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

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

We have studied the metabolic response to changes in calcium in 15 hypercalciuric essential hypertensives, in 8 normotensive hypercalciuric stone formers and in 11 normotensive healthy subjects matched for age and sex. At variance with hypercalciuric stone formers, at low calcium intake hypercalciuric hypertensives did not appropriately reduce urinary calcium excretion and developed mild hypocalcemia. Furthermore, the PTH response to calcium deprivation was not appropriately enhanced in these patients. The data indicate that different mechanisms prevail in these two forms of hypercalciuria: the renal in essential hypertension and the intestinal in urolithiasis.
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PMID:Mechanism of hypercalciuria in essential hypertension and in primary nephrolithiasis. 195 54

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

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

Disorders of calcium metabolism are not generally considered important either clinically or pathophysiologically in essential hypertension. Recent reports, though, suggest that increased parathyroid gland function may be one of the more common endocrine disturbances associated with hypertension. We measured serum parathyroid hormone (PTH) concentrations as well as routine blood and urine chemistries in 34 hypertensives. Their mean PTH, 79.1 +/- 3.1 muliter Eq/muliter, was significantly higher (p less than 0.025) than the mean PTH, 66.9 +/- 3.3, of an age- and sex-matched normotensive control population. The mean serum calcium, 9.5 +/- 0.1 mg%, was identical in the two populations. Compared to a second age- and sex-matched normotensive population, the hypertensives demonstrated a significant (p less than 0.005) relative hypercalciuria. For any level of urinary sodium, hypertensives excreted more calcium. These preliminary data suggest that parathyroid gland function may be enhanced in essential hypertension. This increased gland activity appears, in part, to be an appropriate, physiologic response to a previously unrecognized relative hypercalciuria, or renal calcium leak, associated with essential hypertension. We conclude that the increased prevalence of hypertension in subjects with hyperparathyroidism probably represents the final event in a continuum that begins with obligatory urinary calcium losses in hypertensives, but whose pathological presentation is hyperparathyroidism. The results of this pilot study indicate a need for derivative experiments directed at defining the importance of our preliminary findings in the pathogenesis of human and experimental hypertension.
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PMID:Enhanced parathyroid function in essential hypertension: a homeostatic response to a urinary calcium leak. 738 May 20

Alterations in calcium metabolism have been detected in both human and rat primary hypertension at various levels of the biological organization; in particular, an abnormal renal electrolyte handling, leading to chronically enhanced urinary calcium excretion, has been demonstrated. In keeping with this finding, a significant statistical association between high blood pressure and prevalence of nephrolithiasis has been found in three independent population-based surveys. The first was carried out in the early 1960s in Goteborg, Sweden, on 895 50-year-old men, and showed a higher frequency of a positive history of nephrolithiasis with increasing blood pressure. The second and third studies were performed in Italy, one in the town of Gubbio, with screening of a representative sample (n = 3,431; 84%) of the adult population and the other in Pozzuoli, Naples, at the Olivetti factory, where 688 male workers (88% of the total male workforce) were examined. In both studies, the retrospectively evaluated relative risk of nephrolithiasis in hypertensive persons, after controlling for age, was significantly higher than in normotensive persons, with hypertension contributing by 18% to the overall rate of nephrolithiasis. Hypercalciuria is the most common risk factor for nephrolithiasis and, therefore, also a likely pathogenetic link between nephrolithiasis and hypertension. Dietary factors play an important contributory role in the prevention and treatment of these two widespread conditions, and a dietary approach, with particular regard to electrolyte intake, is a powerful tool for the prevention of hypertension-related kidney stone disease.
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PMID:Hypertension, calcium metabolism, and nephrolithiasis. 814 Nov 46

A statistical association between arterial hypertension and kidney stone disease has been observed in three retrospective epidemiological surveys: the first was conducted in the early 1960s on 895, 50-year-old men living in Goteborg, Sweden; the second on 3,431 in-wall residents of the ancient town of Gubbio in central Italy, and the third on 688 workers (88% of the male work force) of the Olivetti factory in Pozzuoli, Naples, Italy. In all three studies, the participants in the upper part of the respective blood pressure distributions, or on long-term treatment for arterial hypertension had a significantly higher frequency of a positive history of nephrolithiasis compared with normotensives. This statistical association was independent of age, body mass, and biochemical indicators of renal function. The aim of this article is to review the evidence provided by these epidemiological surveys and to discuss a few pathogenetic hypotheses with special reference to the role of hypercalciuria and other alterations of calcium metabolism commonly found in patients with essential hypertension. The higher risk of calcium nephrolithiasis in hypertensive patients has obvious clinical and public health implications, given the large diffusion of both conditions in the population and the elevated social costs of their complications and sequelae. Several nutritional measures are known to be effective for the prevention and treatment of both hypertension and nephrolithisis, and therefore, there is attention in this article to the important role of the micronutrients sodium, potassium, and calcium and to their biological relationships.
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PMID:Hypertension and kidney stones: hypotheses and implications. 858 12

A high prevalence of hypercalciuria has been reported in patients with essential hypertension. Nevertheless, the clinical and therapeutic implications of this finding have scarcely been studied. This study was designed to determine the prevalence of hypercalciuria in an unselected population with essential hypertension and to analyze the relationship between the urinary calcium and the clinical and therapeutic status of these patients. This article presents a prospective study of 112 patients with essential hypertension and 49 healthy normotensive control subjects. Urinary excretion rates of calcium, sodium, chloride, potassium, urinary calcium/creatinine index, the fractional excretion of sodium, potassium and uric acid, the creatinine clearance and serum values of creatinine, urea, uric acid, electrolytes, total proteins, parathormone (intact molecule), plasma renin activity, aldosterone, glucose, and insulin (fasting and after an oral glucose load) were performed in every patient and control subject. Untreated hypertensive patients had a higher prevalence of hypercalciuria (35% had a urinary calcium/creatinine ratio > 0.20 versus 20% of treated hypertensives and 2% of control subjects; P < 0.001). Patients on thiazide or beta-blocker monotherapy had lower urinary excretion rates of calcium and urate than patients on calcium-antagonist monotherapy or untreated patients. Urinary calcium, sodium, and urate correlated positively both in treated and untreated essential hypertension patients. Patients with the higher urinary calcium levels also had higher excretion rates of sodium and urate, higher creatinine clearance rates, and lower serum creatinine and serum uric acid levels. It was concluded that hypercalciuria is a frequent finding of untreated essential hypertension. The association of high urinary calcium levels with high urinary urate excretion rates in the same patient may predispose to development of lithiasis in patients with essential hypertension. Antihypertensive drugs have a variable effect on calciuria-uricosuria, which may constitute an additional criterion in the selection and individualization of therapy. Thiazides and beta-blockers can decrease calciuria and uricosuria and, therefore, the lithogenic risk in these patients.
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PMID:Urinary calcium excretion in treated and untreated essential hypertension. 882 22

Primary aldosteronism represents major cause of secondary hypertension, strongly associated with high cardiovascular morbidity and mortality. Aldosterone excess may influence mineral homeostasis, through higher urinary calcium excretion inducing secondary increase of parathyroid hormone. Recently, in a cohort of PA patients a significant increase of primary hyperparathyroidism was found, suggesting a bidirectional functional link between the adrenal and parathyroid glands. The aim of this study was to evaluate the impact of aldosterone excess on mineral metabolism and bone mass density. In 73 PA patients we evaluated anthropometric and biochemical parameters, renin-angiotensin-aldosterone system, calcium-phosphorus metabolism, and bone mineral density; control groups were 73 essential hypertension (EH) subjects and 40 healthy subjects. Compared to HS and EH, PA subjects had significantly lower serum calcium levels and higher urinary calcium excretion. Moreover, PA patients showed higher plasma PTH, lower serum 25(OH)-vitamin D levels, higher prevalence of vitamin D deficiency (65% versus 25% and 25%; P < 0.001), and higher prevalence of osteopenia/osteoporosis (38.5 and 10.5%) than EH (28% and 4%) and NS (25% and 5%), respectively. This study supports the hypothesis that bone loss and fracture risk in PA patients are potentially the result of aldosterone mediated hypercalciuria and the consecutive secondary hyperparathyroidism.
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PMID:Bone and mineral metabolism in patients with primary aldosteronism. 2486 41