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

A young man developed acute renal failure and hypercalcaemia following severe burns. The hypercalcaemia was initially controlled by haemodialysis, but it persisted after return of renal function. Plasma PTH was inappropriately elevated, but the nephrogenous cyclic adenosine monophosphate level was low; thus the PTH was probably not biologically active, and may have been artefactually elevated by the moderate renal impairment. Bone histology, showed a normal resorbing surface, but a zero forming surface, implying that the bone dissolution leading to hypercalcaemia resulted from a failure of bone formation. Because of widespread infection and impaired renal function, the hypercalcaemia could not be treated by corticosteroid drugs, mithramycin or phosphate, and there was no response to salmon calcitonin. He was therefore treated with intravenous sodium sulphate, which increased urinary calcium excretion and reduced the plasma calcium. Sodium sulphate still has a role in the treatment of patients with hypercalcaemia.
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PMID:Immobilization hypercalcaemia due to low bone formation and responding to intravenous sodium sulphate. 376 50

Sodium-retaining activity of chum salmon prolactin (PRL) was examined in several euryhaline teleosts. Chum PRL was 100 times more potent than ovine PRL in maintaining plasma sodium levels in the hypophysectomized killifish, Fundulus heteroclitus, transferred from 50% seawater to fresh water. The effects of PRLs were parabolic, high doses of the hormones being less effective than low doses. When injected into seawater-adapted fry of the ayu, Plecoglossus altivelis, or into juvenile rainbow trout, Salmo gairdneri, adapted to 50% seawater, a dose-dependent increase in plasma sodium was observed. Chum PRL was 2-10 times more active than ovine PRL, and the effects in the ayu were also parabolic. An increase in plasma sodium also occurred when the PRLs were injected into the seawater-adapted eel, Anguilla japonica; the chum and ovine PRLs were equipotent, and hypercalcemia was also observed. In contrast, both chum and ovine PRLs were without effect on plasma sodium levels of chum salmon fry, either when injected into seawater-adapted fish kept in seawater or into fish subsequently transferred to fresh water. The absence of an effect of PRLs in chum salmon fry seems to be due, at least in part, to their good osmoregulatory ability during the period of seaward migration; effects of the exogenously administered PRLs may be compensated for by other hormones responsible for their hydromineral balance.
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PMID:Sodium-retaining activity of chum salmon prolactin in some euryhaline teleosts. 378 Dec 35

Tubular calcium and magnesium transport was investigated in thyroparathyroidectomized rats following acute elevation of extracellular calcium concentration. Fractional urinary excretion of calcium increased from 0.2 to 8.3% and magnesium increased from 15 to 39%, while sodium increased modestly from 0.1 to 1.1%. Superficial proximal tubules, Henle's loop, and distal tubules were perfused in vivo to determine the segmental effects of hypercalcemia. Fractional calcium absorption within the loop of Henle was significantly less in the hypercalcemic rats (58%) compared with normal animals (86%). Magnesium transport was inhibited to a greater extent compared with calcium in the loop as the fractional reabsorption decreased from 78% in the normal rats to 35% in the hypercalcemic animals. Sodium absorption was inhibited by 8%. Absolute calcium and magnesium absorption within the superficial distal convoluted tubule increased about three- to four-fold with increased delivery to this segment. These data indicate that hypercalcemia inhibits calcium and magnesium transport relatively more than sodium absorption in the loop of Henle and that this action principally accounts for the increase in urinary excretion of these electrolytes.
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PMID:Effect of hypercalcemia on renal tubular handling of calcium and magnesium. 717 16

Sixteen episodes of severe hypercalcaemia (more than 3.25 mmol/l) were treated by rehydration alone. Sodium repletion was invariably achieved within 48 hours (mean deficit 9.24 mmol/kg) although the fall in serum calcium was more protracted. A substantial fall in serum calcium (mean decrease 0.6 mmol/l) was achieved in thirteen patients; poor responses in three patients were associated with a rapidly increasing calcium load. Presentation of the data in terms of calcium excretion per unit of glomerular filtrate (CaE) and the setting of tubular reabsorption (TmCa/GFR) makes it possible to predict the likely effects of rehydration and patients with non-metastatic hypercalcaemia are easily identified. Rehydration is simple and often effective in the early management of this common metabolic problem but it is important that therapeutic goals are realistic and the intrinsic limitations of rehydration recognized. This depends upon a clear idea of the contribution that the kidney makes to the hypercalcaemia of malignant disease.
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PMID:Rehydration in the treatment of severe hypercalcaemia. 734 72

Orally or parenterally administered sodium is known to increase urinary calcium in experimental animals and humans, and there is well-documented correlation between urinary sodium and calcium in 24-h urine collections from normal subjects and renal stone formers. The correlation between urinary sodium and calcium is generally sodium driven, i.e., it is the sodium load that influences urinary calcium rather than vice versa, but the converse may also occur, as after an oral calcium load or in hypercalcemia. When sodium is the determinant, 100 mmol of sodium takes out approximately 1 mmol of calcium in the urine. When calcium load is the determinant, each millimole of calcium appearing in the urine is associated with an extra 10-20 mmol of sodium. Sodium-dependent calcium loss may continue indefinitely, but calcium-dependent natriuresis is self-limiting. There is a significant correlation between calcium and sodium in fasting urine from both pre- and postmenopausal women, but there is more calcium relative to sodium in postmenopausal women than in premenopausal women. In postmenopausal but not premenopausal women, urinary hydroxyproline is also related to obligatory sodium and calcium output, and restriction of salt intake lowers not only urinary sodium but also calcium and hydroxyproline. There is not only an increase in obligatory calcium excretion at the menopause, but also an increase in the fasting urinary sodium, which in turn accounts for some of the increase in calcium output. This rise in fasting urinary sodium represents a delay in sodium excretion that may have a significant effect on calcium homeostasis.
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PMID:The nature and significance of the relationship between urinary sodium and urinary calcium in women. 836 Jul 90

Sodium clodronate is effective in the management of osteolytic lesions, hypercalcaemia and bone pain associated with skeletal metastasis. Clinical and biochemical data underpin a licensed total daily dose of 1600-3200 mg.
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PMID:Bioavailability of two clodronate formulations. 887 4

The relationship between PTH and calcium is best represented as a sigmoidal curve. In the normal animal and human, basal PTH is positioned at approximately 25% of maximal PTH and responds rapidly to small changes in calcium in either direction. Since PTH secretion is designed to respond to either hypo- or hypercalcemia, the study was performed to evaluate whether the parathyroid gland would respond differently to hypocalcemia when the reduction in serum calcium was initiated from sustained hypercalcemia with maximal PTH suppression. Nine dogs were studied and the experimental protocol consisted of two separate parts in which the same dogs were used and the order of study was randomly assigned. For the hypercalcemic part, calcium chloride was infused intravenously to increase serum calcium to between 1.60 and 1.70 mM at 30 minutes and then continued for another 90 minutes to clamp the serum calcium at this level. Sodium EDTA was then infused to lower the serum calcium at a constant rate to less than 0.85 mM. For the normocalcemic part, 5% dextrose in water was infused for two hours to control for fluid volume and time, and then EDTA was infused to lower the serum calcium at a constant rate to less than 0.85 mM. The results show that for the same serum calcium concentration at every 0.05 mM decrement in serum calcium below normal, PTH was less in the hypercalcemic than the normocalcemic dogs (P < 0.02). During the induction of hypocalcemia in the normocalcemic dogs, a characteristic sigmoidal curve was observed in which a small decrease in the serum calcium induced a brisk increase in PTH and a maximal PTH level was rapidly attained; however, during the induction of hypocalcemia in the hypercalcemic dogs, the increase in PTH was progressive, but linear and it was not certain that a maximal PTH level was attained. In conclusion, a sustained period of hypercalcemia resulted in a decreased PTH response to hypocalcemia and reduced the efficiency of the sigmoidal PTH-calcium relationship. Whether the mechanism for this difference in PTH secretion is due to secretory products, modification of the calcium receptor, or changes in intercellular communication among parathyroid cells deserves further study.
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PMID:A reduced PTH response to hypocalcemia after a short period of hypercalcemia: a study in dogs. 894 17

Sodium-hydrogen ion exchange (NHE) is one of the principal mechanisms of restoring intracellular pH following ischemia and reperfusion. However, up-regulation of the NHE process results in a compensatory increase in the activity of the sodium-calcium exchanger. Intracellular hypercalcemia, resulting from the exchange of sodium for calcium, precipitates myocardial stunning and cell death. It has been postulated that NHE inhibition can protect the ischemic/reperfused myocardium, and preclinical studies have uniformly supported this concept. The Guard During Ischemia Against Necrosis (GUARDIAN) trial suggested benefits of NHE inhibition in subjects undergoing coronary artery bypass grafting (CABG). The sodium-hydrogen eXchange inhibition to Prevent coronary Events in acute cardiac conDITIONs (EXPEDITION) trial will further explore the use of cariporide in a randomized, controlled trial of CABG subjects at risk of myocardial necrosis.
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PMID:The role of sodium-hydrogen ion exchange in patients undergoing coronary artery bypass grafting. 1269 76

Primary renal inorganic phosphate (Pi) wasting leads to hypophosphatemia, which is associated with skeletal mineralization defects. In humans, mutations in the gene encoding the type IIc sodium-dependent phosphate transporter lead to hereditary hypophophatemic rickets with hypercalciuria, but whether Pi wasting directly causes the bone disorder is unknown. Here, we generated Npt2c-null mice to define the contribution of Npt2c to Pi homeostasis and to bone abnormalities. Homozygous mutants (Npt2c(-/-)) exhibited hypercalcemia, hypercalciuria, and elevated plasma 1,25-dihydroxyvitamin D(3) levels, but they did not develop hypophosphatemia, hyperphosphaturia, renal calcification, rickets, or osteomalacia. The increased levels of 1,25-dihydroxyvitamin D(3) in Npt2c(-/-) mice compared with age-matched Npt2c(+/+) mice may be the result of reduced catabolism, because we observed significantly reduced expression of renal 25-hydroxyvitamin D-24-hydroxylase mRNA but no change in 1alpha-hydroxylase mRNA levels. Enhanced intestinal absorption of calcium (Ca) contributed to the hypercalcemia and increased urinary Ca excretion. Furthermore, plasma levels of the phosphaturic protein fibroblast growth factor 23 were significantly decreased in Npt2c(-/-) mice. Sodium-dependent Pi co-transport at the renal brush border membrane, however, was not different among Npt2c(+/+), Npt2c(+/-), and Npt2c(-/-) mice. In summary, these data suggest that Npt2c maintains normal Ca metabolism, in part by modulating the vitamin D/fibroblast growth factor 23 axis.
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PMID:Type IIc sodium-dependent phosphate transporter regulates calcium metabolism. 1905 71

Hypercalcemia may follow hypocalcemia in the course of acute renal failure (also named now as acute kidney injury) secondary to rhabdomyolysis. The clinician should be aware of this calcium kinetics to avoid the complications of both hypocalcemia and hypercalcemia that may occur at few days interval during the recovery phase. We present herewith the case of a young gentleman who developed anuric ARF due to a strenuous exercise induced rhabdomyolysis. He was treated with supportive, corrective and dialysis measures. The progress was favourable with a diuretic phase. During the diuretic phase, he developed progressive hypercalcemia that reached up to 3.54 mEq/lwith constipation and drowsiness. Investigations showed besides stigmata of rhabdomyolysis and ARF, low initial levels of vitamin D metabolites. The calcemia eventually normalized with fluids, dialysis and a single dose of Pamidronate Sodium . The patient was discharged 3 weeks after admission with a recovered clinical condition, improved renal functions and normal calcemia. The biphasic kinetics of calcium in this setting is ocumented. We conclude that serum corrected calcium should be monitored in the context of ARF due to rhabdomyolysis.
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PMID:Calcium Kinetic in a patient with acute renal failure due to Rhabdomyolysis. A Case Report and Review of Literature. 2884 16


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