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

Six healthy young volunteers were fed during two period of 9 days each by a strictly constantly liquid formula diet (Fresubin), on an ambulator basis. In a single blind cross-over randomized study, they were given either hydrochlorothiazide, 50 mg p.d., or a placebo during the first seven days of the two periods. The diuretic did not induce significant changes of either magnesemia or magnesiuria. In addition, the magnesium excretion after a challenging intravenous magnesium load remained unchanged. However, the thiazide normally increased the urinary excretion of sodium and potassium. It also induced hypocalciuria and hypercalcemia. The urinary excretion of cAMP and oxalic acid remained stable.
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PMID:[Short-term effect of thiazides on magnesium and calcium metabolism and secondarily on that of phosphorus, uric acid, oxalate and cyclic AMP]. 630 88

To clarify the role of vitamin D in renal phosphate transport, weanling rats were fed a vitamin D-deficient diet containing 1.8% calcium and 1.2% phosphorus. After 5-6 wk, the rats were normocalcemic, normophosphatemic, and had normal levels of PTH. Assays of vitamin D metabolites revealed undetectable plasma levels of 25(OH)D, and 1,25(OH)2D levels of 92 +/- 16 pg/ml in partially vitamin D-depleted (PVDD) rats and 169 +/- 58 pg/ml in normal rats. PVDD rats had increased phosphate excretion, both absolute and fractional, and a decrease in Na+ gradient-dependent Pi transport in proximal tubular brush border membrane vesicles (BBMV) prepared from their kidneys. Vitamin D repletion of PVDD rats with 1,25(OH)2D3, 15 pmol/100 g body wt, decreased fractional excretion of Pi from 22.6 +/- 1.9 to 13.5 +/- 1.3%; the latter values were similar to normal rats. Repletion with 1,25(OH)2D3 also increased Na+-dependent phosphate transport in BBMV from 322 +/- 24 pmol X mg protein-1 X 15 s-1 in BBMV from PVDD rats to 698 +/- 70 pmol X mg protein-1 X 15 s-1. Repletion with larger doses of 1,25(OH)2D3 produced hypercalcemia and hyperphosphatemia from intestinal absorption, an increase in phosphate excretion, and a blunted response of Pi transport to 1,25(OH)2D3. Prevention of hyperphosphatemia by dietary adjustments allowed full expression of the stimulatory effects of 1,25(OH)2D3 on Pi transport. These later data may partially explain the inhibitory effects reported in prior studies in which plasma Pi was not controlled and the larger doses of 1,25(OH)2D3 administered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of 1,25-dihydroxycholecalciferol on phosphate transport in vitamin D-deprived rats. 633 Dec 1

To test the effects of chlorothiazide on vitamin-D2-induced hypercalciuria, we carried out 17 metabolic studies lasting 12 days each in adult Sprague-Dawley male rats. Three groups were studied: (A) control rats receiving only the vitamin-D2 vehicle; (B) vitamin-D2-treated rats receiving 50 IU/day; and (C) rats treated in the same manner as group B with the addition of chlorothiazide 20 mg/day for the last 6 days of the study. Urine was collected during the last 3 days, and a blood sample was obtained at the end of each study period. Analysis of the data showed that there were no significant differences between the groups in changes of serum calcium concentration (A, 6.1 +/- 0.1 mg/dl; B, 6.1 +/- 0.2 mg/dl; C, 6.0 +/- 0.2 mg/dl), serum creatinine concentration (A, 0.5 +/- 0.07 mg/dl; B, 0.52 +/- 0.08 mg/dl; C, 0.48 +/- 0.04 mg/dl), and creatinine clearance (A, 4.8 +/- 0.7 ml/min/kg; B, 5.2 +/- 1.2 ml/min/kg; C, 4.9 +/- 0.5 ml/min/kg). The administration of vitamin-D2 significantly increased the urinary calcium excretion from 6.7 +/- 1.0 mg/kg/day to 19.5 +/- 9.7 mg/kg/day (p less than 0.02), but the calciuria was inhibited in group C rats by the addition of chlorothiazide, which restored urinary calcium excretion to 6.8 +/- 2.5 mg/kg/day (p less than 0.02). Evaluation of the ratio of calcium/creatinine excretion (A, 0.19 +/- 0.03; B, 0.53 +/- 0.25; C, 0.20 +/- 0.07) and calcium/sodium excretion (A, 0.22 +/- 0.05; B, 0.48 +/- 0.25; C, 0.19 +/- 0.04) further confirmed these effects of vitamin-D2 and chlorothiazide on urine calcium excretion. We conclude that in rats conventional doses of vitamin-D2 consistently induce marked hypercalciuria, even without hypercalcemia, and that this hypercalciuria can be effectively prevented by chlorothiazide.
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PMID:Reversal of vitamin-D2-induced hypercalciuria by chlorothiazide. 660 Aug 35

We have determined calcium and sodium excretion rates in three members of a kinship with familial hypocalciuric hypercalcemia (FHH) and in four patients with primary hyperparathyroidism (PHP) under control conditions and following the intravenous administration of chlorothiazide or furosemide. The characteristic hypocalciuria of FHH, evidenced by a significantly reduced urinary calcium/creatinine ratio compared with that of PHP, is present under control conditions (0.08 vs. 0.26 mg calcium/mg creatinine, respectively, P less than 0.05), and after chlorothiazide (0.14 vs. 0.53, respectively, P less than 0.01). However, after furosemide infusion the calcium/creatinine ratio is no longer lower in FHH than in PHP (1.12 vs. 1.14, respectively, P greater than 0.05). These data suggest that, in FHH, tubular calcium reabsorption is enhanced in the thick ascending limb of Henle's loop, the site of action of furosemide. However, the data do not exclude the presence of an abnormality at a more distal site in the nephron.
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PMID:Renal calcium handling in familial hypocalciuric hypercalcemia. 664 9

Familial hypocalciuric hypercalcemia (FHH) is an autosomal dominant trait comprising hypercalcemia, hypophosphatemia, parathyroid hyperplasia, and unusually low renal clearance of calcium. We evaluated the role of parathyroid hormone in the relative hypocalciuria of FHH and characterized the renal transport of calcium in this disorder using three previously hypercalcemic FHH patients with surgical hypoparathyroidism and three controls with surgical hypoparathyroidism. Intravenous infusion of calcium chloride in two patients with FHH and in three controls increased serum calcium from a mean basal of 5.0 to a mean peak of 6.8 meq/liter in two FHH patients and from 4.2 to 5.7 in three control subjects. Urinary calcium in a third FHH patient was studied without calcium infusion during recovery from hypercalcemia of vitamin D intoxication. At all serum concentrations of calcium, calcium clearance was lower in FHH than in controls; at base-line serum calcium, the ratio of calcium clearance to inulin clearance (C(Ca)/C(IN)) in FHH subjects was 32% of that in controls and decreased to 19% during hypercalcemia. Calcium infusion increased the ratio of sodium clearance to inulin clearance in controls from a base line of 0.020 to 0.053 at peak concentrations of calcium in serum, but did not affect this parameter in FHH (0.017 at base-line serum calcium vs. 0.019 at peak). When calcium infusion studies were performed (in two patients with FHH and one control) during administration of acetazolamide, a drug whose principal renal action causes inhibition of proximal transport of solute, C(Ca)/C(IN) in the patients with FHH was 29 and 7% of that of the control at base-line and peak serum calcium, respectively. In contrast, ethacrynic acid, a diuretic that acts in the ascending limb of the loop of Henle, increased C(Ca)/C(IN) more in the FHH patients than in the control subject; C(Ca)/C(IN) was 65% at base-line and 47% at peak serum calcium, compared with that of the control subject. The greater calciuric response to ethacrynic acid than to acetazolamide or calcium infusion alone in FHH indicates that a major renal locus of abnormal calcium transport in this disorder may be the ascending limb of the loop of Henle.Decreased clearance of calcium in patients with FHH and hypoparathyroidism when compared with hypoparathyroid controls indicates that relative hypocalciuria in FHH is not dependent on hyperparathyroidism. Since the parathyroid glands in FHH are not appropriately suppressed by calcium, this implies that FHH represents a disorder of abnormal transport of, and/or response to, extracellular calcium in at least two organs, parathyroid gland and kidney.
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PMID:Urinary calcium excretion in familial hypocalciuric hypercalcemia. Persistence of relative hypocalciuria after induction of hypoparathyroidism. 687 59

In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.
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PMID:[Electrolyte metabolism and emergency]. 688 72

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

Six patients with stable end stage chronic renal failure have been studied while receiving keto-acid supplements that provided a daily calcium load of 42 +/- 2 mM. None of the patients had intercurrent illness. All patients showed elevated serum calcium concentration levels while on keto-acid supplements, reaching significance on 5 occasions. Reciprocal falls in serum phosphate concentrations were noted in all patients, and this observation was not due to an anabolic effect of the keto-acids. In 3 patients, the rise in serum calcium concentration was associated with marked clinical manifestations that required curtailment of treatment. The risk of hypercalcemia occurs early and certain high risk categories can be identified. Recommendations about the use of calcium salts of alpha-keto-acid analogues are given and it is suggested that a choice should be made available between calcium and sodium salt analogues.
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PMID:Changes in serum calcium caused by supplementation of low protein diets with keto-acid analogues in patients with chronic renal failure. 719 26

Sodium sulfate can be used to enhance the conjugation of phenolic drugs with sulfate and to treat hypercalcemia. It is thought that sulfate in is absorbed slowly and incompletely from the digestive tract. The purposes of this investigation were to determine the absorption of large amount of sodium sulfate (18.1 g as the decahydrate, equivalent to 8.0 g of the anhydrous salt) and to compare the bioavailability when this amount is administered orally to normal subjects as a single dose and as four equally divided hourly doses. The 72-hr urinary recovery of free sulfate following single and divided doses was 53.4 +/- 15.8 and 61.8 +/- 7.8%, respectively (mean +/- SD, n=5, p greater than 0.2). The single dose produced severe diarrhea while the divided doses caused only mild or no diarrhea. Thus, a large amount of sodium sulfate, when administered orally in divided doses over 3 hr, is well tolerated and is absorbed to a significant extent. Orally administered sodium sulfate may be useful for the early treatment of acetaminophen overdose.
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PMID:Absorption of orally administered sodium sulfate in humans. 726 5

A 36-year-old with end-stage renal disease secondary to hypertensive nephrosclerosis had a two-day history of epigastric pain and nausea. Soon after admission, multiple grand mal seizures uncontrolled by intravenous phenytoin sodium and diazepam developed. His calcium level was 14 mg/dL and his amylase level was 2,230 mg/dL; lumbar puncture was normal. Hemodialysis lowered his calcium level to 10.7 mg/dL but failed to control his seizures. Secondary hyperparathyroidism was thought to be the cause of his malignant hypercalcemia, and an emergency subtotal parathyroidectomy was performed. Postoperatively, his grand mal seizures resolved. Confusion and aphasia also developed, but they resolved over the ensuing three weeks. Microscopic examination of the parathyroid glands revealed diffuse chief cell hyperplasia. Preoperative parathormone level was 2,196 pg/dL (normal, less than 450 pg/dL). A review of the literature has failed to reveal a similar case.
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PMID:Secondary hyperparathyroidism manifesting as acute pancreatitis and status epilepticus. 728 72


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