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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe two twin sisters in whom calcification of different arteries was detected in the first weeks of life. Transient renal insufficiency, arterial hypertension, and skeletal abnormalities were also observed. One child had anasarca and heart decompensation at birth. Prenatal infarction of one kidney had occurred in the same infant. A kidney biopsy showed calcium deposits in all the layers of the arteries. Most findings in these patients are compatible with idiopathic arterial calcification of infancy (IACI). Investigation of calcium and phosphorus metabolism revealed spontaneously receding hypercalciuria, increased intraerythrocytic calcium levels, and transient X-ray abnormalities of the long bones. Treatment initially consisted of biphosphonate and later, the calcium antagonist flunarizin. A progressive diminution of the arterial calcification was observed in the course of both treatments.
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PMID:Idiopathic arterial calcification of infancy. 200 22

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

We retrospectively reviewed 32 patients who underwent parathyroidectomy at our hospital for the last fourteen years. 1) Clinical appearance of primary hyperparathyroidism was in younger age in women. 2) In previous history or at the time of PTX, 9 patients had malignant tumors including 6 thyroid cancers, 36% of the patients with out bone related symptoms had a remarkable decrease in bone mineral content. 3) After PTX, none of patients had recurrent urolithiasis and bone mineral content of all patients was significantly increased in a short time. In addition, upper GI complaints were improved, or hypertension was partially normalized. However, renal insufficiency remained unchanged. 4) In preoperative localization study, Ultrasound sonography (US) demonstrated the best accuracy rate of 88% when only one gland was involved. US was able to detect multiple gland involvement only in 20% of 5 cases. 5) Hypercalciuria was recognized as one of the risk factors of stone formation in patients with primary hyperparathyroidism.
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PMID:[Clinical study on 32 patients who underwent parathyroidectomy at Osaka City University Hospital]. 232 20

We studied, by dietary recall, the calcium and magnesium intake in 1109 adolescents aged 14-18 years; from 128 we collected a 24-h urine sample to determine electrolyte excretion. Subjects with blood pressure greater than 90th percentile (211) did not consume less calcium or magnesium than those with blood pressure less than 50th (597). Urinary calcium excretion tended to be higher in the adolescents with the highest blood pressure, the difference being statistically significant in males. Urinary sodium excretion also tended to be higher in those adolescents with blood pressure above the 90th percentile than in those with blood pressure below the 50th percentile, the differences being statistically significant in females. A positive significant correlation was found between systolic blood pressure and both calcium and sodium excretion. Our results suggest that hypercalciuria is present in the early phase of hypertension and demonstrate that adolescents at high risk of developing hypertension consume the same amounts of calcium and magnesium as those with low blood pressure.
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PMID:Calcium intake, calcium excretion and blood pressure in adolescents in the upper decile of the distribution: the Torrejon study. 263 23

A retrospective multicentre study of 341 children with persistent/recurrent, isolated haematuria is described. The haematuria was isolated for at least 6 months at the beginning of observation. The duration of follow-up was 2-5 years in 201, 5-10 years in 119, 10-15 years in 19, and over 15 years in 2 cases. Of these patients 47.8% became symptom-free. In 18.4% the haematuria remained isolated; in 13.8% it was combined with proteinuria over 250 mg/day more than 2 years later. The occurrence of associated proteinuria increased progressively with time. It was 8.6% between the 3rd and 5th years, and 37.0% after the 5th year. Renal biopsy was performed because of the symptoms of glomerular disease in 47 cases at an average time of 12 months following the appearance of proteinuria. Proteinuria appeared after a 2-5, 5-10, 10-15 and more than 15 years follow-up period in 16, 23, 6, and 2 patients respectively; 14 of them had Alport's nephropathy. The percentage of more serious azotaemia was 1.7 (creatinine clearance: 10-50 ml/min per 1.73 m2) and 0.3 (creatinine clearance: less than 10 ml/min per 1.73 m2). Mortality was 0.58%. Most of the patients who developed severe azotaemia had persistent microscopic haematuria at the beginning. The prevalence of hypertension was only 1.2%. The time of its appearance was above 5 years in 2 and below 5 years in 2 cases. All these patients had chronic glomerulonephritis. The haematuria was associated with hypercalciuria in 19.9%. In 14.3% of the overall group of patients urolithiasis developed 2-15 years after onset. All of these had hypercalciuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term follow-up of patients with persistent/recurrent, isolated haematuria: a Hungarian multicentre study. 270

A retrospective multicentre study of 341 children with persistent/recurrent, isolated haematuria is described. The haematuria was isolated for at least half a year in the beginning of observation. 47.8% of the patients became symptom-free. In 18.4% the haematuria remained isolated, in 13.8% it was combined with greater than 250 mg/day proteinuria greater than 2 years later. The occurrence of associated proteinuria was 8.6% between the 3rd to fifth years, and 37.0% after the 5th years. 14 cases had Alport's nephropathy. The percentage of more serious azotaemia was 1.7 (Ccreat: 10-50 ml/min/1.73 m2) and 0.3 (Ccreat: less than 10 ml/min/1.73 m2). Mortality was 0.58%, rate of hypertension 1.2%. Most of the patients who developed severe azotaemia, had persistent microscopic haematuria in the beginning. The haematuria was associated with hypercalciuria in 19.9%. In 14.3% of the overall group of patients urolithiasis developed 2-15 years after onset. All of them had hypercalciuria. Our findings suggest that symptoms of isolated haematuria may last for a long-term period and need systematic control. When proteinuria and/or hypertension associates to haematuria a worse prognosis can be expected.
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PMID:[Long-term follow up of chronic recurrent isolated hematuria]. 274 57

A 14-year-old boy with the syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate (Gordon's syndrome) is described. The patient's clinical symptoms consisted of periodic paralysis, slight metabolic acidosis of the proximal type and hypercalciuria. Prostaglandin excretion was normal. Infusion of atrial natriuretic peptide had no effect on electrolyte excretion or glomerular function although a normal increase in cyclic guanosine monophosphate was demonstrated in plasma and urine. This lack of sensitivity to atrial natriuretic peptide offers a new pathophysiological concept in this syndrome. Treatment with hydrochlorothiazide was successful in this case.
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PMID:The syndrome of hypertension and hyperkalaemia with normal glomerular function (Gordon's syndrome). A pathophysiological study. 297 68

In rats given desoxycorticosterone (DOC), the recently reported finding that a normal amount of dietary sodium chloride (NaCl) induces hypertension but an equimolar amount of sodium bicarbonate (NaHCO3) does not, might be a consequence of the differing effects of the two sodium salts on the metabolism of calcium. In accord with this hypothesis, we have found that, in uninephrectomized rats given DOC: Dietary NaCl induces persisting hypercalciuria and hypertension whereas an approximately equimolar amount of dietary NaHCO3 induces neither hypercalciuria nor hypertension. The urinary excretion of calcium becomes greater in rats given NaCl than in those given NaHCO3, before their blood pressures become different. Replacing dietary NaCl with a near equimolar amount of dietary NaHCO3 corrects both the hypercalciuria and the hypertension initially induced by NaCl.
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PMID:Dietary chloride as a determinant of disordered calcium metabolism in salt-dependent hypertension. 298 59

Mild hypercalciuria has been observed in hypertension, but it is not yet established whether the prevalence of urinary stone disease is increased as well. Data from the cross-sectional phase of the Gubbio Study--a population-based survey on hypertension involving 5376 subjects (84% response rate)--have been analysed to address this issue, defining as hypertensive those subjects with diastolic pressure falling within the fifth quintile for each sex- and age-specific category, and/or under regular antihypertensive treatment. The prevalence of a positive history for urinary stone (radiographic and/or surgical evidence, and/or stone excretion) was increased by over 50% (P less than 0.01) in treated and untreated hypertensives. None of the 136 subjects with a positive urinary stone history were hypercalcaemic and none had renal failure.
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PMID:Elevated blood pressure and positive history of kidney stones: results from a population-based study. 324 Dec 40

Abnormalities in Ca metabolism in genetic hypertension have been suggested by studies of the spontaneously hypertensive rat and of humans with essential hypertension. A state of relative Ca deficiency in genetic hypertension was previously hypothesized to explain the reduced serum ionized Ca, increased serum parathyroid hormone levels, and the association between oral Ca loading and mild reduction in blood pressure. Renal Ca leak, reduced intestinal Ca absorption, and diminished Ca intake were further postulated to account for the Ca deficient state. This hypothesis, however, is not supported by the following lines of evidence in genetic hypertension: the absence of fasting hypercalciuria owing to intrinsic tubular defects, increased net Ca absorption in vivo despite greater Ca retention before and during established hypertension, increased intracellular free Ca concentrations, the failure to aggravate the hypertension by 50% reduction in dietary Ca intake, and the failure to ameliorate the hypertension by maneuvers that augment Ca balance (parenteral Ca administration, a high Mg diet, and 1,25-dihydroxyvitamin D3 injections). The available literature may be explained by the alternative hypothesis that genetic hypertension is characterized by generalized membrane defects in Ca regulation, resulting in a relative increase in cytosolic free Ca. The mechanism (or mechanisms) and physiological consequences of the disturbances in Ca homeostasis, however, remain to be defined.
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PMID:The nature and role of disturbances in calcium metabolism in genetic hypertension. 353 40


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