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)

Twenty-four-hour urinary excretion of calcium, oxalic acid, inorganic phosphorus, magnesium and citric acid was examined in fifty-nine stone formers with bladder stones. Hypercalciuria and hyperoxaluria were present in 18.6% and 44.1%, respectively, while 11.9% of patients had both abnormalities. Hypomagnesuria and hypocitraturia were present in 67.8% and 69.5%, respectively, while 45.7% had both of these abnormalities. Normal urine chemistry in respect of parameters studied was observed only in 1.7% of cases. In 15.2% one risk factor was present, while 83.1% had two or more risk factors. "Path" analysis of the urinary parameters directly related to calcium lithiasis showed that magnesium and oxalic acid have substantial influence on calcium excretion, whereas citric acid had none. The influence of phosphorus did not provide any consistent trend.
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PMID:Interdependence of urinary factors in calcareous bladder stone patients. 274 86

Adult cats with normal renal function were fed a nutritionally balanced, vitamin A-replete, experimental dry diet with or without ammonium chloride (NH4Cl) for 6 mo to study the effects of chronic dietary acidification on acid-base parameters and the metabolism of selected minerals. Dietary balance studies were performed monthly. Blood and urine samples were collected monthly to evaluate acid-base parameters, plasma parathyroid hormone (PTH) and 1.25-dihydroxycholecalciferol levels. Ammonium chloride-treated cats had significantly lower blood and urinary pH, and lower blood bicarbonate concentrations. Treated cats also had higher blood ionized calcium concentrations, hypercalciuria and lower intestinal calcium absorption relative to baseline (prior to feeding the experimental diet) and to control cats. This resulted in the development of lower calcium balance in the first several months. PTH levels were unaffected by dietary acidification; however, 1.25-dihydroxycholecalciferol levels were significantly decreased in treated cats. Treated cats had negative potassium balance during 5 mo of dietary acidification. Magnesium, sodium, and phosphorus balances were lower, but positive, in treated cats compared to control cats. Cats consuming the NH4Cl-supplemented diet had increased chloride balance. Thus, chronic dietary acidification with 1.5% NH4Cl produced chronic metabolic acidosis and lower or negative, calcium and potassium balance.
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PMID:The effect of chronic dietary acidification using ammonium chloride on acid-base and mineral metabolism in the adult cat. 274 72

In 19 preterm infants fed a standard formula for prematures (calcium (Ca) 13.5 mmol/l; phosphorus (P) 12.9 mmol/l), biochemical parameters of blood, serum and urine were determined before and during supplementation with Ca-L-lactate (final Ca concentration 20 mmol/l). In 8 preterm boys Ca and P balance were evaluated in addition. During Ca supplementation, the serum Ca levels, urine pH (without supplement 6.31, with supplement 6.73), and calciuria (46 mumol/kg/d vs. 98 mumol/kg/d) were increased, and urinary P (1.05 mmol/kg/d vs. 0.65 mmol/kg/d) and net acid excretion (1.70 mEq/kg/d vs. 0.89 mEq/kg/d) were decreased. Balance studies showed increased net intestinal Ca absorption during supplementation (37% vs. 56%) as well as improved Ca (0.8 mmol/kg/d vs. 1.85 mmol/kg/d) and P retention (0.97 mmol/kg/d vs. 1.45 mmol/kg/d). These data show that increased Ca intake given to optimize the Ca:P ratio improves mineral retention in preterm infants fed a standard formula. Ca and P intake should be thoroughly balanced to avoid side-effects like hypercalciuria or high renal net acid excretion.
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PMID:Effect of calcium supplementation on calcium and phosphorus balance and renal net acid excretion in preterm infants fed a standard formula. 278 67

A 14-year-old Turkish boy had severe rickets that had been clinically evident since he was 2 years of age. When he was 5 years of age, he had normal serum calcium and phosphorus levels and increased alkaline phosphatase activity. Treatment with modest dosages of vitamin D (5000 U/d for 3 weeks) resulted in hypercalcemia. At 10 years of age, high-dose vitamin D (40,000 U/d) plus phosphorus (1.1 g/d) therapy for 20 days resulted in symptomatic nephrolithiasis. When, 14 years of age, he had normocalcemia, hypophosphatemia, increased alkaline phosphatase activity, and normal circulating parathyroid hormone concentration. Levels of 25-hydroxyvitamin D were normal but those of 1,25-dihydroxyvitamin D were markedly increased. Rickets and osteopenia were evident on radiographs, and osteomalacia was present on trabecular bone obtained at biopsy. Balance study results showed increased intestinal absorption of calcium and phosphorus, hypercalciuria, and increased urinary phosphorus excretion. This patient manifests an unusual form of hypophosphatemic rickets in which hypercalciuria is a cardinal feature. In contrast with most varieties of hypophosphatemia, this disorder is characterized by appropriately increased production of 1,25-dihydroxyvitamin D in response to hypophosphatemia. It is recommended that urinary calcium excretion be assessed in all patients with hypophosphatemic rickets so that appropriate therapy will be instituted.
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PMID:Hypercalciuric hypophosphatemic rickets, mineral balance, bone histomorphometry, and therapeutic implications of hypercalciuria. 278 97

The causes of impaired calcium, phosphorus and vitamin D metabolism in diabetic patients which in the long run lead to demineralization of bone can be summarized into several main groups. Above all disorders of calcium absorption from the small intestine are involved, associated with impaired absorption of vitamin D and its reduced conversion into active metabolites in the liver and kidneys. An increased elimination of calcium from the organism may also play a part (hypercalciuria, excretion in the faeces and sweat), hormonal changes (secondary hyperparathyroidism) and finally changes in the metabolism of the organic bone constituent--osteoid. Subsequent work will deal with the prevalence of osseous changes in diabetics, early diagnosis and rational treatment and possible prevention of these changes.
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PMID:[Diabetic osteopathies. 1. Etiologic factors and theoretical prerequisites for the development of bone demineralization in diabetics]. 280 Mar 64

The treatment of premature infants with the diuretic furosemide appears to be a contributory factor in the development of metabolic bone disease presumably because of furosemide-induced hypercalciuria. In this study, we measured calcium and phosphorus balance in furosemide-treated very low birth weight infants (VLBW) infants with bronchopulmonary dysplasia (BPD) who were fed a specialized premature formula containing increased amounts of calcium and phosphorus. Furosemide-treated infants received 166 +/- 37 mg/kg/day and retained 80 +/- 34 mg/kg/day of calcium, and 87 +/- 19 mg/kg/day and retained 52 +/- 14 mg/kg/day of phosphorus. The amounts retained were approximately 65% of the calcium and 72% of the phosphorus requirements for in utero mineral accretion. Compared to a group of similarly fed VLBW infants without BPD and not treated with the diuretic, the furosemide-treated infants excreted a larger percent of the calcium intake in the urine but had similar total urinary calcium and phosphorus losses (mg/kg/day) and serum calcium, phosphorus, alkaline phosphatase, and parathyroid hormone (PTH) levels. From the latter two findings, we suggest that the extra mineral content of the formula may have promoted bone mineralization and prevented the occurrence of secondary hyperparathyroidism.
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PMID:Effect of high calcium and phosphorus intake on mineral retention in very low birth weight infants chronically treated with furosemide. 280 41

Vitamin D deficiency is associated with a generalized aminoaciduria which has been shown to be independent of parathyroid hormone (PTH) and urinary cyclic AMP excretion. To further characterize the mechanism underlying the tubulopathy, weanling rats were placed on one of the following diets for 5 weeks: (1) control [0.7% phosphorus (P), 5.5 micrograms % vitamin D]; (2) D-P- (0.1% P, 0 vitamin D); (3) D+P- (0.1% P, 5.5 micrograms % vitamin D); (4) D-P+ (0.3% P, 0 vitamin D); (5) D-P++ (0.7% P, 0 vitamin D). All diets contained 1.2% calcium (Ca). A group of rats raised on D-P++ for 4 weeks were fed D-P- for 7 days after which they received 500 pmol of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3; SUPP] or an equal volume of the vehicle (ETH). The above diets resulted in partial vitamin D depletion in that 1,25(OH)2D levels were 50.25-79 pg/ml in the presence of very low 25(OH)D concentrations. Augmentation in the urinary excretion of 6 out of 8 amino acids measured was observed in P depletion irrespective of vitamin D status. For the most part, acute supplementation with 1,25(OH)2D3 did not ameliorate the tubulopathy. Plasma PTH and Ca concentrations remained normal in all diets, except D+P-, where plasma Ca was 15.88 +/- 0.54 mg/dl. P depletion was associated with hypercalciuria, hypophosphatemia, avid reabsorption of P and growth retardation, irrespective of vitamin D status. Using taurine as a representative of the amino affected, there was a strong correlation between urinary taurine on the one hand and dietary P content (r = 0.613), plasma P (r = 0.399) and 1,25(OH)2D levels (r = -0.576) on the other. The present study suggests that the aminoaciduria of vitamin D deficiency is not related to elevated levels of PTH. A similar defect may be produced by P depletion, suggesting the possibility of a common pathway for the effect.
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PMID:Effect of vitamin D deficiency on amino acid excretion in the phosphate-depleted rat. 281 86

To evaluate the cause of hypercalciuria, we carried out the oral calcium tolerance test before and after parathyroidectomy in a patient with primary hyperparathyroidism who had recurrent and multiple nephrolithiasis. Preoperative laboratory examination showed hypercalcemia, hypophosphetamia, hypercalciuria, decrease in % tubular reabsorption of phosphorus and strikingly elevated urinary cyclic AMP excretion. The oral calcium tolerance test indicated a significantly greater increase in serum calcium (delta serum calcium: 1.4 mg/dl vs 0.8 mg/dl) and a significantly greater suppression of urinary cyclic AMP excretion (delta U-cyclic AMP:-3.56 moles/gCre vs-1.17 moles/gCre) before parathyroidectomy than after. These results showed that hypercalciuria in this case was induced not only by the significant increase in the filtrated load of calcium but by the reduction in the resorption of calcium in the distal tubule caused by the significantly suppressed parathyroid hormone effect.
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PMID:[A case report: primary hyperparathyroidism--comparison before and after parathyroidectomy by oral calcium tolerance test]. 283 26

116 normocalcemic and 8 primary hyperparathyroid (PHPT) patients with calcium (Ca) nephrolithiasis and 10 normal controls underwent 1 g of oral Ca tolerance test following 4 days of Ca restricted diet (400 mg/day). On the basis of urinary Ca/creatinine (Cr) ratio obtained by the test, the 116 patients with normocalcemic nephrolithiasis were divided into 3 groups (normocalciuric nephrolithiasis; NN, absorptive hypercalciuria; AH, renal hypercalciuria; RH) according to our criteria which were slightly modified from Pak et al. Changes in urinary Ca/Cr ratio, and those in serum Ca and phosphorus (P), tubular maximum reabsorption of phosphate/glomerular filtration rate (TmPO4/GFR), nephrogenous adenosine 3',5'-monophosphate (NcAMP) and plasma immunoreactive parathyroid hormone (iPTH) were determined. As a result, the 116 patients were divided into 82NN, 13AH and 21RH. In general, a rise in serum Ca and fall in NcAMP were seen first, followed by rises in urinary Ca/Cr ratio, serum P and TmPO4/GFR although the changes were small. The group PHPT showed abnormality in the changes of TmPO4/GFR, NcAMP and plasma iPTH. The former one decreased constantly during the test and the latter two did not fall to within the normal range, suggesting parathyroid autonomy or abnormal suppressibility. Regarding the normal controls, all the changes were smallest among the 5 groups and clear parathyroid suppression was not observed while it was seen in the groups NN, AH and RH. In conclusion, oral Ca tolerance test is useful not only to separate NN, AH and RH, but also for the diagnosis of PHPT by demonstrating parathyroid autonomy or abnormal suppressibility assessed by NcAMP and/or TmPO4/GFR.
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PMID:Biochemical changes before and during oral calcium tolerance test in calcium stone formers. 284 10

In a short-term prospective study 36 patients with absorptive hypercalciuria were initially treated with diet alone followed by either trichlormethiazide (4 mg. per day) or oral neutral phosphate (1,500 mg. of elemental phosphorus per day) for 6 weeks. Study subjects were then crossed over to the second drug for an additional 6 weeks. In response to dietary treatment urinary calcium decreased from a pre-treatment value of 346 +/- 63 mg. per 24 hours to 308 +/- 90 mg. per 24 hours. Oral phosphate therapy caused a further decrease in urinary calcium to 218 +/- 85 mg. per 24 hours, an over-all decrease of 37 per cent. Parathyroid function did not change significantly with phosphate administration but circulating levels of 1,25-dihydroxyvitamin D decreased by 22 per cent (73 +/- 12 to 57 +/- 16 pg. per ml., p less than 0.001). Pre-treatment renal phosphate threshold did not correlate with the response to oral phosphate administration. Trichlormethiazide treatment led to a 34 per cent decrease in urinary calcium with a mean value on treatment of 228 +/- 80 mg. per 24 hours. 1,25-Dihydroxyvitamin D levels decreased by 10 per cent. Pre-treatment fasting calcium excretion, parathyroid function and 1,25-dihydroxyvitamin D levels did not correlate with the response to trichlormethiazide. We conclude that both drugs by pharmacological means improve the biochemical abnormalities in absorptive hypercalciuria and should be efficacious in its treatment.
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PMID:Trichlormethiazide and oral phosphate therapy in patients with absorptive hypercalciuria. 291 43


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