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

The effect of short term hydrochlorothiazide therapy on urinary calcium excretion was compared to that of low calcium and a combined low calcium and low sodium diet in 30 children with postglomerular hematuria. On basal conditions 9 children were normocalciuric, 11 had absorptive, 10 renal hypercalciuria. The effect of thiazide treatment on the haematuria was also evaluated. Thiazide revealed to be more effective in reducing calcium excretion than low calcium diet alone in all groups (p less than 0.001 in normocalciuria; p less than 0.01 in both hypercalciuric groups). Combined low calcium--low sodium diet and thiazide treatment were equally effective in reducing calcium excretion in the hypercalciuric groups. On the first 3 days of thiazide treatment a slight increase of hematuria was observed; in the following period a significant decrease in the occurrence (p less than 0.01 in both hypercalciuric groups) and degree (p less than 0.01 in absorptive; p less than 0.02 in renal hypercalciuria) of hematuria was noted. These data furnish further evidence on the relation of hypercalciuria and post-glomerular hematuria.
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PMID:Effect of thiazide on urinary calcium excretion and hematuria in children with postglomerular hematuria. 342 38

As a practical contribution to an understanding of the usefulness of measuring some electrolytes in urine, the author first recalls that elements measured in a 24-h urine sample provide nutritional informations, whereas those assayed in fasting morning urine generate data on renal tubular function. To illustrate the first point the author describes assessment of the etiology of hypercalciuria based on a knowledge of concomitant 24-h excretions of sodium, phosphate, urate and creatinine. On the second point, the author suggests dissociating the parameters of which only the urinary concentration is of interest (pH, lysozyme, gamma-glutamyl-transferase) from the parameters of which the excretion--either fractional (Na, K, Cl, P, Mg) or absolute (Ca)--should be calculated. Finally, the reader is reminded how to use the nomogram of Peacock, Robertson and Nordin to evaluate fasting urinary excretion of calcium, and how to use the nomogram of Walton and Bijvoet to estimate the renal threshold phosphate concentration.
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PMID:[Usefulness of urinary electrolyte determination]. 356 52

The anterior pituitary (AP) grafted, adrenalectomized, steroid hormone-replaced male rat is characterized by hyperprolactinemia and hypercalciuria. To determine the origin of the hypercalciuria, clearance experiments were performed under Inactin anesthesia in adrenalectomized Fischer rats 8-10 wk after implantation of extra AP glands under the kidney capsule. Glomerular filtration rate, ultrafilterable calcium, and fractional sodium excretion were comparable in the AP and control groups. However, fractional calcium excretion was significantly higher in the AP-implanted rats, P less than 0.05, resulting in a marked dissociation of the calcium/sodium clearance ratio. Because filtered calcium load did not change, these results clearly demonstrate that AP-implanted animals have a defect in tubular calcium reabsorption. The dissociation of calcium transport from sodium transport suggests the distal tubule as a likely site of action. Parathyroidectomy did not alter the calciuric response to AP implantation. To test whether hyperprolactinemia was responsible for decreased calcium reabsorption in AP-implanted rats, purified rat prolactin was infused into normal rats to achieve high blood prolactin levels, or was injected into normal rats daily for 8 days. Changes in fractional calcium excretion and the ratio of calcium to sodium clearance were identical in animals receiving prolactin or control infusions. Thus, hypercalciuria in the AP-implanted rat may be attributed to an unidentified factor, perhaps secreted from the implanted anterior pituitaries, rather than to prolactin excess.
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PMID:Examination of hypercalciuria in anterior pituitary-implanted rats. 357 34

The effect of changes in urinary sodium, induced by dietary manipulation in normal subjects (NS) and in stone formers (SF) was studied by observing crytalluria qualitatively and by determining calcium, oxalate and phosphate crystallization quantitatively in an experimental model. In SF the calcium crystallization was significantly higher than in NS at all the three levels of urinary sodium studied. However, no difference was observed in oxalate and phosphate crystallization rates between these two groups. Calcium and oxalate (p less than 0.05) and oxalate and phosphate (p less than 0.001) were found to be correlated in NS but were non-significant in SF. The wide changes in the urinary sodium induced by dietary changes did not influence the crystallization rate of calcium, nor of oxalate and phosphate in NS as well as in SF. The results suggested that a sodium intake with lower and upper limits of 124 mg and 6,009 mg respectively did not act as "inhibitor" of crystallization rate nor did it induce hypercalciuria severe enough to pose a "risk" of stone formation. The results did not suggest that a high urinary sodium increases the solubility of calcium phosphate.
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PMID:Sodium is neither a risk nor a protective factor in urolithiasis? 359 Apr 27

Between 1981 and 1983, 49 children aged 2 to 15 years were diagnosed as having idiopathic hypercalciuria (IH). They were divided into 3 groups based on their response to dietary manipulation: group I (32/49) had absorptive hypercalciuria; group II (8/49) had renal hypercalciuria and group III (6/49) had sodium-dependent hypercalciuria. Response to diet was more reliable than Pak's test in differentiating between the three groups. A control group (CG) of 45 healthy, age matched children determined baseline levels for all metabolic parameters. At the time of presentation IH children did not differ from the CG in height or weight. Fifty percent of IH children had first degree relatives with urolithiasis. Yet, only 16% of the IH children had urolithiasis, the majority presenting with gross hematuria and urinary tract infections (UTI). With few exceptions the clinical symptoms resolved when urine calcium excretion was controlled. Severe calcium restriction in a few patients produced osteoporosis and delayed bone age although growth velocity was unaffected. Thiazide therapy in a few patients produced some metabolic derangements. The authors conclude that IH in childhood is a benign disease which may present with UTI or hematuria. They further propose a new classification method based on response to dietary manipulation.
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PMID:Idiopathic hypercalciuria in children. Classification, clinical manifestations and outcome. 359 Dec 93

Out of 89 stone formers with idiopathic hypercalciuria, 51 remained hypercalciuric on a low calcium diet over 5 days: a renal leak of calcium could thus have been suspected in them. Dietary factors such as high sodium or high animal protein intake, and metabolic factors such as obesity with or without hyperinsulinemia, which all might account for the hypercalciuria of these patients, have been evaluated. This evaluation revealed conditions known to be associated with hypercalciuria in 37 of these 51 patients: 15 had hypercalciuria related to a high sodium intake, 7 had severe hyperuricosuria (greater than 1 g/24 h) reflecting a high animal protein intake, 20 were obese (greater than 120% of ideal weight) with (7 cases) or without (13 cases) concomitant high fasting plasma level of insulin (greater than 18 microU/ml). A careful retrospective analysis of the intravenous pyelograms disclosed medullary sponge kidneys in 8 cases which had remained undiagnosed so far. One of them was studied histologically. Only 14 out of 51 patients had an otherwise unexplained hypercalciuria on a low calcium diet. It is concluded that dietary causes appear to play a key role in 'idiopathic' hypercalciuria, that the incidence of a primary renal leak of calcium among idiopathic stone formers is much smaller than initially thought, and that this condition can hide unrecognized medullary sponge kidneys.
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PMID:Dietary factors and medullary sponge kidneys as causes of the so-called idiopathic renal leak of calcium. 368 38

There is evidence that prolactin (PRL) excess plays a role in the etiology of osteoporosis associated with human prolactinoma. Calcium balance in human hyperprolactinemia has not been thoroughly investigated. In the present study, rats with excess circulating PRL levels (male anterior pituitary-grafted Fischer 344 rats) had urinary calcium excretion twice that of control rats (4.16 +/- 0.43 v 2.25 +/- 0.30 mg/24h X 100 g BW). Calcium excretion expressed per mg of calcium intake was also high in pituitary-grafted rats. The excess calcium excretion in hyperprolactinemic rats was not accompanied by a concomitant rise in sodium excretion. This dissociation suggests that PRL has an effect on the renal handling of calcium. Since thiazide diuretics have a well-described hypocalciuric action, their effect was tested in these rats. In normal rats, benzthiazide, a long-acting agent, significantly reduced urinary calcium excretion in a dose-dependent fashion. Hyperprolactinemic rats responded to benzthiazide in a manner similar to control rats. In pituitary-grafted rats, benzthiazide also decreased the calcium excretion to intake ratio and normalized the calcium to sodium excretion ratio. Since the hypercalciuria of experimental hyperprolactinemia can be corrected by thiazide diuretics, these agents may have therapeutic potential in human PRL excess.
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PMID:Hypercalciuria in hyperprolactinemic rats: effects of benzthiazide. 372 59

A case of renal failure due to sarcoidosis with hypercalciuria and nephrocalcinosis is described. Prolonged treatment with inorganic absorbable phosphate significantly deteriorated the patient's renal function. After a sodium cellulose phosphate treatment, renal failure was completely reversed. We suggest that sodium cellulose phosphate is the treatment of choice in sarcoidotic renal failure induced by nephrocalcinosis.
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PMID:Sarcoid nephrocalcinotic renal failure reversed by sodium cellulose phosphate. 374 Jan 31

Furosemide produces chronic hypercalciuria. The source of the additional urinary calcium is not known but must be either bone mineral or calcium absorbed by the intestine. Without bone calcium dissolution or increased absorption the filtered load of calcium would fall and urinary calcium excretion would return to pretreatment levels. To determine whether furosemide alters intestinal calcium absorption, we fed furosemide (75 mg . kg body-1 wt . day-1) to 11 rats eating 15 g/day of a 0.60% calcium diet. Compared with 11 control rats, furosemide increased urine calcium (15.6 +/- 0.8 mg/5 days vs. 4.1 +/- 0.3, P less than 0.001). Fecal calcium excretion fell (194 +/- 7 mg/5 days vs. 223 +/- 12, P less than 0.05), indicating an increase in intestinal calcium absorption sufficient to sustain the hypercalciuria. The increase in absorption occurred without an increase in the level of serum 1,25-dihydroxycholecalciferol (180 +/- 20 pg/ml vs. 220 +/- 16, furosemide vs. control, respectively, P = NS). To determine whether the intestinal effect of furosemide persists after the initial sodium diuresis abates, we analyzed only the last 3 days of balance. Again, rats fed furosemide had increased urine excretion and intestinal absorption of calcium, so that net calcium balance was not different from that of controls. Twelve additional rats were fed a 0.02% calcium diet to which 35 mg . kg body wt-1 . day-1 of furosemide was added. Compared with eleven controls, urine calcium increased and fecal calcium excretion again fell, but balance was not different. Chronic administration of furosemide increases intestinal calcium absorption enough to permit urine calcium excretion to remain elevated without the necessity for bone dissolution.
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PMID:Mechanism of chronic hypercalciuria with furosemide: increased calcium absorption. 375 94

Chronic mineralocorticoid excess results in the predicted retention of salt and water followed by a period of escape from sodium retention and hypercalciuria. We studied a rat model during mineralocorticoid escape (ME) with clearance and micropuncture studies to ascertain the nephron site and possible role of parathyroid hormone. Rats during ME were hypercalciuric compared with a matched saline group. Clearance studies revealed a marked difference in the calcium-to-sodium fractional excretion ratio (FECa/FENa) between saline-expanded and mineralocorticoid (desoxycorticosterone acetate, DOCA)-escaped animals (saline-expanded, 0.40 +/- 0.09 vs. DOCA, 1.02 +/- 0.14; P less than 0.01). The addition of either hydrochlorothiazide (HCTZ) or amiloride (AMIL) to the ME animals significantly lowered this ratio from that seen in the intact ME group (DOCA-HCTZ, 0.47 +/- 0.07; DOCA-AMIL, 0.83 +/- 0.14). Neither parathyroidectomy (PTX) nor parathyroid hormone infusions (PTH) in ME animals altered the FECa/FENa from that seen in the intact ME group (DOCA-PTX, 1.15 +/- 0.20; DOCA-PTH, 1.25 +/- 0.18). Segmental micropuncture along the length of superficial nephrons demonstrated no differences in calcium delivery to late proximal, early distal, and late distal sites. However, FECa was markedly increased in ME animals compared with saline controls (saline, 0.48 +/- 0.13% vs. DOCA, 1.62 +/- 0.24%; P less than 0.05). We conclude that the hypercalciuria of ME is independent of PTH and can be significantly reduced by HCTZ or AMIL. Micropuncture and clearance data suggest that the hypercalciuria of ME is mediated in the terminal nephron. The differences in the results when superimposing various factors that influence distal nephron calcium reabsorption on ME may be related to differences in their site(s) of activity on calcium transport.
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PMID:Hypercalciuria of mineralocorticoid escape: clearance and micropuncture studies in the rat. 377 84


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