Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The association of hypercalciuria, salt losing renal disease, and a defect in urine concentrating ability with high renin and aldosterone levels is described in two brothers. One child had marked nephrocalcinosis by the age of 3 and the other severe growth retardation. In one child all the abnormalities were abolished with indomethacin which was responsible for a marked decrease in urinary. The data and the family study suggest that this condition is a proximal tubular disorder with atuosomal recessive inheritance.
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PMID:[Familial tubulopathy associating hypercalciuria and saline diabetes. Favorable results of indomethacin therapy]. 48 70

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

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.
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PMID:Disturbed calcium metabolism in offspring of hypertensive parents. 159 47

To test the hypothesis that hyperfiltration in essential hypertension is linked to alterations in calcium metabolism, we studied the relationship between urinary calcium excretion and glomerular filtration rate (GFR, creatinine clearance) in 38 untreated essential hypertensives on a free diet. We also studied the influence of changes in calcium intake on GFR in 30 essential hypertensives (15 with well-defined hypercalciuria and 15 with normal urinary calcium excretion) and in 11 normotensive healthy subjects. In the patients on a free diet, urinary calcium excretion was directly and independently related to GFR (r = 0.56, P less than .001), while serum calcium showed an opposite trend (r = -0.27, P = .12). In patients on fixed calcium diets, GFR was significantly higher (P = .008) at low calcium intake (115 +/- 31 mL/min/1.73 m2) than at high calcium intake (98 +/- 22 mL/min/1.73 m2). Further analysis showed that the hyperfiltering effect of low calcium almost exclusively occurred in hypercalciuric patients and in hypertensive women. In hypercalciuric hypertensives there was a highly significant inverse correlation between GFR and serum calcium (r = -0.51, P = .004) and a similar correlation between GFR and plasma renin activity (r = -0.70, P = .003) in the high calcium phase of the study. Changes in calcium intake had no influence on GFR in normal subjects (Low Ca 103 +/- 22 mL/min/1.73 M2, High Ca 110 +/- 23 mL/min/1.73 m2). The data indicate that alterations in calcium metabolism interfere to an important extent with mechanism(s) regulating GFR in essential hypertension.
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PMID:Hyperfiltration and calcium metabolism in essential hypertension. 181 51

Several abnormalities of calcium metabolism have been described in patients with essential hypertension, and they have been linked to the pathogenesis of hypertension. Intestinal calcium absorption has been shown to be decreased in rats with spontaneous hypertension, but it has not been studied in patients with essential hypertension. In these studies we have for the first time measured intestinal absorption of calcium (using oral and intravenous administration of 47Ca), along with other parameters of calcium metabolism, in 14 patients with essential hypertension and normal renal function and in 16 normal subjects. There was no difference in serum total or ionized calcium, serum phosphorus, parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D), and 24,25-dihydroxy-vitamin D(24,25(OH)2D) among hypertensives and normotensives. The urinary excretion of calcium, on the other hand, was greater in hypertensive than in normotensive subjects (195 +/- 33 v 107 +/- 13 mg/24 h, P less than .05). There was also no difference in intestinal absorption of calcium after 2 and 24 h among hypertensives and normotensives. When hypertensive patients were stratified according to plasma renin activity (PRA) we found that patients with low PRA had higher intestinal absorption of calcium at 2 h (23 +/- 2.9 v 18 +/- 0.6%, P less than .05) but not at 24 h. Serum total and ionized calcium, PTH, and 1,25(OH)2D were not different between patients with low and those with normal-high PRA. The major derangement of calcium metabolism in patients with essential hypertension is hypercalciuria. This abnormality is more pronounced in patients with low PRA, and it may lead to increased vitamin D-dependent intestinal absorption of calcium.
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PMID:Intestinal absorption of calcium and calcium metabolism in patients with essential hypertension and normal renal function. 206 73

Various studies have shown that a high protein (HP) diet, compared to a low protein (LP) diet, leads to hypercalciuria and alterations in renal and systemic hemodynamics. The authors compared the effects of HP diet to those of normal protein diet (NP) to determine the possible mechanisms by which changes in systemic hemodynamics and hypercalciuria occurred. The studies were conducted in awake rats; the effects of dietary sodium content on the changes induced by HP also were evaluated. The relationship of prostaglandins (PG), renin (PRA), and aldosterone (PA) to changes in blood pressure (BP) was assessed. Two weeks after HP and normal sodium feeding (40%), glomerular filtration rate (GFR) and urine flow (V) were not different from the same values in a group on an NP diet (23%). When HP was fed with low sodium, there was a rise in V as a consequence of greater fluid intake. Although plasma calcium remained constant, the hypercalciuria correlated with high protein and sodium content. Alterations in 1,25(OH)2 vitamin D3 or PTH (cyclic AMP excretion) function did not explain the hypercalciuria induced by HP. This suggests that HP leads to inhibition of tubular calcium reabsorption by mechanism(s) yet to be elucidated. Although HP did not alter GFR, it led to an increase in BP, a fall in renal vascular resistance, and an increase in RPF, regardless of sodium intake. PRA and urine PGE2 excretion were significantly higher in the rats on HP diet, whereas PA remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal and systemic effects of short-term high protein feeding in normal rats. 254 89

The immature kidney may be adversely affected by a variety of vasoactive or diuretic drugs, either administered to the mother during pregnancy, or to the neonate. Inhibitors of the angiotensin-converting enzyme administered to the hypertensive pregnant woman can severely and sometimes definitely impair renal function in the fetus, leading to postnatal anuria. Pathogenesis involves interference with the renin-angiotensin system and the prostaglandins. Beta-adrenergic agents administered during labor depress glomerular filtration rate transiently. Tolazoline, an alpha-adrenergic blocking agent useful in the treatment of persistent pulmonary hypertension of the neonate induces intense renal vasoconstriction with consequent hypoperfusion. Indomethacin, a prostaglandin synthetase inhibitor used for the pharmacological closure of a patent ductus arteriosus, also increases renal vascular resistance, and decreases urine output. Furosemide, the drug most often used in oliguric neonates, may also adversely affect the newborn infant. Its use has been associated with an increase in the incidence of patent ductus arteriosus, hypercalciuria, nephrocalcinosis and secondary hyperparathyroidism. These observations demonstrate that the proper use of drugs requires that the therapeutic endpoint be clearly defined and the predictable side effects be anticipated.
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PMID:Adverse effects of drugs on the immature kidney. 290 Dec 76

The case of a two month-old child admitted because of dystrophy is presented. At physical examination she presented a growth retardation (-2DS) as well as cutaneous and mucosal pallor. Metabolic acidosis, hyponatremia, hyperkaliemia and salt loss were demonstrated. Aldosterone, both plasmatic and urinary, was increased. Plasma renin activity, was also increased. In respect to renal function, hypercalciuria was found but not other abnormalities neither in the renal nor suprarrenal function were noticed. The electrolytic levels in sweat, saliva and feces were also normal. The clinical and laboratory findings were not modified with the DOCA test. Spirolactone caused an increase in salt loss. Treatment with indometacine improved both the clinical and analytical findings. On the other hand, treatment with chloride sodium (4 gr p.o. per day) also improved dramatically the disturbances. In the last 12 months she has growth up normally. At the same time, the renal loss of sodium has decreased and aldosterone, both plasmatic and urinary, is not so increased as it was at diagnosis. Finally, electrolytic parameters are fully normal.
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PMID:[Review of pseudohypoaldosteronism. Apropos of a clinical case in a 2-month-old girl]. 639 46

An 8-year-old boy presented with precocious puberty and hypertension. He had hypokalemia, increased serum aldosterone and testosterone levels and low plasma renin activity. An adrenal adenoma was found using imaging methods and was removed. Postoperatively aldosterone, testosterone and blood pressure returned to normal. Renal ultrasonography findings were consistent with nephrocalcinosis, which might be explained by long lasting hypokalemic metabolic alkalosis and hypercalciuria. Precocious pseudopuberty progressed into true puberty due to the maturational effect of testosterone. Nephrocalcinosis was still present 8 years later and hypertension was recurring obviously as a consequence of increased peripheral resistance.
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PMID:Aldosterone and testosterone producing adrenal adenoma in childhood. 775 88

Sodium chloride deficiency (SCD) was observed within the 1st year of life in 12 of 46 cystic fibrosis (CF) patients between July 1989 and September 1992. All patients showed sweating, loss of appetite, fever, vomiting, irritation, dehydration, weakness, and cyanosis during an attack. Mean plasma sodium, potassium and chloride levels were 122.9 (range 106-135), 2.5 (range 1.6-3.5), and 73.3 (range 60-90) mEq/l respectively. Alkalosis and elevated plasma renin activity were detected in all patients. Of the patients, 50% showed microscopic haematuria, and hypercalciuria was detected in two out of four patients. Low urinary sodium and high urinary potassium were observed in the four examined patients. Increased creatinine, BUN and uric acid values returned to normal with treatment. All the patients were treated initially with intravenous fluids and electrolyte solutions. All patients were less than 7 months of age during the first attack, five received only breast milk and the others breast milk with formula milk. Their oral salt supplement was 2-4 mEq/kg per day, which is recommended for CF patients, but could be deficient in excessively sweating infants. The genotype of these patients might be cause of high salt losses. F508 is the most common mutation with the frequency of 38% in our CF patients with SCD, but the frequency of unknown mutations is high (54%).
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PMID:Sodium chloride deficiency in cystic fibrosis patients. 784 98


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