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

The urine-concentrating mechanism was studied in chronic hypokalemia (seven dogs given a low K(+), high NaCl diet plus injections of deoxycorticosterone acetate [DOCA]) and chronic hypercalcemia (seven dogs given vitamin D). In the potassium-depleted dogs, muscle, serum, and urine K(+) fell markedly, but glomerular filtration rate (GFR) and body weight varied little. Maximum urine osmolality fell in all dogs (mean decrease = 45%); however, solute-free water reabsorption (T(CH2O)) at high rates of solute excretion remained normal in three of four dogs. Free water excretion (C(H2O)) increased normally or supranormally as a function of increasing Na(+) delivery to Henle's loop in six dogs so tested. Hypercalcemia of several weeks duration caused a decrease in both GFR (mean 36%) as well as in maximum urine osmolality (mean 57%). Maximum T(CH2O) was not invariably depressed; in fact, when the values were adjusted for the reduced number of functioning nephrons (T(CH2O)/C(In)), four of seven studies were normal. C(H20)/C(In) increased normally (or supranormally) with increasing fractional Na delivery to Henle's loop in four of five dogs.I conclude that the lowered maximum urine osmolality in these hypokalemic and hypercalcemic dogs was not related to abnormal water reabsorption from the collecting ducts. Although not specifically measured in this study, it is very likely that solute accumulation in the renal medulla was reduced. This probably was not caused by abnormal delivery of sodium to, nor reabsorption of sodium from Henle's loop. It is likely that a more subtle defect exists in the countercurrent mechanisms for establishing a steep concentration gradient in the renal medulla. In the few hypercalcemic dogs in whom GFR was very low, I believe that injury to, and blockage of medullary tubules could account for most of the reduction in maximum U(Osm). Although not specifically ruled out, there is no evidence here to suggest that high serum Ca(+) or low serum K(+) per se causes a defect in sodium and water reabsorption in the mammalian nephron.
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PMID:Urine concentration and dilution in hypokalemic and hypercalcemic dogs. 543 74

Porcine calcitonin in a slow-release gelatin vehicle was given by intramuscular injection to 10 patients-four with primary hyperparathyroidism, four with Paget's disease, and two with carcinoma of the breast and hypercalcaemia. All cases showed a fall in serum calcium with an immediate rise in urine calcium. All except three patients with primary hyperparathyroidism showed a fall in serum phosphorus, but an immediate rise in urine phosphorus occurred in all cases. Urine hydroxyproline output fell in three patients with severe Paget's disease. Urine sodium rose in all cases, but the effects on potassium, magnesium, water, and pH were not appreciably different from results obtained in four control subjects who were given the gelatin vehicle alone.The data suggest that calcitonin caused a decrease in the tubular resorption of calcium and phosphorus. The hypocalcaemic effect appeared to be due to a decrease in bone resorption in the patients with Paget's disease but in the remaining cases could be accounted for in part or entirely by the rise in urine calcium.
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PMID:Renal effects of calcitonin. 546 Aug 39

Two elderly patients suffering from manic-depressive psychosis/depressive reaction had concurrently hypercalcaemia from vitamin D intoxication. They developed hypernatraemia with severe potassium and water depletion. Hypercalcaemia was pronounced, but both patients recovered quickly and their depressive symptoms resolved following water and potassium repletion and corticosteroid therapy.
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PMID:Vitamin D intoxication, with hypernatraemia, potassium and water depletion, and mental depression. 572 27

Significant alterations in the structure and functions of the kidney are caused by a number of metabolic disturbances and deficiencies of physiological substances. These include intercapillary glomerulosclerosis, gout, hypercalcemia, hereditary cystinuria, potassium depletion, pyrophosphates deficiency, vitamin D deficiency and liver disorders. Some of these metabolic disorders are secondary to drug ingestion.
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PMID:Renal disease secondary to metabolic disorders or physiological deficiency states. 604 89

Reduced concentrating and diluting capacity of the kidney in acute and chronic hypercalcemia may partly be due to inhibition of transcellular sodium reabsorption (RNa) in the thick ascending limb of Henle's loop. To examine this hypothesis, local heat production and RNa were measured during normo- and hypercalcemia at comparable glomerular filtration rate (GFR) in volume expanded, anesthetized dogs. Changes in proximal RNa which might occur during CaCl2 infusion, were minimized by infusing acetazolamide (75 mg/kg body wt iv). When ultrafiltrable calcium was increased from 1.12 +/- 0.09 to 2.95 +/- 0.10 mmol/l, cortical heat production was unchanged, whereas outer medullary heat production fell by 32 +/- 4%. RNa was reduced by 32 +/- 6%. Bicarbonate reabsorption did not change but calcium reabsorption and potassium excretion increased significantly. The potassium content of cortex and outer medulla increased during hypercalcemia, whereas ouabain, an inhibitor of Na+, K+-ATPase reduces the potassium content. We conclude that hypercalcemia does not inhibit transcellular RNa in the diluting segment by a direct effect on the Na+, K+-ATPase or the mitochondria, but by interfering with the coupled NaCl transport across the luminal cell membrane.
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PMID:Inhibition of transcellular NaCl reabsorption in dog kidneys during hypercalcemia. 609 15

Pharmacological treatment of hypertension can cause clinically significant alterations in endocrine function through effects on glucose homeostasis, thyroid and parathyroid hormones, adrenal steroid metabolism and reproductive/pituitary physiology. Long term use of thiazide diuretics causes deterioration in glucose tolerance, probably secondary to potassium depletion. Hypoglycaemic complications of beta-blockers (mainly the non-selective compounds) can be dramatic, especially in type I diabetics. Clonidine, diazoxide and calcium antagonists have all been associated with deterioration in glucose tolerance and their long term use should be avoided in type II diabetics if possible. Propranolol lowers T3 levels by decreasing the conversion of T4 to T3. Prazosin causes elevations in T4 and thyroid-stimulating hormone, while sodium nitroprusside use may result in hypothyroidism. Numerous agents are associated with sexual dysfunction, including methyldopa, reserpine, clonidine and spironolactone. Thiazide diuretics may cause hypercalcaemia, particularly in patients with hyperparathyroidism, by decreasing urinary calcium as well as directly influencing bone and gut calcium handling. Conversely, propranolol may decrease circulating parathyroid hormone levels and correct the hypercalcaemia seen in hyperparathyroidism. Awareness of drug-induced changes in endocrine function will facilitate the rational management of the hypertensive patient.
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PMID:Effects of antihypertensive drugs on endocrine function. 614 2

Severe hypokalemia (2.6 mEq/l), hypomagnesemia (0.6 mg/dl), mild hypercalcemia (10.9 mg/dl), and secondary hyperaldosteronism developed in a patient receiving viomycin for pulmonary tuberculosis. Reversible renal wasting of both potassium (K+) and magnesium (Mg++) was documented. Viomycin administered to 40 rats resulted in severe damage to the proximal tubule and mild damage to the distal tubule. THe case report and experimental data suggest viomycin induces proximal tubule dysfunction that results in renal wasting of sodium, K+ and Mg++ and secondary hyperaldosteronism. Hypercalcemia, not previously associated with viomycin therapy, may be secondary to hypomagnesemia-induced hyperparathyroidism.
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PMID:Viomycin-induced electrolyte abnormalities. 626 92

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

Two patients with both primary hyperparathyroidism and primary hyperaldosteronism are described. Each presented with high blood pressure and a history of renal calculi. Mild hypercalcaemia was associated with raised plasma parathyroid hormone concentrations and a parathyroid adenoma was excised from each. Both patients also had hypokalaemia, hyperaldosteronism and low plasma renin concentrations. Quadric analysis, adrenal vein plasma aldosterone concentrations, adrenal venography and CT scanning all suggested an adrenal adenoma in each patient. This suspicion was confirmed at operation in one patient; the other patient is unfit for adrenal surgery but her blood pressure and plasma potassium concentration have remained within the normal range during prolonged treatment with either spironolactone or amiloride. Because of this unusual association a search was made for parathyroid hormone excess in patients with primary hyperaldosteronism and for aldosterone excess in primary hyperparathyroidism. None was found.
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PMID:Primary hyperparathyroidism associated with primary hyperaldosteronism. 634 7

To evaluate the efficacy and safety of a simple approach to intravenous phosphorus therapy, we prospectively studied ten adult patients with severe hypophosphatemia (less than or equal to 1 mg/dl), two or more clinical reasons for the hypophosphatemia, and normal renal function. They were treated with a solution containing 0.32 mmol of phosphorus per kilogram of body weight. This amount of phosphorus was infused intravenously over 12 hours and repeated every 12 hours until the serum phosphorus was greater than or equal to 2 mg/dl. The serum phosphorus, potassium, magnesium, and calcium levels were measured at six hours, 12 hours, and every 12 hours thereafter. The serum phosphorus level was greater than or equal to 2 mg/dl in one patient at six hours, three patients at 12 hours, three patients at 24 hours, four patients at 36 hours, and one patient at 48 hours. The serum calcium was measured every 12 hours and at no time was any patient dangerously hypocalcemic. Administration of 0.32 mmol of phosphorus per kilogram of body weight intravenously over a 12-hour period is both efficacious and safe in severely hypophosphatemic patients with multiple causes of hypophosphatemia, normal renal function, and no hypercalcemia.
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PMID:High-dose intravenous phosphorus therapy for severe complicated hypophosphatemia. 663 36


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