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)

Patients with recurrent stone disease and hypercalciuria were cleared up according to Nordin's schedule. In cases of absorptive hypercalciuria, an ion exchanger operating in the intestine, sodium cellulose phosphate (SCP), is applied under strict control of oxalate, calcium and magnesium excretion as well as ionized calcium in serum. Under treatment with SCP (27 patients), we found a reduction in the renal excretion of calcium and magnesium, and, as a side effect, a significant augmentation of the renal oxalate excretion. In cases of resorptive or resorptive/absorptive hypercalciuria, except in patients with primary HPT, 23 patients were mediated by thiazides (Esidrix). This drug effects a marked decrease of urinary calcium based on a higher rate of reabsorption of calcium in the distal tubule. No severe side effects especially primary HPT were observed.
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PMID:Resorptive and absorptive hypercalciuria. Therapy with sodium cellulose phosphate or thiazides. 42 8

A persistent hypercalciuria and normal serum levels of calcium were measured in a 5-year-old boy suffering from recurrent macro- and microhaematuria and bilateral nephrolithiasis (stone analysis was positive for calcium-oxalate). No growth retardation or any other relevant clinical parameters concerning hypercalciuria e.g. vitamin D-intoxication or renal tubular acidosis could be observed. A slight secondary hyperparathyroidism and increased calcium excretion during fasting or calcium depleted diet indicates a primary failure of calcium reabsorption as previously described by Bordier (hypercalciuria type 2). Treatment with a combination of hydrochlorothiazide (Esidrix) and sodium chloride depleted diet resulted in a long-lasting normalization of calcium excretion and thus disappearance of symptoms in the child.
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PMID:[Idiopathic hypercalciuria due to primary decrease in the renal tubular reabsorption of calcium. Hypercalciuria type 2 according to Bordier (author's transl)]. 51 92

Results of investigation of 800 patients with renal calculi are presented. The high incidence of medullary sponge kidneys (tubular ectasia) in patients of either sex is stressed as is the low incidence of idiopathic hypercalciuria in the female. Hydrochlorothiazide has been found to be highly effective in preventing recurrence of calcium stones in our personal experience with over 300 patients who have been treated for as long as 14 years with this agent. The efficacy and mode of action of other measures advocated for stone prevention is reviewed.
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PMID:The management of the patient with calcium stones. 101 24

Hydrochlorothiazide is employed to reduce calcium excretion in patients with urinary stone disease secondary to renal leak hypercalciuria. Because the drug also has been reported to be a competitive inhibitor of oxalate excretion by the renal tubules, we sought to determine whether chronic use indeed affected the amount of oxalate excreted. Patients taking hydrochlorothiazide 50 mg daily did not have a statistically significant reduction in twenty-four-hour urinary oxalate on their customary diets (pretreatment 37 +/- 3 mg/day [mean +/- S.E.M.; N = 22]; at one year 36 +/- 3 mg/day [N = 22]; at two years 37 +/- 3 mg/day [N = 16]). In 12 patients who voluntarily collected twelve-hour urine specimens after dinner on the third day of a low-oxalate diet and again the next day after a 1 g oxalate load, hydrochlorothiazide had no significant effect on oxalate excretion (19 +/- 2.3 mmol oxalate/mol creatinine on hydrochlorothiazide versus 20.6 +/- 2.6 mmol off the drug after low oxalate meal; 50 +/- 7.8 mmol/mol creatinine on hydrochlorothiazide versus 56.2 +/- 7.5 mmol off the drug after an oxalate load). As expected, there was a significant reduction in urinary calcium excretion and thus of calcium oxalate urinary saturation during hydrochlorothiazide administration. Hydrochlorothiazide by itself is not sufficient to reduce oxalate excretion in patients with renal leak hypercalciuria.
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PMID:Urinary excretion of oxalate by patients with renal hypercalciuric stone disease. Effect of chronic treatment with hydrochlorothiazide. 201 97

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

Hydrochlorothiazide (HTZ) therapy reduces the urinary excretion of calcium (UCa V) in patients with idiopathic hypercalciuria (IH). To test the role of parathyroid hormone (PTH), namely the possibility that HTZ sensitizes the kidney to PTH as the sole or contributory cause of decreased UCa V associated with HTZ therapy, we measured urinary excretion of calcium (UCa V) and cAMP (UcAMP V), the tubular reabsorption of phosphate (TRP), plasma immunoreactive PTH, and the renal response to infused PTH (change in UcAMP V and TRP) in 10 patients with IH. Patients were studied before (control) and after 4 weeks of treatment with HTZ (100 mg/day). HTZ therapy significantly reduced UCa V (mean change, -122 +/- 19 mg/24 h). The UcAMP V, TRP, and plasma levels of calcium, phosphorus, and immunoreactive PTH were initially within the normal range and did not change significantly during HTZ therapy. PTH infusion resulted in a significant increase in the UcAMP V and a significant decrease in TRP during both control and HTZ therapy studies. There was, however, no significant difference in the degree of these renal responses to PTH infusion during the control vs. HTZ therapy studies. We conclude that the hypocalciuric effect of HTZ in patients with IH is independent of changes in PTH secretion, and that HTZ does not cause general sensitization of the nephron, namely proximal tubules, to PTH, as assessed by an increase in UcAMP V and a decrease in TRP.
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PMID:Idiopathic hypercalciuria: hydrochlorothiazide decrease urinary calcium without altered renal response to parathyroid hormone. 628 1

1. Chronic administration of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] can normalize plasma calcium in human hypoparathyroidism and in thyroparathyroidectomized animals. The effect of 1,25(OH)2D3 on plasma calcium is associated with an increase in urinary calcium excretion. In an attempt to prevent this increase thyroparathyroidectomized rats receiving 1,25(OH)2D3 were also treated with hydrochlorothiazide for 9-11 days. 2. Calcium clearance studies show that hydrochlorothiazide stimulated the tubular reabsorption of calcium in thyroparathyroidectomized rats treated with 1,25(OH)2D3. 3. Calcium balance and kinetic studies indicated that hydrochlorothiazide decreased 1,25(OH)2D3-induced hypercalciuria in thyroparathyroidectomized rats. Hydrochlorothiazide did not affect the 1,25(OH)2D3-induced increase in plasma calcium. The hypocalciuric effect of hydrochlorothiazide was not associated with significant changes in calcium deposition into or release from bone. 4. In thyroparathyroidectomized rats treated with 1,25(OH)2D3 the hypocalciuric effect of hydrochlorothiazide was associated with a fall in intestinal calcium absorption. Overall, the calcium balance was unaffected. 5. Thus it appears that hydrochlorothiazide reduces the 1,25(OH)2D3-induced hypercalciuria in parathyroid hormone-deficient animals by decreasing intestinal calcium absorption. Despite the decreased absorption, hydrochlorothiazide does not reduce the 1,25(OH)2D3-induced increase in plasma calcium.
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PMID:Effect of hydrochlorothiazide on 1,25-dihydroxyvitamin D3-induced changes in calcium metabolism in experimental hypoparathyroidism in rats. 689 67

Recent studies have shown that, not only in hypertensive animals but even in normotensive rats, dietary salt (sodium chloride) produces a dose-related increase in the left ventricular and renal mass. In the present study the effects of the angiotensin converting enzyme inhibitor (ACEI) enalapril and the thiazide-type diuretic, hydrochlorothiazide, on the development of the salt-induced left ventricular and kidney hypertrophy were examined in normotensive Wistar-Kyoto and Wistar rats. A high intake of sodium chloride (6% of the dry weight of the chow to mimic the level found in many human food items) during eight weeks produced a marked increase in the mass of the left ventricle and the kidneys in both rat strains with little or no effect on blood pressure. The cardiac hypertrophy correlated strongly with the renal hypertrophy. These salt-induced changes in the heart and in the kidneys were completely blocked by hydrochlorothiazide, while enalapril was devoid of any significant effects during the high-salt diet. However, during a low-salt diet enalapril, but not hydrochlorothiazide, effectively lowered the blood pressure and decreased the left ventricular mass of the normotensive rats. There was a 3- to 4-fold increase in the urinary excretion of calcium during the high intake of sodium chloride. Hydrochlorothiazide decreased the urinary excretion of calcium even during the low salt diet, and it completely blocked the salt-induced hypercalciuria. Enalapril had no significant effect on the urinary calcium excretion. During the low-salt diet hydrochlorothiazide increased the calcium and decreased the potassium concentration in the heart while enalapril increased the phosphorus concentration. In conclusion, a high intake of sodium chloride produced hypertrophy both in the heart and in the kidneys, even in the absence of a rise in blood pressure. Salt also remarkably increased the urinary calcium excretion. These harmful effects of salt were blocked by the thiazide diuretic hydrochlorothiazide but not by the ACEI enalapril. However, this study does not allow to make any direct comparison between the effects of enalapril and hydrochlorothiazide.
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PMID:Effects of enalapril and hydrochlorothiazide on the salt-induced cardiac and renal hypertrophy in normotensive rats. 784 79

Hypercalciuria is a biological syndrome defined as excretion in the urine of more than 0.1 mmol/kg/24 hours of calcium in the absence of dietary manipulation. A number of endocrine, renal, and bone diseases can cause hypercalciuria. Urinary calcium excretion is substantially influenced by dietary intakes of calcium, sodium, protein, carbohydrates, alcohol, and potassium: a poorly balanced diet can result in hypercalciuria. Recently, there has been a burst of interest in the molecular underpinnings of rare nephrolithiasis syndromes, which have been shown to result from mutations in the CLCN5 chloride channel gene. Mutations affecting the calcium-sensing receptor (CaSR) have been identified in other forms of hypercalciuria. Idiopathic hypercalciuria is defined as hypercalciuria that persists after correction of dietary imbalances and has no detectable cause. The classification suggested by Pak ("absorptive" hypercalciuria [with three types] and "renal" hypercalciuria) is controversial and of little assistance in clinical practice. Three mechanisms can be incriminated in idiopathic hypercalciuria: increased intestinal absorption of calcium, defective reabsorption of calcium by the renal tubule, and increased bone resorption. Overexpression of the vitamin D receptor (VDR) and deficiencies in renal tubule enzymes may also be involved. Bone mineral density is moderately decreased in idiopathic hypercalciuria, particularly in the renal type. The risk of vertebral fracture seems increased, however. Overproduction of calcitriol and cytokines that stimulate bone resorption have been incriminated in the bone loss. Treatment of the cause is essential in secondary hypercalciuria (dietary advice, treatment of an underlying disease, etc.). A diet low in sodium and meat and containing no more than 800 mg of calcium per day is advocated in idiopathic hypercalciuria. Hydrochlorothiazide therapy is warranted in patients with osteopenia and an inadequate response to dietary therapy.
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PMID:Hypercalciuria. 1119 13

Gain-of-function mutations of the calcium-sensing receptor (CaR) gene cause autosomal dominant and/or sporadic hypocalcemia with hypercalciuria. Because treatment of the hypocalcemia with vitamin D and/or calcium in patients with such mutations results in increased hypercalciuria, nephrocalcinosis, and renal impairment, its use should be limited to alleviating the symptoms of symptomatic patients. Because thiazide diuretics have been successfully used to treat patients with hypercalciuria and hypoparathyroidism, they are theoretically useful in reducing urine calcium excretion and maintaining serum calcium levels in patients with gain-of-function mutations of the CaR gene. In this study, we report on the clinical course, molecular analysis, and effects of hydrochlorothiazide therapy in two Japanese patients with gain-of-function mutations of the CaR gene. Within a few weeks after birth, they developed generalized tonic seizures due to hypocalcemia (serum calcium values: 1.1 mmol/liter and 1.3 mmol/liter, respectively). Despite treatment with the standard dose of 1,25-dihydroxyvitamin D(3) in one patient and 1alpha-hydroxyvitamin D(3) in the other, acceptable serum calcium levels near the lower limit of normal were not established, and their urinary calcium excretion inappropriately increased. Addition of hydrochlorothiazide (1 mg/kg) reduced their urinary calcium excretion and maintained their serum calcium concentrations near the lower limit of normal, allowing the 1,25-dihydroxyvitamin D(3) and 1alpha-hydroxyvitamin D(3) doses to be reduced, and it alleviated their symptoms. A heterozygous missense mutation was identified in both patients. In one patient, the mutation was A843E in the seventh transmembrane domain of the CaR, and in the other it was L125P in the N-terminal extracellular domain. In vitro transient transfection of their mutant CaR cDNAs into HEK293 cells shifted the concentration-response curve of Ca(2+) to the left. In conclusion, two sporadic cases of hypercalciuric hypocalcemia were due to de novo gain-of-function mutations of the CaR gene. Hydrochlorothiazide with vitamin D(3) successfully reduced the patients' urinary calcium excretion and controlled their serum calcium concentrations and symptoms. Thiazide diuretics are effective in patients with gain-of function mutations of the CaR gene.
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PMID:Hydrochlorothiazide effectively reduces urinary calcium excretion in two Japanese patients with gain-of-function mutations of the calcium-sensing receptor gene. 1210 2


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