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

In a retrospective study of 120 patients with surgically proved primary hyperparathyroidism, 71 patients who were normotensive and 49 patients (41 percent) who were either hypertensive at the time of parathyroidectomy or had a history of hypertension were compared. The mean serum calcium levels in the normotensive and hypertensive patients were very similar (11.6 +/- 0.1 [SEM] mg/dl, and 11.8 +/- 0.1), ruling against the hypothesis that hypercalcemia per se is the dominant cause of the hypertension of hyperparathyroidism. The mean serum creatinine levels in the two groups were also very similar (1.02 +/- 0.05 and 1.09 +/- 0.05 mg/dl), indicating that the hypertension of hyperparathyroidism is not the consequence of advanced renal parenchymal damage. The hypertensive patients did not have a significantly higher prevalence of urolithiasis. A review of the data in this and related studies leads to the conclusion that the hypertension of hyperparathyroidism is heterogeneous in origin. The mean serum phosphate level in the hypertensive patients was significantly lower than that in the normotensive patients (2.20 +/- 0.06 mg/dl versus 2.69 +/- 0.09 mg/dl, p less than 0.02), which may be due to a decrease in renal tubular phosphate reabsorption secondary to hypertension.
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PMID:Hypertension and hyperparathyroidism. Inverse relation of serum phosphate level and blood pressure. 685 80

A patient with hypertension and chronic renal disease was evaluated for hypercalcemia and hypophosphatemia. Serum parathyroid hormone and urine nephrogenous cyclic adenosine monophosphate levels were both elevated. Absolute and fractional urine excretion of calcium was low, thereby raising the suspicion of hypocalciuric hypercalcemia. Surgical removal of a parathyroid adenoma led to normalization of the serum calcium, and phosphate values associated with the complete absence of calcium from the 24-hour urine collection returned to normal.
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PMID:Hypocalciuric hyperparathyroidism with chronic renal failure. 687 85

1. The effect of acute hypercalcaemia on blood pressure, blood volume, haemodynamic indices, plasma catecholamines, renin and aldosterone levels was investigated in 10 patients. 2. Calcium infusion (15 mg/kg over 3 h) increased (P < 0.05) plasma calcium and adrenaline levels, blood pressure, total peripheral resistance and packed cell volume. Plasma volume was decreased, and heart rate, cardiac output and plasma renin, aldosterone or dopamine levels were not significantly changed. Plasma noradrenaline was increased only minimally after 3 h of calcium infusion. 3. Mean blood pressure before and during calcium infusion correlated with concomitant serum calcium (r = 0.39; P < 0.02) or adrenaline levels (r = 0.57; P < 0.01); changes in blood pressure correlated with variations in plasma adrenaline (r = 0.68; P < 0.001). 4. Acute hypercalcaemic hypertension is mediated by an increase in peripheral vascular resistance and may be induced by a direct effect of calcium on blood vessels. The calcium-mediated increase in adrenaline release may play a contributory, and plasma volume contraction an inhibitory, role.
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PMID:Role of haemodynamics, catecholamines and renin in acute hypercalcaemic hypertension in man. 700 29

The effect of acute hypercalcemia on blood pressure, blood volume, hemodynamic parameters, plasma norepinephrine, epinephrine, dopamine, renin, and aldosterone concentrations was investigated. After 1 hour of equilibration, 10 patients received an infusion of calcium gluconate in 5% dextrose (calcium 15 mg/kg of body wt in 3 hours). The calcium infusion increased the mean serum calcium from 8.7 to 13.0 mg/dl, the systolic blood pressure from 144 +/- 10 to 184 +/- (SEM) 12 mm Hg (P less than 0.001), the diastolic pressure from 78 +/- 4 to 93 +/- 5 mm Hg (P less than 0.01). The plasma volume was decreased by 9% (P less than 0.001), whereas the hematocrit was increased (P less than 0.05). Heart rate and cardiac output remained unchanged. Total peripheral resistance was increased from 1643 +/- 223 to 2256 +/- 387 dyne.sec/cm5 (P less than 0.05). The plasma epinephrine concentration rose from 4.5 +/- 0.7 to 6.9 +/- 1.2 ng/dl (P less than 0.01). The plasma norepinephrine concentration was unchanged after 2 hours and increased only slightly after 3 hours of calcium infusion. Plasma renin, aldosterone, and dopamine concentrations were not significantly changed. These findings demonstrate that acute hypercalcemic hypertension is mediated by an increase in peripheral vascular resistance. Hypercalcemic hypertension may be induced by a direct effect of calcium on blood vessels; calcium-mediated increase in adrenal epinephrine release may play a mild contributory role, and plasma volume contraction, an inhibitory role.
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PMID:Acute hypercalcemic hypertension in man: role of hemodynamics, catecholamines, and renin. 702 19

A 38-year-old woman with hypercalcemia, severe hypertension, and high renin levels was treated with the angiotensin-converting enzyme inhibitor captopril. This therapy, together with spironolactone, normalized blood pressure (BP), but even with three daily administrations of the converting enzyme inhibitor, intermittent rebound hypertension could not be avoided. The administration of only verapamil, an antagonist of calcium transport, did not induce BP control, but when verapamil therapy was combined with administration of captopril and spironolactone, BP could be normalized with only twice-daily administration of the converting enzyme inhibitor. Thus, high plasma calcium levels seem to sensitize the arterioles to the intermittent increase of angiotensin II levels that accompanies captopril therapy.
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PMID:Hypertension in a patient with hypercalcemia: captopril and verapamil. 703 43

Persistent hyperparathyroidism and its attendant hypercalcemia have been implicates as possible etiologic factors in posttransplant hypertension. To better define the role of parathyroid hormone (PTH) and calcium in posttransplant blood pressure homeostasis, we measured the acute response of blood pressure, ionized calcium (Ca++), plasma renin activity (PRA), and parathyroid hormone (PTH) to a 4-hr infusion of calcium (15 mg/kg) and an isoproterenol injection (0.15 mg SC) in seven normal subjects and 13 renal transplant (Tx) recipients with stable graft function and persistent hyperparathyroidism. Transient hypercalcemia produced a significant (p less than 0.01) increase in the systolic blood pressure (delta SBP) and suppression of PTH (p less than 0.001) in the posttransplant subjects. There was a significant (p less than 0.02) inverse correlation between changes (delta) in PTH and delta SBP in these subjects. There was no correlation between the delta SBP and either the change in Ca++ (delta Ca++) or the change in PRA (delta PRA) observed in the Tx recipients administered calcium. Following isoproterenol administration, SBP increased (p less than 0.01), PTH fell (p less than 0.05) and Ca++ was only minimally increased in the Tx recipients. A virtually identical, significant (p less than 0.05) inverse correlation existed between the delta PTH and delta SBP observed in the transplant subjects. Greater suppression of PTH was associated with a larger increase in systolic blood pressure. Transient hypercalcemia of comparable degree in normal subjects caused an insignificant increase in their blood pressure. The fact that PTH suppression in the normals was substantially (0.01) less (delta PTH -13 microliter/Eq/ml versus -65 microliter/Eq/ml in the transplant group) with a similar increase in serum calcium suggests that the blood pressure response to transient hypercalcemia is more dependent on PTH suppression than the level of ionized calcium. Plasma renin activity was unchanged during the blood pressure fluctuations induced by either the calcium or the isoproterenol administration to the normal subjects. Under the conditions of this study, endogenous parathyroid hormone has the characteristics of a vasodepressor hormone and may have a role in blood pressure regulation in transplant recipients with hyperparathyroidism. Since the vasodepressor effect can be dissociated from delta Ca+ and delta PRA, such a conclusion seems warranted. The implications of these findings for all subjects with renal disease requires further investigation.
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PMID:Parathyroid hormone: a determinant of posttransplant blood pressure regulation. 703 14

Neoplasia-induced hypercalcemia in the Fischer rat results in hypertension 1 wk after Leydig cell tumor transplantation. Systolic blood pressure, plasma catecholamine, prolactin, plasma renin activity (PRA), and aldosterone responses to immobilization stress were evaluated in Fischer rats 10 days after tumor transplantation and in age-matched nontransplanted controls. Basal systolic blood pressure, norepinephrine, and PRA levels at 10 days after tumor transplantation were higher in association with elevated calcium levels in tumor-transplanted rats than in controls. Systolic pressure, norepinephrine, and epinephrine responses to immobilization stress were greater in the hypercalcemia 10-day transplanted rats. Although basal levels of prolactin and aldosterone were similar in the two groups. These observations suggest that elevated levels of the vasoactive hormones norepinephrine and angiotensin may play a pivotal role in development of hypertension in association with neoplasia-induced hypercalcemia. Further, neoplasia-induced hypercalcemia in the Fischer rat is associated with a relative hyperreninemic hypoaldosteronism state.
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PMID:Hormonal changes associated with hypertension in neoplasia-induced hypercalcemia. 704 41

To elucidate the pathophysiology of elevated blood pressure in hypercalcemic patients, we studied the plasma concentration of catecholamines and their major metabolites (as an index of sympathetic function) and the blood pressure response to norepinephrine infusion (vascular reactivity) in patients with primary hyperparathyroidism, in patients with primary hypertension, and in normal controls. In addition, we evaluated the hemodynamic response to calcium infusion in normotensive and hypertensive subjects. Plasma levels of both norepinephrine and epinephrine and the metabolites normetanephrine and dihydroxyphenyl-glycol were significantly higher in the hypercalcemic group than in the other two groups. Norepinephrine infusion increased blood pressure by 8.5 +/- 1.4 mm Hg in the control group, by 19 +/- 2 mm Hg in the hypercalcemic group and by 29 +/- 3 mm Hg in the primary hypertensive group. Infusion of calcium produced a significant rise in both systolic and diastolic blood pressures and in peripheral resistance in the hypertensives, whereas in the normotensive group only systolic blood pressure increased, associated with a rise in cardiac output. We conclude that the observed increased activity of the sympathetic nervous system in hypercalcemia could account for the elevation in blood pressure and the enhanced vascular reactivity could explain the hypertension in some patients with primary hyperparathyroidism.
Hypertension
PMID:Sympathetic system function and vascular reactivity in hypercalcemic patients. 706 99

Hypercalcemia developed in our teen-aged patient after extended immobilization for a femoral fracture. In all patients immobilized from whatever cause, both blood pressure and serum calcium should be monitored. Since both the hypertension and hypercalcemia respond well to mobilization, every effort should be made to encourage activity as soon as possible.
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PMID:Immobilization hypercalcemia. 707 52

Sarcoidosis may involve the kidneys in several ways. Most commonly, aberrations of calcium metabolism, including hypercalcemia, hypercalciuria, and nephrocalcinosis, are responsible for the renal manifestations of sarcoidosis. Granulomatous infiltration of the renal interstitium may also produce severe derangements of renal function. Glomerulonephritis can occur with sarcoidosis, although the pathogenesis remains unclear. Besides renal insufficiency and frank renal failure, nephrotic syndrome, nephrolithiasis, hypertension, and a variety of tubular defects may complicate sarcoidosis. The sensitivity of "sarcoid nephropathy" to corticosteroids usually warrants therapeutic trial.
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PMID:Renal manifestations of sarcoidosis. 722 44


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