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

The serum concentration of ionized calcium is the physiologically active circulating calcium fraction, and its level is influenced by protein binding, pH and free fatty acid levels. Hypocalcemia is common in critically ill patients and primarily results from abnormalities in the parathyroid-vitamin-D axis and circulating chelators. Hypercalcemia is less common and primarily results from malignancy, hyperparathyroidism and posthypocalcemic hypercalcemia. Mild degrees of hypocalcemia and hypercalcemia are well tolerated. However, severe hypocalcemia may cause cardiovascular compromise and impair drug action. In ischemic and shock states, hypercalcemia may be detrimental, and calcium channel blockers may be useful.
Magnesium 1989
PMID:Calcium homeostasis in the critically ill patient. 268 44

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

High circulating concentrations of calcium are toxic to the heart and may cause cardiac arrhythmias and arrest. To investigate the therapeutic use of calcium antagonists in hypercalcemia, we evaluated the efficacy of verapamil hydrochloride and magnesium chloride in the treatment of experimental calcium-induced cardiac arrest in laboratory rats. Verapamil rapidly reversed the experimental calcium-induced arrest and improved survival (83% survival versus 0% in controls). Magnesium failed to reverse this toxic event. We conclude from these experimental studies that verapamil may be useful in the treatment of hypercalcemic cardiac toxicity.
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PMID:Verapamil reverses calcium cardiotoxicity. 357 66

To assess the consequences of hypercalcemia on systemic and renal hemodynamics, vasoactive hormones, and water and electrolyte excretion in intact, conscious mongrel dogs, measurements in 10 dogs receiving 100 mg/kg calcium gluconate and 10,000 U/kg vitamin D daily for 2 weeks were compared with measurements made in 10 time-control dogs not receiving calcium or vitamin D. Hypercalcemia induced by dietary supplementation with calcium and vitamin D resulted in profoundly reduced glomerular filtration rate (40 vs 78 ml/min in controls; p less than 0.005), estimated renal plasma flow (145 vs 267 ml/min in controls; p less than 0.005), and renal blood flow (254 vs 441 ml/min in controls; p less than 0.005). Renal resistance was significantly increased in the hypercalcemic dogs (0.57 +/- 0.07 vs 0.28 +/- 0.01 mm Hg/ml/min; p less than 0.005). Hypercalcemia also resulted in increased fractional excretion of water (4.8 vs 1.4% in controls; p less than 0.005), sodium (1.4 vs 0.6% in controls; p less than 0.005), calcium (1.7 vs 0.7% in controls; p less than 0.01), and magnesium (10.2 vs 4.1% in controls; p less than 0.005). Systolic blood pressure (160 vs 172 mm Hg in controls; p less than 0.05) and stroke volume were lower (0.024 vs 0.036 L/beat in controls; p less than 0.005) in hypercalcemic dogs, presumably because of the diuresis, while total peripheral resistance was higher (36 vs 31 mm Hg/L/min; p less than 0.05) in controls. Magnesium levels were significantly lower in the experimental group (1.3 vs 1.7 mg/dl in controls; p less than 0.0005). Aldosterone levels, plasma renin activity, and urinary prostaglandin excretion were not significantly affected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Systemic and renal vascular responses to dietary calcium and vitamin D. 377 Aug 72

The TmMg and renal Mg threshold were assessed in normal subjects and in a number of pathological conditions. The TmMg in normal subjects was 1.4 mg/100 ml glomerular filtrate (GF) 1.73 m2 and numerically equalled the renal Mg threshold of 1.4 mg/100 ml. No significant difference was seen in patients with primary hyperparathyroidism or hypoparathyroidism. Patients with familial hypocalciuric hypercalcemia, however, tended to have an elevated renal Mg threshold. Investigation of 3 patients with idiopathic renal Mg wasting demonstrated a normal TmMg but reduced renal Mg threshold. Urinary Mg excretion was also assessed in normomagnesemic alcoholic patients. Retention of a parenterally administered Mg load and renal Mg retention were significantly greater than normal despite normal serum Mg concentrations. These data suggest that determination of TmMg and renal Mg threshold may provide useful information in understanding Mg homeostasis in normal subjects and in disorders which may result in abnormal Mg metabolism.
Magnesium 1986
PMID:TmMg and renal Mg threshold in normal man and in certain pathophysiologic conditions. 380 21

Hypercalcemic conditions are commonly associated with hypertension and with abnormal magnesium homeostasis. The mechanism by which the hypertension of hypercalcemia is mediated is not clear, and the role that magnesium may play in its generation has not been examined. We review here the available clinical and experimental data and propose a role for abnormal magnesium metabolism in the mediation and generation of the hypertension of hypercalcemia.
Magnesium 1984
PMID:The possible role of magnesium in hypercalcemic hypertension. 609 41

In Sarotherodon mossambicus prolactin cell activity is related to ambient Ca2+ levels, and prolactin has hypercalcemic activity in this species. To study whether prolactin has a direct action on calcium metabolism, or whether prolactin's relationship with calcium is indirect and connected with control of gill permeability, the effects of external Ca2+ and Mg2+ on prolactin secretion and gill permeability were compared. It appeared that high external Mg2+ was associated with reduced prolactin secretion, even though high Mg2+ resulted in a marked hypocalcemia. Exposure of fish to high Ca2+ levels led to hypercalcemia. Both high Mg2+ and high Ca2+ concentrations in the ambient water reduced the osmotic water permeability of the gills. These results represent further evidence that prolactin secretion in S. mossambicus may be affected by any external factor that interferes with branchial permeability. It is concluded that prolactin's main function in this species is connected with control of branchial permeability rather than calcium metabolism, although internal calcium may be implicated in permeability control.
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PMID:Effects of external Mg2+ and Ca2+ on branchial osmotic water permeability and prolactin secretion in the teleost fish Sarotherodon mossambicus. 665 34

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

Our understanding of renal Mg handling has been expanded in recent years with the use of electron probe, ultramicroanalysis, and fluorescent dye techniques to determine total Mg and free Mg2+ in individual tubule segments and cells, respectively. Recent studies have shown that [Mg2+]i is a highly mobile cation that may be altered by a number of influences including hormones. It is likely that the hormonal changes in [Mg2+]i, reported here and elsewhere, are involved in intracellular metabolism and regulation rather than transepithelial transport. The role of intracellular Mg2+ in control of cell function is poorly understood. However, it is evident that [Mg2+]i may be rapidly charged through a number of different influences that may have important effects on cell function. These kinds of data have enlarged our understanding of Mg conservation by the renal tubule but have posed many questions for further study. Magnesium is handled in different ways along the nephron. About 80% of the total plasma Mg (1.5-2.0 mM) is ultrafilterable across the glomerular membrane. Of the ultrafilterable Mg (1.2-1.6 mM), only 20-25% is reabsorbed by the proximal tubule, including the convoluted and straight portions. This is in contrast to Na and Ca reabsorption, which amounts to approximately 70 and 60%, respectively, in the proximal nephron. Accordingly, the fractional delivery of Mg to the thick ascending limb of the loop of Henle is much greater than that of Na or Ca. It is now evident from micropuncture studies that proportionally greater amounts of Mg (50-60%) are reabsorbed in the loop compared with Na (20-25%) or Ca (30-35%). Because the terminal nephron segments, including the DCT and collecting tubule, reabsorb only a small portion of the filtered Mg (approximately 5%), the loop of Henle plays a major role in the determination of Mg reabsorption, and it is in this segment that the major regulatory factors act to maintain Mg balance. Magnesium reabsorption in the thick ascending limb takes place in the cortical segments, at least in the mouse and rat. Evidence summarized here suggests that Mg is passively reabsorbed via the paracellular pathway in the cTAL of the loop of Henle. Several factors affect Mg reabsorption in the loop of Henle. Hypermagnesemia and hypercalcemia inhibit reabsorption leading to increased urinary excretion of Mg and Ca. These effects have been reviewed in detail elsewhere (113, 149). Magnesium depletion, for instance through dietary Mg deprivation, enhances Mg reabsorption in the loop of Henle before the fall in plasma Mg concentration and filtered Mg load.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renal magnesium handling and its hormonal control. 817 Nov 16

The normal fractional urinary excretion of filtered magnesium is about 5%. In magnesium deficiency in man, the kidneys can normally reduce the 24-hour urinary magnesium excretion to less than 1 mmol (24 mg) via unknown mechanisms, and initially without a fall in plasma magnesium concentration. Renal magnesium wasting may be defined as a urinary excretion greater than 1 mmol/day in the presence of hypomagnesemia (plasma magnesium < 0.7 mmol/l). Congenital renal magnesium wasting occurs in several syndromes including Bartter's syndrome in which it is associated with hypercalciuria, and the defect may be in the thick ascending limb of Henle's loop, and Gitelman's syndrome in which there is hypocalciuria, and the defect may be in the distal convoluted tubule. Other causes of renal magnesium wasting include diabetes mellitus, hypercalcemia and diuretics. Magnesium wasting may also result from various toxicities including those of cis-platinum, in which the biochemical features resemble Gitelman's syndrome, and those of aminoglycosides, pentamidine and cyclosporin. Calcitriol deficiency may also contribute to renal magnesium wasting in some circumstances. Mild hypermagnesemia may occur in familial hypocalciuric hypercalcemia and may reflect abnormal sensitivity of the loop of Henle to calcium and magnesium ions. By contrast, the hypermagnesemia that occurs in chronic renal failure results from the reduced glomerular filtration of magnesium.
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PMID:Abnormal renal magnesium handling. 826 9


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