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)

Mechanisms involved in the hypercalciuria caused by high levels of protein intake were investigated. Six healthy males participated in a 20-day metabolic study. During the first 10-day period, all subjects were given a 47 g protein diet and during the second 10-day period, a 142 g protein diet. Calcium, magnesium and phosphorus intakes were kept constant at 515, 320 and 1,110 mg daily, respectively. Urinary calcium was elevated significantly when the protein intake was increased. Glomerular filtration rate and calcium clearance were increased significantly when the high protein diet was fed; the fractional tubular reabsorption of calcium was decreased from 98.4 to 97.4%. Thus, the increase in urinary calcium caused by the high protein diet appears to be due in part to an increase in the filtered load of calcium by the glomeruli and in part to a decrease in calcium reabsorption by the renal tubules. The level of protein intake had no effect on the fasting serum concentrations of parathyroid hormone, total calcium, magnesium or inorganic phosphorus or plasma ultrafiltrable calcium.
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PMID:Effect of level of protein intake on calcium metabolism and on parathyroid and renal function in the adult human male. 45 94

Metabolic evaluation of patients with multiple or recurrent calcium stones has been fruitful. The great majority of cases has demonstrated abnormalities contributing to stone formation. Hypercalciuria on the basis of increased intestinal absorption of calcium was a common finding. The evaluation led to improved guide lines for therapy.
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PMID:The benefits of evaluation of the patient with recurrent or multiple calcium stones. 45 48

We studied weanling rats fed 0.06% (group 1) and 0.10% (group II) magnesium (Mg) during phosphate depletion (PD) in order to evaluate the role of Mg in the bone, soft tissue, and serum changes of PD. The following results were obtained: 1) serum Mg remained stable in the face of a negative Mg balance; 2) the hypercalcemic and hypercalciuric response to PD was the same in both groups; 3) bone Mg content was decreased with PD in both groups and was associated with a significant decrease in bone calcium and phosphorus. We conclude that: 1) the hypomagnesemia of PD is dependent mainly on the dietary intake of Mg; 2) the hypercalcemia and hypercalciuria of PD are not caused by primary changes in Mg homeostasis; 3) low-dietary Mg during PD may cause a defect in soft tissue utilization of P in the growing rat.
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PMID:Influence of dietary magnesium in experimental phosphate depletion: bone and soft tissue mineral changes. 46 91

Two families are reported affected with hereditary renal hypouricaemia associated with uric acid lithiasis. The propositi of both families were found also to have hyperabsorptive hypercalciuria. Based on the study of the effect of pyrazinamide and probenecid on uric acid excretion in both propositi, it is suggested that the defect in uric acid reabsorption is most probably at the pre-secretory site.
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PMID:Familial renal hypouricaemia: two additional cases with uric acid lithiasis. 46 79

Eighty-eight urinary tract stone formers (74 men) with idiopathic hypercalciuria were treated by dietary calcium restriction alone. Short-term control of hypercalciuria was achieved in only 27 patients and all but 12 eventually escaped control. Failure of control was twice as likely in patients with severe hypercalciuria. Almost all patients lived in a hard water area. In such areas at least, attempts to control hypercalciuria by diet alone are likely to fail and early introduction of additional treatment is advisable. In most severe hypercalciurics, such treatment should be introduced from the start.
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PMID:Dietary treatment of idiopathic hypercalciuria. 46 84

The causes of, and physiopathological factors underlying the most common metabolic disorders implicated in the formation of renal stones are reviewed. These include hypercalciuria, hyperoxaluria, renal tubular acidosis, cystinuria and disturbances of purine metabolism. Apart from metabolic disorders the risk of stone formation is also influenced by a low inhibitor activity in urine. Though some aspects in the pathogenesis of urolithiasis remain uncertain, the exact knowlege of important aetiological factors of stone formation is the basis of correct treatment and the prevention of recurrence of urinary calculi.
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PMID:[The evaluation of patients with urinary calculi discloses disturbances of metabolism in 75% of all cases (author's transl)]. 47 69

Inborn hypouricemia due to isolated renal tubular defect is a rare disorder. Thus far eight documented families with this condition have been reported. In reviewing the data on these families, hyperuricosuria was found to be a constant associate of the hypouricemia, and hypercalciuria, mainly of the absorptive type, was frequently associated. Urolithiasis appears to be common. The mode of inheritance of this hypouricemia was autosomal, probably recessive. The magnitude of renal urate clearance and the effects on it of probenecid and pyrazinamide suggest the inborn renal hypouricemia to be of two types, due to defective re-secretory tubular urate reabsorption and to total defective tubular urate reabsorption. The question of the renal tubular abnormality for urate transport being the primary defect or secondary to an abnormal metabolite is discussed.
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PMID:Inborn hypouricemia due to isolated renal tubular defect. 47 67

A 9 year old girl with idiopathic Fanconi syndrome and hypercalciuria is described. In order to determine whether the increased calcium excretion was directly or indirectly due to the disturbed phosphate metabolism, the behavior of the calcium excretion during therapy, the serum levels of 1,25-dihydroxyvitamin D and parathyroid hormone, and the effect of parathyroid hormone on the renal tubules were investigated. Normal serum 1,25-dihydroxyvitamin D and parathyroid hormone levels, lack of a correlation between the serum phosphate concentration and the degree of hypercalciuria, as well as unsuccessful therapy of the hypercalciuria with oral phosphate indicate that the increased calcium excretion cannot be explained by impaired renal phosphate reabsorption. The hypercalciuria in the patient was therefore regarded as being due to a primary decrease of tubular calcium reabsorption.
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PMID:Hypercalciuria in idiopathic Fanconi syndrome. 47 82

Two methods of oral calcium load or tolerance test for the indirect assessment of calcium absorption were compared. In 16 patients in whom the diagnosis of absorptive hypercalciuria was made independently, an exaggerated urinary total calcium excretion during four hours following calcium load, indicative of increased calcium absorption according to the method of Pak et al., was found in 15 patients. An abnormally high increment in urinary calcium during third and fourth hours post-calcium load, suggestive of enhanced calcium absorption by the criteria of Broadus et al., was encountered in 14 patients. However, an exaggerated urinary total calcium following calcium load was found in all 7 patients with renal hypercalciuria, whereas only 4 were shown to have an enhanced increment in calcium excretion. It is concluded that both methods are equally reliable in the detection of increased calcium absorption in absorptive hypercalciuria. However, the technique of Broadus et al. is probably superior to that of Pak et al. in the disclosure of increased calcium absorption in renal hypercalciuria.
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PMID:Critical appraisal of oral calcium load test for indirect assessment of intestinal calcium absorption. 48 99

The association of hypercalciuria, salt losing renal disease, and a defect in urine concentrating ability with high renin and aldosterone levels is described in two brothers. One child had marked nephrocalcinosis by the age of 3 and the other severe growth retardation. In one child all the abnormalities were abolished with indomethacin which was responsible for a marked decrease in urinary. The data and the family study suggest that this condition is a proximal tubular disorder with atuosomal recessive inheritance.
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PMID:[Familial tubulopathy associating hypercalciuria and saline diabetes. Favorable results of indomethacin therapy]. 48 70


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