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)

Calcium metabolic balance determinations, which have been done in various clinical and experimental conditions, were applied to the study of 8 spinal cord injured patients receiving a diet with 1600 mg calcium and 85 to 120 gm protein daily. All of the patients had hypercalciuria prior to ambulation. Those with spinal cord injuries of less than 3 months duration (early group) had a calcium balance of -27 mg before ambulation and 235 mg after ambulation. Patients with spinal cord injuries of 6 months or more duration (late group) had calcium balances of 55 mg before ambulation and 175 mg after ambulation. Ambulation significantly decreased the hypercalciuria and modified the calcium balance in a positive direction. Smaller changes were noted in the responses of the late group than in those of the early group. Early ambulation will probably prevent bone loss, calcium stones in the genitourinary tract, and other sequellae of negative calcium balance.
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PMID:Calcium balance in paraplegic patients: influence of injury duration and ambulation. 71 7

Absorptive hypercalciuria was treated in 27 patients with cellulose phosphate. In all patients urinary calcium decreased and stone formation virtually ceased. The most striking side effect was an excessive hyperoxaluria, necessitating withdrawal of the drug in 8 patients. Succinate decreased the hyperoxaluria in 14 of 19 patients. All patients had mild hypercalciuria and hypermagnesiuria. This study was done to determine the therapeutic value and the side effects in the treatment of absorptive hypercalciuria with sodium cellulose phosphate and of hyperoxaluria with succinate.
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PMID:Calcium oxalate stone disease: effects and side effects of cellulose phosphate and succinate in long-term treatment of absorptive hypercalciuria or hyperoxaluria. 73 12

The calcium tolerance test is of diagnostic importance only in osteomalacia, which it helps to identify before bone biopsy when the static phosphocalcic parameters are not a deciding factor. However, the test does not make it possible to distinguish an osteoporosis from a cortisone osteopathy or an idiopathic hypercalciuria. In the first two diseases, the rates of urinary calcium elimination are comparable to that of normal individuals. It seems that the rate of urinary elimination of I.V. administered calcium is, approximately, all the more elevated as the level of iPTH is low; and, when the level of iPTH is low, the osteoid tissue seems less calcified than normally.
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PMID:[The provoked hypercalciuria test. Significance and limitations]. 74 25

The frequency of hypercalciuria was determined in the families of nine hypercalciuric patients with idiopathic hypercaliuria who formed recurrent calcium oxalate renal stones. Idiopathic hypercalciuria occurred in 26 of 73 relatives, in three consecutive generations of two families and in two successive generations of four other families. Multiple siblings or children of the probands were affected in three families. Nineteen of 44 first-degree relatives (43 per cent) had idiopathic hypercalciuria, as compared to seven of 29 (29 per cent) other relatives; there was no relation to age or sex. Renal stones were formed by 19 of the 44 first-degree relatives but by none of the others; nine of the 19 were women. We conclude that there is a familial form of hypercalciuria, which appears to be transmitted as an autosomal dominant trait. Stone disease is frequent in first-degree relatives, and affects both sexes equally.
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PMID:Familial idiopathic hypercalciuria. 75 93

In a double-blind controlled clinical study, 71 patients with recurrent calcium oxalate stones were divided into three treatment groups: those who received potassium acid phosphate, those who received an inert placebo, and those who received a low calcium diet only. Follow-up periods averaged 2.9 years. Although the mean urinary calcium level of the patients who received phosphate was reduced 33 per cent, their renal stone disease did not diminish. Mean urinary phosphorus increased 88 per cent with phosphate treatment but did not correlate with the decrease in urinary calcium, or with treatment success. The data did not suggest that phosphorus and its metabolites retard calcium oxalate crystallization in urine. No evidence appeared for an association of hypercalciuria with severe stone disease, or with a specific clinical or chemical response to phosphate therapy. Patients whose urinary calcium level fell more than 25 percent when dietary calcium was reduced may have excessive gastrointestinal calcium absorption, which appears to be associated with improved chemical response to phosphate therapy.
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PMID:Recurrent nephrolithiasis: natural history and effect of phosphate therapy. A double-blind controlled study. 78 40

A case of renal transplantation is presented in which the donor had idiopathic hypercalciuria. The hypercalciuria persisted in the donor, but was not observed in the recipient. This fact suggests that, in this case, the cause of the hypercalciuria is the intestinal hyperabsorption of calcium ions.
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PMID:Kidney transplant from a patient with idiopathic hypercalciuria. 78 44

Vitamin D-dependent CaBP isolated from Rat renal cortex (rCaBP) was measured in phosphorus-depleted (OP) and control (C) Rats, either vitamin D-deficient (OD) or vitamin D-supplemented (1 or 10 i. u.). A low molecular weight fraction was isolated from renal cortex by "Sephadex G-100" chromatography and rCaBP activity quantitated by saturation analysis using a 45 Ca chelex assay. The results indicated that phosphorus deprivation resulted in the increase in the vitamin D-dependent rCaBP as well as in the intestinal CaBP. As a marked hypercalciuria was noted in all OP Rats and as the rCaBP activity was high in vitamin D-supplemented Rats and hardly detectable in vitamin D-deficient Rats, the implication of the rCaBP in the large hypercalciuria can be definitely ruled out. Furthermore when vitamin D-supplementation ranged from 1 to 10 i. u. vitamin D, while the serum calcium level was increasing a decrease could be noticed in the large hypercalciuria. This deserves to be related to the increase in rCaBP activity. The high CaBP activity probably resulting from the renal synthesis of 1,25-dihydroxycholecalciferol stimulated by phosphorus-deprivation could represent the molecular basis of the calcium tubular reabsorption increased by vitamin D. Thus a vitamin D-dependent protein implicated in an ion-selective transport could be involved in the tubular calcium reabsorption as well as in the intestinal calcium absorption.
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PMID:[Increase in the renal calcium-binding protein (CaBPr) in the presence of vitamin D in growing, phosphate deficient rats. Possible role in tubular calcium reabsorption]. 82 36

Four patients having high-level quadriplegia developed elevated serum calcium concentrations (11 to 15.8 mg/100 ml) within three months of injury. All were young males (ages 15 to 19 years) and quadriplegic (C4-C7). Presenting symptoms were nausea, vomiting, polydipsia, polyuria and lethargy. In two patients severe muscle wasting and cachexia with clinical symptoms developed and persisted for several months. Laboratory studies in all patients showed negative calcium balance with hypercalciuria. Reduced renal function was seen in all patients but returned to normal with return of normal serum calcium. Alkaline phosphatase level was normal in three and elevated in one. Serum parathormone levels were normal. Roentgenograms revealed diffuse demineralization. Nephrocalcinosis and soft tissue calcifications developed in one patient. Primary treatment included reduced calcium intake, correction of dehydration, sodium infusion and remobilization. Corticosteroids, oral phosphates, furosemide and mithramycin were used with varying success to control prologned symptoms and severe hypercalcemia.
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PMID:Immobilization hypercalcemia in spinal cord injury. 83 59

The effect of hydrochlorothiazide on the formation of renal stones was evaluated by quantitative assessment of the propensity of urine to undergo crystallization of calcium oxalate. In seven patients with calcium urolithiasis (three with absorptive hypercalciuria, one with renal hypercalciuria, and three with normocalciuric nephrolithiasis), the urinary activity product ratio and formation product ratio of calcium oxalate were measured both on and off therapy with hydrochlorothiazide (50 mg orally twice a day). The activity product ratio (state of saturation with respect to calcium oxalate) decreased in the majority of cases, primarily as a result of the fall in urinary calcium. The formation product ratio (limit of metastability) increased in all cases; the cause of the increase was not readily apparent. Both changes reduced the propensity of urine to undergo crystallization of calcium oxalate, and therefore may account for the clinical improvement reported during thiazide therapy in nephrolithiasis.
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PMID:Effect of hydrochlorothiazide therapy on the crystallization of calcium oxalate in urine. 83 53

In two patients (father and daughter) with idiopathic hypoparathyroidism, one of whom was resistant to the action of vitamin D2 and AT-10, 1alpha-hydroxycholecalciferol (1alpha-(OH)D3) in doses of 2-5 mug/day restored the serum calcium concentration to the normal range. The calcemic effect of 1alpha (OH)D3 was in both patients due to an increased intestinal calcium absorption and increased calcium mobilization from bone. In one of the patients 1alpha-(OH)D3 also increased the renal tubular calcium reabsorption; in the other it did not have this effect, resulting in hypercalciuria as serum calcium rose. The lack of effect on tubular calcium reabsorption probably accounts for the relative resistance to the action of 1alpha-(OH)C3 in this patient compared with other.
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PMID:1alpha-hydroxycholecalciferol in the treatment of hypoparathyroidism. 83 68


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