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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifteen cases of hypervitaminosis D in childhood are reviewed. In all of them, vitamin D was given following medical prescription. In four occasions, excessive dosage of vitamine D impaired the evolution of a previous nephropathy. The clinical, analytical, radiological and histological findings as well as the therapeutical aspects are commented. Hypercalcemia, hypercalciuria, polyuria with hypostenuria, renal failure, bone lesions and nephrocalcinosis are the most prominent features of the picture. Occasionally, arterial hypertension and glycosuria were found. Prednisone, thyrocalcitonine and phosphates were used as therapeutical means. In spite of nephrocalcinosis and renal failure generally present at diagnosis, the clinical course was rather good.
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PMID:[Hypervitaminosis D. Review of fifteen cases]. 44 41

We report a 14-year-old boy with severe hypertension who was cured by surgical removal of a pheochromocytoma. The tumor was shown biochemically and morphologically to secrete predominantly noradrenaline. The metabolic effects noted in this patient were raised free fatty acid levels and depressed insulin levels, hyperreninemia, hypercalcemia, and hypercalciuria with normal parathyroid function. All these abnormalities returned to normal after removal of the tumor. It is suggested that these effects were mediated via beta-adrenergic stimulation of the excess noradrenaline.
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PMID:The metabolic effects of excess noradrenaline secretion from a pheochromocytoma. 90 78

Renal disease was detected in 21 of 56 progeny from a specific line of inbred Norwegian Elkhound (NE) dogs. Results of hematologic and clinical chemistry examinations revealed that minor differences existed between affected and nonaffected NE dogs. Of 21 NE dogs with renal disease, 3 had persistent glucosuria without hyperglycemia. The 21 affected dogs had impaired ability to concentrate urine. According to renal function tests, glomerular filtration rate of normal NE dogs was less than that of normal mixed breed dogs. Although a few affected NE dogs excreted large amounts of amino acids in urine, statistically significant differences did not exist between normal and affected NE dogs with regard to alpha-amino acid nitrogen content of their plasma or urine. By paper chromatographic separation techniques, free amino acids of plasma, urine, and extracts of liver and kidney were not qualitatively different for mixed breed dogs, normal NE, and NE with renal disease. Statistically significant differences were not detected between serum calcium concentrations of normal and affected NE dogs. In NE dogs with renal disease, there was significant hypercalciuria, but a few normal dogs excreted more than did some dogs with disease. Blood pressure values of normal mixed breed dogs and affected NE dogs were similar. It was concluded that hematologic and blood chemical abnormalities, derangement of amino acid or calcium metabolism, and hypertension were not associated with renal disease in these NE dogs.
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PMID:Familial renal disease in Norwegian Elkhound dogs: physiologic and biochemical examinations. 94 38

Despite the bewildering number of diuretics available to the physician, these drugs can be divided into 4 main groups, characterised by their site of action on sodium reabsorption in the kidney. Drugs acting on the ascending limb of the loop of Henle have a powerful but short acting diuretic effect; they include frusemide, ethacrynic acid and bumetanide. The benzothiadiazines and related compounds have a moderate diuretic action spread over a longer period, whilst the potassium-sparing diuretics, triamterene, amiloride and spironolactone, have only a weak diuretic effect but a marked ability to diminish urinary potassium excretion. The fourth group is made up of miscellaneous substances which function as vasodilator or osmotic agents. The pathogenesis of oedema formation in heart failure is outlined and a logical approach to treatment suggested. Duiretics are being increasingly used in the treatment of non-oedematous states, in particular hypertension, diabetes insipidus and hypercalciuria; their exact role in pregnancy and acute renal failure remains controversial. Side-effects can be related to their effect on electrolyte excretion and include hypokalaemia, hyponatraemia, hyperkalaemia and hyperuricaemia. The incidence of disturbed carbohydrate tolerance in previously normal individuals is low. Other less common side-effects are also discussed.
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PMID:Diuretics: mechanism of action and clinical application. 109 41

A 52 year old man with a long history of marked hypertension, peptic ulcer disease, nephrocalcinosis and intermittent hypercalcemia was referred to be evaluated for primary aldosteronism suspected on the basis of low plasma renin activity, hypokalemia and blood pressure responsive to spironolactone. Aldosterone excretion, however, was extremely low. Alkaluria, high urinary sodium excretion and hypercalciuria were observed. The patient admitted to chronic ingestion of large amounts of baking soda. Upon cessation of alkali abuse, his blood pressure fell dramatically; orthostatic hypotension, concomitant azotemia, hemoconcentration, hyperkalemia and weight loss occurred. Despite dramatic elevation in plasma renin activity, urinary aldosterone excretion remained low during this period. Adrenal glucocorticoid secretion was intact. All abnormalities of sodium, potassium and aldosterone subsequently returned to normal. A 10 day challenge with oral sodium bicarbonate was associated with a rise in blood pressure, but serum calcium remained normal. The patient remains normotensive 15 months after discontinuing alkali abuse.
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PMID:Hypertension corrected by discontinuing chronic sodium bicarbonate ingestion. Subsequent transient hypoaldosteronism. 111 72

Diuretics act primarily by blocking reabsorption of sodium at four major sites in the nephron. Clinically useful agents that block sodium reabsorption effectively in the proximal tubule are lacking. Furosemide (Lasix), ethacrynic acid (Edecrin), and possibly organomercurial agents are effective in the ascending limb of Henle's loop. Thiazides are the major agents acting in the early distal tubule. In the late distal tubule and collecting duct, spironolactone (Aldactone) and triamterene (Dyrenium) are useful, especially in combination with diuretics which act more proximally. In treating edematous states, initial therapy with thiazides is effective in most patients who do not exhibit moderate or severe renal insufficiency, severe hyperaldosteronism with excessive distal reabsorption of sodium in exchange for potassium, or excessive sodium reabsorption in the proximal tubule or ascending limb. Nonedematous states in which diuretic therapy is useful include hypertension, hypercalcemia, hypercalciuria, diabetes insipidus, and acute renal failure.
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PMID:Diuretic agents. Mechanisms of action and clinical uses. 126 95

Renal ultrasound examination, performed following a urinary tract infection in a 4.5-year-old girl with triple X syndrome, showed multiple echogenic foci at the corticomedullary junction in both kidneys. She was asymptomatic but had hypertension with echocardiographic evidence of left ventricular hypertrophy. Computerised tomographic scan revealed foci of calcification in the kidneys, spleen and pancreas. On biopsy calcification was found in the internal and external elastic laminae of the superficial temporal artery and in the internal elastic lamina of a renal arcuate artery. Intimal fibrosis was mild and focal. No other arterial calcification was demonstrated radiographically or by ultrasound. Biochemical and hormonal profiles revealed no abnormality except hypercalciuria. The aetiology and prognosis of this child's condition are unknown. Although similar ultrasound and histological appearances have been described in pseudoxanthoma elasticum and in idiopathic arterial calcification of infancy, there is no evidence that the child has either of these conditions.
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PMID:Hypertension associated with diffuse small artery calcification: a case report. 148 46

To assess a possible heritability of a disturbed calcium metabolism in relation to blood pressure regulation, 28 young normotensive offspring of either hypertensive or normotensive parents were studied while administered a defined diet with daily sodium chloride of 6 and 20 g/day for 7 days each. Before the high salt diet was begun, the cytosolic calcium concentration ([Ca2+]i) in platelets was elevated in offspring of hypertensive parents, whereas serum electrolytes, plasma renin activity, plasma catecholamines, and 24-hour urinary excretion of sodium and calcium showed no difference between the two groups. On exposure to a high salt diet, the mean blood pressure increased (from 80 +/- 2 to 85 +/- 2 mm Hg, p less than 0.05) in offspring of hypertensive parents. These changes in mean blood pressure were positively correlated with the basal platelet [Ca2+]i (r = 0.61, p less than 0.01), whereas [Ca2+]i did not demonstrate any significant changes. When the subjects were administered the high salt diet, plasma ionized calcium decreased (from 2.37 to 2.21 meq/l, p less than 0.05) and 1,25-dihydroxyvitamin D3 increased (from 32.7 to 40.8 pg/ml, p less than 0.05) with a transient relative hypercalciuria in offspring of hypertensive parents. This increase of 1,25-dihydroxyvitamin D3 was significantly correlated with the changes in mean blood pressure (r = 0.62, p less than 0.01). Disturbed intraplatelet and systemic calcium metabolism may be of predictive value in the development of hypertension.
Hypertension 1992 Jun
PMID:Disturbed calcium metabolism in offspring of hypertensive parents. 159 47

Recent research provides evidence that parathyroid hormone is implicated in the pathogenesis of genetic hypertension. Abnormalities in calcium metabolism in genetic hypertension have been reported. These include hypercalciuria, depressed serum ionized calcium associated with enhanced serum parathyroid hormone levels. Calcium supplement resulted in normalization of calcium metabolism and reduction in blood pressure. In addition, removal of parathyroid glands attenuated the rise in blood pressure in genetic hypertensive rat. This review focuses on the links between calcium metabolism and calcium endocrine system abnormalities and the etiology of experimental genetic hypertension. The mechanisms by which dietary supplement and parathyroidectomy lower genetic hypertension are also discussed. Although the causality of raised parathyroid hormone in genetic hypertension is not yet fully understood, we conclude that this hormone may play a permissive effect in the development of hypertension.
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PMID:Parathyroid hormone and genetic hypertension. 161 92

Urinary excretion of sodium and calcium was examined in hypertensive (n = 8) and normotensive (n = 7) subjects following infusion of 2% saline at a rate of 11 mL/min for 90 min. The urinary sodium excretion was 204 +/- 38 (mean +/- SEM) muEq/min in normotensives and 233 +/- 28 muEq/min in hypertensives before infusion of saline and increased maximally to 499 +/- 114 muEq/min (P less than .05) and to 928 +/- 68 muEq/min (P less than .01), respectively, after saline infusion. In normotensives, urinary calcium excretion did not change significantly; however, in hypertensives excretion increased markedly (P less than .01) from 6.1 +/- 0.7 muEq/min to 12.3 +/- 1.6 muEq/min. Plasma atrial natriuretic peptide (ANP) levels increased significantly (P less than .05) in both groups. Serum ionized calcium and plasma parathyroid hormone (PTH) levels did not change significantly. The increments of urinary sodium and calcium and of plasma ANP, as well as the preinfusion plasma PTH level, were significantly (P less than .05) higher in hypertensives than in normotensives. The present study showed that exaggerated natriuresis was accompanied by hypercalcinuria and an enhanced rise in plasma ANP in hypertensives. Basal levels of plasma PTH were elevated in hypertensives. The calcium deficiency may be attributable to a close relationship between urinary sodium and calcium, and causally related to the disturbance of sodium and volume homeostasis in hypertension, which results in exaggerated natriuresis.
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PMID:Effect of saline infusion on urinary calcium excretion in essential hypertension. 182 96


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