased kidney slice ammonia-genesis from glutamine and glutamine and kidney slice oxygen consumption while not affecting gluconeogenesis. Based upon our findings, we propose that hypercalcemia decreases urine ammonia excretion by depressing renal ammonia production.
Nephron 1976
PMID:The effects of high calcium concentrations on renal ammoniagenesis by rat kidney slices. 101 6

Three adolescents with uraemic osteodystrophy were treated for 7 months with daily oral doses of 1alpha-hydroxycholecalciferol (0.25-10.0 mug). All the patients were hypocalcaemic and had high serum levels of alkaline phosphatase before the treatment. A rapid rise in serum calcium and a slow, but pronounced decline in serum alkaline phosphatase concentration were observed during the period of treatment. 1alpha-Hydroxycholecalciferol induced hypercalcaemia in two situations. In both cases the hypercalcaemia was transient, serum calcium being normalized in a few days by withdrawal of the drug. Withdrawal of the drug also in other situations resulted in a fall in serum calcium concentration in a couple of days. This suggests that 1alpha-hydroxycholecalciferol should be given daily or every other day. The response did not subside during 7 months of treatment. On the contrary, the maintenance dose necessary to keep serum calcium constant was smaller than the initial dose necessary to normalize serum calcium. Bone mineral content, estimated by photon absorptiometry, rose. The rachitic bone lesions seen radiologically were significantly ameliorated during the treatment.
Nephron 1976
PMID:1alpha-hydroxycholecalciferol. Long-term treatment of patients with uraemic osteodystrophy. 126 9

The purpose of this study is to evaluate the place of intravenous 1 alpha-hydroxyvitamin D3 (1 alpha-OH-D3) in the prevention of radiologically obvious hyperparathyroidism (HPT) in patients on maintenance dialysis while excluding aluminium phosphate binder and using a dialysate calcium concentration of 1.62 mmol which keeps the intradialytic calcium balance neutral. Therefore, 47 patients without subperiosteal resorption and previously treated by oral CaCO3 and if necessary Mg(OH)2 as phosphate binder while their dialysate calcium had a Ca level of 1.62 and a Mg level of 0.2 mmol/l were randomized into a control group of 24 who were maintained on the same treatment and an experimental group of 23. This group discontinued CaCO3 and received intravenous 1 alpha-OH-D3 after each dialysis at increasing doses up to 4 micrograms and increased Mg(OH)2 as their sole phosphate binder. When plasma Ca increased above 2.7 mmol/l, the dose of 1 alpha-OH-D3 was decreased. When plasma PO4 increased above 2 mmol/l, the dose of Mg(OH)2 was increased to the highest dose not inducing diarrhea, hypermagnesemia (less than 2 mmol/l) or hyperkalemia (less than 6 mmol/l). In case of persistent hyperphosphatemia, the dose of 1 alpha-OH-D3 was decreased. Since mean plasma alkaline phosphatase was normal, HPT was monitored on the plasma concentration of 1-84 PTH for which a previous histological study showed that frank osteitis fibrosa was present only when they were above 70 pg/ml, i.e. (about twice the upper limit of the normal value). Before the study, plasma PTH was below this limit in 16 patients of the CaCO3 group and in 14 patients of the 1 alpha-OH-D3 group. After 6 months, they remained below this limit in all patients except 2 of each group. Plasma PTH was initially above 70 pg/ml in 8 of the CaCO3 and did not change significantly throughout the study, 2 patients having at 6 months a PTH level below 70 pg/ml. In contrast with intravenous 1 alpha-OH-D3, all the 9 patients with initial frank HPT decreased their PTH levels after 2 months, the levels being below 70 pg/ml in 6 cases. However, because of hypercalcemia and/or of hyperphosphatemia in spite of a highest tolerable dose of Mg(OH)2, 1 alpha-OH-D3 doses had to be decreased down to 0.4 microgram per dialysis at the 6th month so that at 6 months 6 of 9 patients had their PTH levels above 70 pg/ml, a number comparable to that of patients treated with CaCO3 (6 of 8).(ABSTRACT TRUNCATED AT 400 WORDS)
Nephron 1992
PMID:Prevention of hyperparathyroidism in patients on maintenance dialysis by intravenous 1-alpha-hydroxyvitamin D3 in association with Mg(OH)2 as sole phosphate binder. A randomized comparative study with the association CaCO3 +/- Mg(OH)2. 155 99

Since Mai et al. found, with the intestinal lavage technique, that the same dose of elemental calcium given as acetate (Ca Ac) complexed in the gut of uremic patients twice as much phosphate as calcium carbonate (CaCO3) while inducing a rather low calcium absorption, we wanted to see if half the dose of elemental calcium given as Ca Ac could control, on medium term, the predialysis plasma phosphate as well as CaCO3 while inducing less frequent hypercalcemia. This was evaluated in a cross-over study of 3 periods of 10 weeks according to the sequence Ca Ac, CaCO3 and Ca Ac, in 12 compliant patients on chronic dialysis previously treated by CaCO3. Because of poor tolerance of Ca Ac during the first period, 4 patients were excluded and the results were assessed only on the 8 patients who completed the study. For half the doses of elemental calcium (620 +/- 250 mg versus 1,310 +/- 560 mg versus 710 +/- 200 mg/day), Ca Ac allowed the same control of predialytic hyperphosphatemia (1.67 +/- 0.34; 1.74 +/- 0.32; 1.75 +/- 0.38) with paradoxically comparable normal mean plasma calcium concentration (2.61 +/- 0.14; 2.56 +/- 0.13; 2.55 +/- 0.14 mmol/l). Plasma alkaline phosphatases and intact PTH concentrations remained also stable during the 3 periods. The frequency of hypercalcemia greater than 2.75 mmol/l (12; 9; 20%) and of hyperphosphatemia greater than 2 mmol/l (17; 22; 27%) were comparable with the 2 treatments. In conclusion, Ca Ac controls predialytic hyperphosphatemia as efficiently as CaCO3 for half the dose of elemental calcium without, however, decreasing the frequency of hypercalcemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephron 1992
PMID:Control of predialytic hyperphosphatemia by oral calcium acetate and calcium carbonate. Comparable efficacy for half the dose of elemental calcium given as acetate without lower incidence of hypercalcemia. 173 15

We measured the serum parathyroid hormone (PTH) levels in 20 patients treated with continuous ambulatory peritoneal dialysis before and after oral treatment with 24,25-dihydroxyvitamin D3- 24,25(OH)2D3. This metabolite was given in addition to existing treatment with 1 alpha-OH-D3 and calcium carbonate. Administration of 24,25(OH)2D3 led to a significant decrease in PTH levels (intact molecule) from 382 +/- (SE) 65 to 245 +/- 54 pg/ml in 9 patients whose initial levels were extremely high (p = 0.01). No side effects were observed. On the average, calcium values were unchanged and within the normal range throughout the study period; however, a few episodes of mild asymptomatic hypercalcemia occurred which responded quickly to reduction of the calcium carbonate dosage. The present study suggests that oral administration of 24,25(OH)2D3 combined with 1 alpha-OH-D3 is safe and capable of suppressing the raised serum PTH levels of end-stage renal disease patients without the danger of significant hypercalcemia.
Nephron 1991
PMID:Oral administration of 24,25(OH)2D3 suppresses the serum parathyroid hormone levels of dialysis patients. 189 92


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