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

The etiology of hypercalciuria remains unknown in spontaneously hypertensive rats (SHR). In order to differentiate absorptive versus renal hypercalciuria, serial measurements of urinary calcium (UCaV) excretion were made weekly under fasting (3-hour urine collection) and after oral administration of CaCl2 (50 mg/100 g; 4-hour urine collection) from age 8 to 14 weeks in SHR (n = 14) and normotensive Wistar Kyoto rats (WKY; n = 14). Fasting UCaV was significantly greater in WKY than in SHR throughout the periods of observation. In contrast, after oral Ca loading UCaV was greater in SHR after 13 weeks of age (13 weeks: SHR UCaV = 954 micrograms/mg creatinine, WKY UCaV = 541 p less than 0.01; 14 weeks: SHR UCaV = 988 micrograms/mg creatinine, WKY UCaV = 534, p less than 0.01). Fasting urinary cyclic adenosine monophosphate (AMP) excretion was not different between WKY and SHR. However, cyclic AMP excretion of SHR, but not WKY, was decreased after calcium loading when compared to the fasting values. The cyclic AMP was also significantly lower in SHR than in WKY rats after calcium loading. Calcium handling by the kidney was not different between SHR and WKY with or without parathyroidectomy. Calcium disposition kinetic studies were performed on these animals at age 15 and 16 weeks. No significant difference of intravenous 45Ca was observed between WKY (n = 6) and SHR (n = 6) in total plasma clearance, nonrenal clearance, biologic half-life, and elimination rate constant from the central compartment. However, the WKY had a significantly greater renal clearance of 45Ca than the SHR (0.48 +/- 0.04 vs. 0.24 +/- 0.02 ml/n, p less than 0.001). Since tissue disposition of intravenous 45Ca was not different between WKY and SHR, the increased renal excretion of calcium after oral administration in SHR, therefore, reflects increased intestinal absorption of calcium. Correction of established hypertension did not abolish the hypercalciuria. We believe that increased gastrointestinal absorption of calcium is responsible for the hypercalciuria in SHR.
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PMID:Pathogenesis of hypercalciuria in spontaneously hypertensive rats. 396 17

12 adult patients with medullary sponge kidney (MSK), followed up for 1 to 14 years (mean 7 years) are presented. MSK was initially diagnosed in 4 cases. In 8 cases the initial diagnosis included pyelonephritis, nephrocalcinosis, and nephrolithiasis. Renal calculi (4 patients), urinary tract infection (8) and hematuria (5) were the most frequent symptoms. Renal tubular acidosis was documented in 2 patients and hypercalciuria without hyperparathyroidism in 2. Over the years renal calculi increased in size in 4 patients. Renal function was stable in 11. In one patient with associated, well controlled hypertension, serum creatinin rose from 141 to 298 mumol/l over 14 years.
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PMID:[Medullary sponge kidney. Diagnosis and course in 12 cases]. 397 81

To define the mechanism for the hypercalciuria in spontaneously hypertensive rats (SHR), Ca clearance was evaluated in fasted 23-wk-old SHR and normotensive Wistar Kyoto (WKy) controls. There was no exaggerated calciuria before or after parathyroidectomy. Ca balance was therefore measured in the nonfasted animals, which revealed hyperabsorption in SHR of both sexes with increments 10-fold that of Ca excretion, supporting the primacy of intestinal hyperabsorption. In situ duodenal Ca uptake was also increased in the SHR. Parathyroidectomy did not affect the hyperabsorption. Hypercalcemia (total and ionized) and hypercalciuria in SHR associated with reduced adenosine 3',5'-cyclic monophosphate excretion, were abolished by fasting. Correction of hypertension for 6 mo failed to abolish the hypercalciuria. Bone Ca deposits were increased in 1-yr-old SHR. Ten-week-old SHR, in contrast, displayed mild malabsorption. Our data do not support the "renal leak" hypothesis. Instead, the adult SHR is characterized by increased Ca retention due to primary hyperabsorption, absorptive hypercalciuria, and increased bone Ca deposition. These phenomena are independent of sex, parathyroid hormone, and treatment of the established hypertension.
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PMID:Evidence for an intestinal mechanism in hypercalciuria of spontaneously hypertensive rats. 649 32

Of 117 formers of relapsing calcium oxalate calculi 75.2% showed a hyperuricaemia, 64.1% a hyperlipoproteinaemia, 19.7% a diabetes mellitus, 44.4% a hypertension, 11% a hyperuricuria (greater than 1.0 g/a day) and 7.5% a hypercalciuria. In 30 formers of relapsing uric acid calculi we could establish a hyperuricaemia in 93.3%, a hyperlipoproteinaemia in 76.7%, a diabetes mellitus in 36.7%, a hypertension in 80%, a hyperuricuria in 11% and a hypercalciuria in 3.8%. In comparison to formers of calcium oxalate calculi patients with uric acid calculi had a significantly higher body-weight. The results of our examinations make clear that in relapsing formation of urinary calculi frequently a complex disturbance of the metabolism is present which in every case must be established and treated.
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PMID:[Incidence of metabolic disorders in patients with recurrent urinary calculi]. 722 5

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

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.
Hypertension
PMID:Enhanced parathyroid function in essential hypertension: a homeostatic response to a urinary calcium leak. 738 May 20

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

Hypertension and calcium nephrolithiasis show some common features, such as the high prevalence of hypercalciuria and of elevated urinary sodium excretion. 28 patients with idiopathic calcium stone disease and 17 normals were studied: all the subjects were evaluated for the mean arterial pressure, and for the metabolic risk factors for calcium stone disease. The mean arterial pressure proved to be higher in patients with calcium nephrolithiasis than in normals. In normals the mean arterial pressure showed a direct relationship with the urinary calcium, while in the group of stone patients it had a direct relationship with the urinary sodium excretion. The lack of relationship between the mean arterial pressure and calcium excretion, in patients with calcium stones, suggests an impaired tubular calcium handling in such patients.
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PMID:[Arterial pressure in idiopathic calcium nephrolithiasis]. 803 56

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

Abnormalities in renal handling of calcium, magnesium, or phosphate have been implicated in the development and/or maintenance of human hypertension. We have shown recently that renal excretion of these ions is correlated to blood pressure in Dahl salt-sensitive as well as salt-resistant rats. The present study was designed to determine whether renal perfusion pressure per se could affect excretion of these ions. Urinary excretion of calcium, magnesium, and phosphate was studied in anaesthetized Sprague-Dawley rats under basal conditions and during an intravenous infusion of angiotensin II (ANG II), vasopressin (AVP) or phenylephrine (PE). A cuff, placed around the aorta between the two renal arteries, allowed maintenance of normal perfusion pressure in the left kidney, while that in the right kidney was allowed to rise. Infusion of pressor agents raised mean arterial blood pressure to comparable levels (means +/- SE): ANG II (n = 7), before = 102 +/- 4, during = 133 +/- 3 mmHg, AVP (n = 8), before = 110 +/- 7, during = 136 +/- 5 mmHg, PE (n = 6), before = 111 +/- 6, during = 141 +/- 6 mmHg. Although there was no difference in excretion of calcium, magnesium and phosphate between the two kidneys under basal conditions, infusion of ANG II or PE induced hypercalciuria, hypermagnesiuria and hyperphosphaturia in the right kidney which was exposed to the increased arterial pressure. Such effects did not appear in the pressure-controlled left kidney. Infusion of AVP was associated with reduced excretion of calcium and magnesium, and increased excretion of phosphate, in the normotensive kidney. The response to the similarly increased renal perfusion pressure in this group was also reduced for calcium and magnesium, and enhanced for phosphate. The results indicate (1) renal excretion of calcium, magnesium and phosphate is renal perfusion pressure-dependent; the higher the renal perfusion pressure, the greater the excretion of these ions. (2) Independently of perfusion pressure, AVP can inhibit phosphate reabsorption and stimulate divalent cation reabsorption.
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PMID:Effect of renal perfusion pressure on excretion of calcium, magnesium, and phosphate in the rat. 856 1


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