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)

The effect of different dietary regimens and of an oral calcium (Ca) load was studied in 30 children with postglomerular hematuria, 8 of whom were renal stone formers. In addition we investigated the urinary inorganic phosphate complex composition in 12 of them, based on the principles of complex equilibria. Twenty-one of the 30 hematuric children with a urinary Ca/creatinine (Ca/cr) ratio of greater than or equal to 0.6 (mmol/mmol) were regarded as hypercalciuric. Low calcium intake normalised the ratio in 11 patients, fulfilling the definition of absorptive hypercalciuria, but not in the other 10 patients with renal hypercalciuria. Sodium restriction combined with low calcium diet induced a further significant decrease of the urinary Ca/cr ratio to a normal range in both forms of hypercalciuria (mean +/- SD: 0.325 +/- 0.112 in absorptive hypercalciuria; 0.533 +/- 235 in renal hypercalciuria). There was a significant difference in the composition of phosphate complexes between the 6 normocalciuric patients and the 6 children with renal hypercalciuria investigated. Lithogenic urinary phosphate complexes (CaHPO4, MgHPO4) were excreted by the latter group in a significantly higher amount under basal conditions. On the basis of these data sodium restriction added to low calcium diet could represent a dietary approach in preventing excessive calcium excretion in idiopathic hypercalciuria, and therefore renal stone formation.
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PMID:Studies on the urinary calcium excretion in children with hematuria of postglomerular origin: effects of the variation of dietary calcium and sodium intake. 381 82

Six children with idiopathic hypercalciuria and their families were examined with an oral calcium loading test. Family members were divided into two clinical categories: group 1 consisted of the six index children and their parents and siblings with urolithiasis or unexplained hematuria; group 2 comprised the remaining parents and siblings without signs or symptoms associated with hypercalciuria. The results revealed that fasting urinary excretion of calcium was similar in both groups, but group 1 displayed a greater calciuric response to an oral calcium load. Serum concentrations of calcitriol (1,25-dihydroxyvitamin D3) and calcium were higher in group 1 than in group 2, while parathyroid activity was lower in group 1 patients. Urinary excretion of sodium, phosphorus, and magnesium, urine pH, serum levels of calcifediol (25-hydroxyvitamin D3) and phosphorus, and the renal tubular threshold for phosphate were not significantly different in the two groups. These findings suggest that idiopathic hypercalciuria may arise from a disturbance in the regulation of vitamin D metabolism that mediates enhanced intestinal absorption of calcium.
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PMID:Families of children with idiopathic hypercalciuria. Evidence for the hormonal basis of familial hypercalciuria. 383 4

The effects of thiazide diuretics on serum phosphate concentration, renal tubular threshold for phosphate, and urinary calcium excretion in children with renal hypophosphatemic rickets were studied. There were nine controlled acute studies conducted in five patients, and, in addition, seven long-term studies of up to 26 months were performed. During the acute studies, the children continued to receive the same doses of oral calcitriol and phosphate supplementation as at home. Hydrochlorothiazide, 1.50 to 2.25 mg/kg/d, was used alone in the first four studies; hydrochlorothiazide and amiloride at a dose of 1 mg for each 5 mg of hydrochlorothiazide were used in the other five studies. Administration of the diuretics for four days gave rise to a significant increase in serum phosphate concentration from 3.1 +/- 0.4 mg/dL to 3.7 +/- 0.9 mg/dL (P less than .01) and in tubular threshold for phosphate from 1.31 +/- 0.45 mg/dL to 1.74 +/- 0.60 mg/dL (P less than .01). These changes were accompanied by significant reductions in urinary sodium excretion from 135 +/- 39 mEq/24 h during the control period to 99 +/- 42 mEq/24 h on the fourth day of therapy (P less than .05), fractional sodium excretion from 0.99% +/- 0.42% to 0.81% +/- 0.42% (P less than .05), and urinary calcium excretion from 57.3 +/- 28.9 mg/24 h to 19.0 +/- 13.1 mg/24 h (P less than .01). Fractional excretion of phosphate divided by fractional excretion of sodium after the treatment with diuretics was not significantly different from that observed at the end of the control period. Increments in serum phosphate concentrations were correlated with elevations in serum albumin concentrations (r = .739; P less than .02). As an additional index of intravascular volume contraction, the elevations in serum phosphate concentrations were correlated with the increase in BUN, (r = .793; P less than .01). The addition of amiloride in the last five studies prevented the hypokalemia and alkalosis that had complicated the administration of hydrochlorothiazide. Long-term follow-up studies for a total of 119 therapy-months on six children and one adult, who continued to receive the diuretics concomitantly with calcitriol and phosphate supplementation, showed that they were free of complications except for a transient episode of hypercalcemia and hypercalciuria in one patient. In comparison with the previous period of treatment with calcitriol and phosphate without diuretics, linear growth velocity and healing of the rickets were not changed in two children and improved in the other four after the addition of hydrochlorothiazide and amiloride.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of hydrochlorothiazide and amiloride in renal hypophosphatemic rickets. 388 56

The long-term effects of potassium citrate therapy (usually 20 mEq. 3 times daily during 1 to 4.33 years) were examined in 89 patients with hypocitraturic calcium nephrolithiasis or uric acid lithiasis, with or without calcium nephrolithiasis. Hypocitraturia caused by renal tubular acidosis or chronic diarrheal syndrome was associated with other metabolic abnormalities, such as hypercalciuria or hyperuricosuria, or occurred alone. Potassium citrate therapy caused a sustained increase in urinary pH and potassium, and restored urinary citrate to normal levels. No substantial or significant changes occurred in urinary uric acid, oxalate, sodium or phosphorus levels, or total volume. Owing to these physiological changes, uric acid solubility increased, urinary saturation of calcium oxalate decreased and the propensity for spontaneous nucleation of calcium oxalate was reduced to normal. Therefore, the physicochemical environment of urine following treatment became less conducive to the crystallization of calcium oxalate or uric acid, since it stimulated that of normal subjects without stones. Commensurate with the aforementioned physiological and physicochemical changes the treatment produced clinical improvement, since individual stone formation decreased in 97.8 per cent of the patients, remission was obtained in 79.8 per cent and the need for surgical treatment of newly formed stones was eliminated. In patients with relapse after other treatment, such as thiazide, the addition of potassium citrate induced clinical improvement. Thus, our study provides physiological, physicochemical and clinical validation for the use of potassium citrate in the treatment of hypocitraturic calcium nephrolithiasis and uric acid lithiasis with or without calcium nephrolithiasis.
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PMID:Long-term treatment of calcium nephrolithiasis with potassium citrate. 389 44

Vitamin K promotes the formation of gamma-carboxylated glutamate (GLA) in several protein species. GLA residues have a high affinity for the Ca ion. In the present study, we tested the hypothesis that experimental vitamin K deficiency in rats could induce changes in Ca metabolism. Vitamin K depletion, which was associated with a reduction in urinary GLA excretion, induced within 7 days a significant increase in cumulative urinary Ca excretion that persisted throughout the 21 days of study. The hypercalciuria of vitamin K-deficient rats was corrected on vitamin K supplementation. No concomitant changes were observed in intestinal Ca absorption determined by a balance technic or of skeletal resorption and apposition rates determined by bone histomorphometry. Plasma Ca, but not total protein concentration, of vitamin k-depleted rats showed a transient decrease at day 15 that disappeared at day 21. plasma sodium, phosphate and 1,25(OH)2 vitamin D concentration, and urinary phosphate, sodium, and creatinine excretion remained unchanged. In conclusion, vitamin k deficiency in the rat induced hypercalciuria that could be of renal origin. Its possible relationship to vitamin K-dependent renal GLA protein remains to be clarified.
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PMID:Hypercalciuria during experimental vitamin K deficiency in the rat. 392 70

An animal model was established to test the effect of a calcium antagonist on nephrocalcinosis, which was induced by an atherogenous diet, and its effect on the excretion of calcium and other parameters relevant for stone formation. With the administration of nifedipine (Adalat), the grade of nephrocalcinosis could be significantly reduced. Furthermore, with nifedipine the excretion of calcium and sodium in the urine was raised, while phosphate and potassium levels were lowered. The excretion of magnesium and citrate, reduced by an atherogenous diet, could be raised significantly with the administration of nifedipine. The pathophysiological mechanisms underlying the effect of nifedipine on nephrocalcinosis and on the excretion of the urine parameters are discussed. Apparently hypercalciuria is the result of a reduced reabsorption of calcium in the tubulus. The inhibitory effect on the genesis of nephrocalcinosis is possibly due to the lower calcium influx into the tubular cells.
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PMID:[Effect of calcium antagonists (nifedipine) on nephrocalcinosis and calcium excretion in the rat]. 397 86

Recent data have shown that administration of indomethacin to patients with hypercalciuric nephrolithiasis decreased urinary calcium excretion, implying a possible pathogenic role for renal prostaglandins in hypercalciuria. To explore this hypothesis we administered indomethacin, ketoprofen and aspirin to normal volunteers for 6 days and assessed daily creatinine clearance and urinary excretion of sodium and calcium. In contrast to previous studies, subjects were maintained on a constant metabolic diet. These nonsteroidal anti-inflammatory drugs decreased urinary sodium excretion but had no effect on creatinine clearance or urinary calcium excretion. In summary, our data do not support an important physiologic role of renal prostaglandins in renal calcium excretion in normal subjects.
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PMID:Lack of effect of prostaglandin inhibition on calcium excretion in normal volunteers. 399 16

The effects of a 2 Gm oral phosphorus load in a family with idiopathic hypercalciuria (IH) consisting of 3 symptomatic (DT, CS, DS) and 2 asymptomatic (MS, PD) members were compared with 12 normal control subjects. Biochemical parameters measured included: total and ionized calcium, phosphorus, intact and carboxyl-terminal parathyroid hormone, urinary calcium, phosphorus, and sodium. Water loading had no effect on these parameters. After the phosphorus load, serum phosphorus rose 1.60 mg/dl in the control subjects but only 1.34 mg/dl in the IH family at the end of one hour. Basal tubular reabsorption of phosphate (TRP) were comparable in the control subjects and the IH family. After the phosphorus load, the TRP in the control subjects fell (average 9.2%) accompanied by a significant (P less than 0.02) rise in the carboxyl-terminal parathyroid hormone. Except for DT who had been taking hydrochlorothiazide, the TRP fell dramatically in the rest of the IH family (DS 25%, CS 12%, PD 26%, MS 50%) in the absence of any perturbations in either the intact or carboxyl-terminal parathyroid hormone. A hypocalciuric effect was observed in the IH family but not in the control subjects after phosphorus loading. The oral phosphorus challenge unmasked a parathyroid hormone independent renal phosphate leak in both symptomatic and asymptomatic members in a family with idiopathic hypercalciuria.
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PMID:Oral phosphate load unmasks underlying renal phosphate leak in symptomatic and asymptomatic members of family with idiopathic hypercalciuria. 401 72

The effect of borogluconate on plasma calcium fractions was studied in vitro and in vivo in sheep. In vitro calcium chloride was more effective in raising ionised plasma calcium than calcium borogluconate. Sodium borate or gluconate added to blood caused only small decreases in blood ionised calcium. However, together, a synergistic reduction in ionised calcium was observed. Following calcium borogluconate infusions into sheep, total plasma calcium rose primarily because of an increase in the unionised ultrafiltrable fraction. Other changes observed following the infusion were hypercalciuria, decreased glomerular filtration rate and acidosis. Sodium borogluconate administered subcutaneously lowered total plasma calcium. This probably resulted from enhanced calcium excretion. It is suggested that since the anionic component of calcium solutions alters the availability and retention of calcium, it is likely to affect clinical efficacy significantly.
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PMID:Formation of calcium complexes by borogluconate in vitro and during calcium borogluconate infusion in sheep. 403 94

Patients with hypercalciuria have been reported to have an exaggerated response to hydrochlorothiazide (HCTZ), implying a renal tubular defect in solute reabsorption. To determine whether this disturbance is generalized or unique to a particular pathogenetic type of hypercalciuria, we measured the increments in urinary sodium (delta Na), calcium (delta Ca), and magnesium after a 100-mg dose of oral HCTZ in 10 normal subjects and 31 patients with different types of hypercalciuric nephrolithiasis. Eleven patients with renal hypercalciuria had significantly greater delta Na (P less than 0.005) and delta Ca (P less than 0.005) than the normal subjects. Ten patients with absorptive hypercalciuria and 10 patients with fasting hypercalciuria without parathyroid stimulation had delta Na and delta Ca indistinguishable from those of normal subjects. In all groups, urinary HCTZ and basal 24-h urinary Na did not differ. The results suggest that the unique natriuretic and calciuric responses to HCTZ occur only in renal hypercalciuric patients with secondary hyperparathyroidism. The data support a renal tubular defect in renal hypercalciuric in contrast to other diagnostic categories of hypercalciuric nephrolithiasis.
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PMID:Exaggerated natriuretic and calciuric responses to hydrochlorothiazide in renal hypercalciuria but not in absorptive hypercalciuria. 404 75


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