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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirteen urolithiasis patients with unilateral obstructive uropathy were treated with percutaneous nephrostomy (PCN) either for urinary diversion, endopyelotomy, nephrolithtotmy or chemolysis. After percutaneous nephrostomy, the individual urine volume, creatinine clearance (Ccr), urinary absolute and fractional excretions of sodium, potassium, calcium, magnesium and inorganic phosphate were measured separately in timed urine collections from a pigtail catheter and from the urethra. The data showed that Ccr and the absolute urinary excretions of sodium, potassium, calcium, magnesium and inorganic phosphate were significantly lower in the PCN kidney immediately or 2 days after relief of obstruction. The ratio of total urinary calcium excretion to urinary creatinine excretion in the obstructed kidney was significantly greater than that in the contralateral kidney. The fractional excretions of calcium and magnesium increased as renal function decreased. The results showed that when the total Ccr is below normal, the apparent excretion of urinary calcium will be underestimated. However, when the total Ccr of patients is within normal range, hypercalciuria may be detected adequately and thus favors early implementation of an appropriate therapeutic strategy.
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PMID:Reduction of calcium excretion in the stone-forming kidney in unilateral ureteral obstruction. 188 28

To elucidate the pathophysiology of dietary calcium independent hypercalciuria, 42 calcium stone formers (Ca SF) were selected because they had on free diet a calciuria greater than 0.1 mmol/kg/day. For four days they were put on a diet restricted in calcium (Ca RD) by exclusion of the dairy products. They collected 24 hour urines on free diet and on day 4 of Ca RD as well as the two-hour fasting urines on the morning of the day 5 and the four-hour urines passed after an oral calcium load of 1 g, for measurement of creatinine, Ca, PO4, urea and total hydroxyprolinuria (THP). On day 5 fasting plasma concentrations of Ca, PO4, intact PTH, Gla protein, calcidiol and calcitriol were measured. The patients were firstly classified into dietary hypercalciuria (DH, 18 patients) and dietary calcium-independent hypercalciuria (IH, 24 patients) on the basis of the disappearance or not of hypercalciuria on Ca RD. Then the patients with IH were subclassified into absorptive hypercalciuria (AH) because of normal fasting calciuria (8 patients) and into fasting hypercalciuria (16 patients). Fasting hypercalciuric patients were subsequently divided according to the PTH levels into renal hypercalciuria (RH, 1 patient) with elevated fasting PTH becoming normal after the Ca load and undetermined hypercalciuria (UH, 15 patients) with normal PTH levels. Furthermore, their vertebral mineral density (VMD) was measured by quantitative computerized tomography which was normal in DH (91 +/- 6% of the normal mean for age and sex) but was decreased in IH to 69 +/- 4%. No difference in VMD was observed between AH and UH. Urinary excretions of urea, phosphate and THP was higher in IH than in DH and comparable in AH and UH. Sodium excretion Ca RD was the same in all groups and subgroups as well as the plasma parameters. Plasma calcitriol was increased in IH and DH comparatively to normal in spite of normal plasma calcidiol. Calciuria increase after oral calcium load, an index of Ca absorption, was higher in IH than in controls and comparable in IH and DH as well as in the three subgroups of IH. From these data and correlation studies in IH it is concluded: (1.) VMD is decreased in Ca stone formers with IH but not in those with DH, making the distinction of these two groups of hypercalciuria patients clinically relevant.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diet, vitamin D and vertebral mineral density in hypercalciuric calcium stone formers. 189 73

A series of 182 calcium stone formers with idiopathic hypercalciuria underwent treatment with rice bran for 1 to 94 months. Urinary calcium excretion was considerably reduced, but there was some increase in urinary phosphate and oxalate. Urinary excretion of magnesium and uric acid, serum calcium, magnesium, phosphate, uric acid, parathyroid hormone (PTH) and ALP was unaffected. There were no obvious changes in serum iron, zinc and copper even when patients were treated for long periods. Rice bran was well tolerated in almost all cases and there were no serious side effects; 49 patients have undergone treatment for more than 3 years (average duration of administration 5.09 years). The frequency of new stone formation was drastically reduced (individual stone formation rate (no./year) from 0.720 +/- 0.533 to 0.125 +/- 0.204; group stone formation rate (no./patient-year) from 0.721 to 0.120) compared with the 3-year period before treatment. During treatment, 61.2% of patients remained in remission. Although rice bran therapy should be effective in correcting absorptive hypercalciuria, there may be limits to the overall ability of rice bran monotherapy to prevent recurrence.
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PMID:Results of long-term rice bran treatment on stone recurrence in hypercalciuric patients. 190 88

The synergistic interaction of fructose and magnesium (Mg) deficiency on kidney calcification was compared in male and female rats. Male and female weanling rats were divided into four dietary groups: fructose or starch, with or without Mg. Rats were fed their respective diets for 9 weeks, and 24 h urine was collected to measure urinary output, pH, Mg, calcium (Ca), and oxalic acid. Rats were fasted overnight. After decapitation, blood was collected immediately, and kidneys were removed to determine their Mg and Ca content. Dietary fructose significantly increased kidney Ca in female rats fed deficient or adequate Mg diet and in male rats fed Mg-deficient diet only; the greatest kidney calcification occurred in female rats fed Mg-deficient diet (P less than 0.0001). Even in starch groups female rats fed the Mg-deficient diet showed some kidney Ca accumulation. The synergistic interaction of fructose and magnesium deficiency on nephrocalcinosis was significantly greater in female than in male rats. Low urinary output, optimal pH 6.8 for calcium phosphate precipitation, hypercalcaemia, hypercalciuria, hypomagnesuria, and low ratio of urinary Mg to Ca may independently or multifactorially contribute to nephrocalcinosis. The possible mechanism of this interaction is discussed.
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PMID:Dietary fructose produces greater nephrocalcinosis in female than in male magnesium-deficient rats. 191 Oct 97

Our primary objective was to test the hypothesis that a defect in acidification is more common in patients who have idiopathic calcium phosphate kidney stones than in those whose stones are formed mainly of calcium oxalate. Additionally, other risk factors might differ for these 2 stone types. Urine pH was measured serially over 24 hours, and along with ammonium and titratable acid, it was measured before and serially after ingestion of ammonium chloride in 3 groups of subjects: 24 patients with predominantly calcium phosphate stones, 30 patients with calcium oxalate stones, and 15 health non-stone-formers. Twenty-six parameters potentially related to stone formation and acidification were assayed on urines collected over 24 hours, and 15 parameters on blood. The data base was a computerized list of 5900 analyses of stones from patients living in Newfoundland. Patients not known by their physician to have had urinary tract infection, anatomical abnormality, hyperparathyroidism, or renal tubular acidosis were asked to participate in the study. Differences between means were considered significant if p values were less than 0.05 for F by analysis of variance and also less than 0.01 by t-test. In all patients with calcium oxalate stones and all non-stone-formers, urine acidified to pH less than 5.25, but in 8 of the 23 phosphate stone formers who completed the ammonium chloride study urine failed to acidify to pH less than 5.25. As all 8 had normal values for venous pH, total CO2, and chloride, they were considered to have incomplete renal tubular acidosis (IRTA). The 8 phosphate stone formers with IRTA had greater mean values for urine pH on all 9 specimens collected serially over 24 hours (all means greater than 6.2), and after administration of ammonium chloride (p less than 0.01), as well as lower mean values for urine titratable acid excretion (p less than 0.01), both after administration of ammonium chloride and in 24-hour urine samples, compared with the remaining phosphate stone formers whose urine acidified and the oxalate and non-stone-forming control groups. Nearly all the phosphate stone formers had 1 or more risk factors for stone formation, but with frequencies not significantly higher than those found in the oxalate group. Hypercalciuria and hypocitruria were the commonest, but increased oxalate or urate also occurred. Thus, idiopathic calcium phosphate stone formation can be associated with 1 or more of several risk factors, and, with the possible exception of those with IRTA, treatment should be similar to that given to patients with calcium oxalate stones.
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PMID:Comparison of patients with idiopathic calcium phosphate and calcium oxalate stones. 195 78

Nephrolithiasis is a heterogeneous disorder, with varying chemical composition and pathophysiologic background. Although kidney stones are generally composed of calcium oxalate or calcium phosphate, they may also consist of uric acid, magnesium-ammonium phosphate, or cystine. Stones develop from a wide variety of metabolic or environmental disturbances, including varying forms of hypercalciuria, hypocitraturia, undue urinary acidity, hyperuricosuria, hyperoxaluria, infection with urease-producing organisms, and cystinuria. The cause of stone formation may be ascertained in most patients using the reliable diagnostic protocols that are available for the identification of these disturbances. Effective medical treatments, capable of correcting underlying derangements, have been formulated. They include sodium cellulose phosphate, thiazide, and orthophosphate for hypercalciuric nephrolithiasis; potassium citrate for hypocitraturic calcium nephrolithiasis; acetohydroxamic acid for infection stones; and D-penicillamine and alpha-mercaptopropionylglycine for cystinuria. Using these treatments, new stone formation can now be prevented in most patients.
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PMID:Etiology and treatment of urolithiasis. 196 46

We characterized the bone disease of transilial biopsy specimens from children with hereditary hypophosphatemic rickets with hypercalciuria (HHRH) and genetically related asymptomatic hypercalciuric subjects. All HHRH patients showed irregular mineralization fronts, markedly elevated osteoid surface and seam width, increased number of osteoid lamellae, and prolonged mineralization lag time. These findings are consistent with a mineralization defect and indicate unambiguously that the bone disease in HHRH is osteomalacia. The only abnormality seen in the asymptomatic hypercalciuric subjects was slightly extended osteoid surface. Parametric and nonparametric statistical analyses performed on a pooled sample of HHRH patients and asymptomatic hypercalciuric subjects revealed a very high inverse correlation and a tight linear relationship between serum phosphorus and osteoid parameters. Serum 1,25-dihydroxyvitamin D, which is low in other forms of hereditary hypophosphatemia and osteomalacia, is elevated in HHRH and correlated positively with osteoid parameters and the mineralization lag time. Serum alkaline phosphatase showed similar relationships. These results as well as the clinical, biochemical, and radiological remission of bone disease consequent to phosphate therapy strongly suggest that in HHRH 1) hypophosphatemia alone is sufficient to cause osteomalacia; and 2) the elevation of 1,25-dihydroxyvitamin D reflects the degree of the primary renal phosphate leak, but is not involved in the pathogenesis of the bone disease.
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PMID:Osteomalacia in hereditary hypophosphatemic rickets with hypercalciuria: a correlative clinical-histomorphometric study. 198 23

We present what we believe is the first case of rickets following prolonged treatment with aluminum containing antacids that bind phosphate, in an 18-year-old mentally retarded boy with cerebral palsy and spastic quadriplegia. As expected, serum calcitriol was increased and urinary phosphate excretion was very low. However, in contrast to all published cases of antacid induced hypophosphatemic osteomalacia in adults, despite a substantial increase in bone resorption reflected by urinary total hydroxyproline excretion, urinary calcium excretion was low rather than high, and significant hypocalcemia occurred after antacids were ceased and a phosphate salt administered. We suggest that the skeleton was so under-mineralized because of growth during prolonged phosphate deficiency, possibly augmented by anticonvulsant administration and immobilization, that increased bone resorption did not release enough calcium to cause hypercalciuria, or to prevent hypocalcemia during resumption of normal mineralization.
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PMID:Hypophosphatemic rickets with hypocalciuria following long-term treatment with aluminum-containing antacid. 179 81

To investigate our impression that hypercalciuria is relatively common in children with osteogenesis imperfecta, we performed a retrospective study of data accumulated from our pediatric population with this skeletal disorder. Children with osteogenesis imperfecta (17 girls, 30 boys; mean (+/- SD) age 7.8 +/- 4.6 years; range 0.7 to 16.8 years) had undergone detailed inpatient evaluation of mineral homeostasis during periods of clinical stability and controlled dietary calcium intake. Hypercalciuria was found in 36% of the patients and averaged (+/- SEM) 6.1 +/- 0.3 mg/kg per 24 hours (0.15 +/- 0.01 mmol/kg per 24 hours) or 392 +/- 28 mg/gm of creatinine (1.10 +/- 0.07 mmol calcium/mmol creatinine) in the group with hypercalciuria. There were no statistically significant differences in age, gender, or dietary calcium intake (per kilogram of body weight) between the normocalciuric and hypercalciuric children. However, the group with hypercalciuria was shorter than the normocalciuric group and had a greater lifelong fracture rate. When patient height z scores were regressed against urinary calcium levels, a significant negative correlation was found in the group with hypercalciuria (r = -0.76; p less than 0.001). Although serum alkaline phosphatase activity was lower in the group with hypercalciuria, no difference was found between groups with regard to serum levels of calcium, phosphate, magnesium, creatinine, immunoreactive parathyroid hormone, or osteocalcin. The groups were also similar with respect to both their total body mineral density, as determined by dual-photon absorptiometry (n = 17), and their static indexes of bone formation and resorption, as assessed histomorphometrically with iliac crest specimens (n = 19). We conclude that hypercalciuria occurs frequently in children with osteogenesis imperfecta, and that its magnitude appears to reflect the severity of the skeletal disease.
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PMID:Hypercalciuria in children severely affected with osteogenesis imperfecta. 206 61

Reference values for the urinary calcium/creatinine ratio (Ca/Cr ratio) in the first morning urine were established in 361 healthy children aged 5 to 15 years, on unrestricted diets. The urinary Ca/Cr ratio in the urine upon arising was independent of sex but dependent upon age. The measurement of the urinary Ca/Cr ratio in the urine upon arising while on unrestricted diets may be a reasonable screening test for elevated calcium excretion. On the basis of the urinary Ca/Cr ratios in the urine upon arising during unrestricted diets and the calciuric response to calcium restricted diets and the oral calcium loading test, idiopathic hypercalciuria (IH) was subclassified into three groups: (1) absorptive hypercalciuria; (2) renal hypercalciuria; (3) dietary hypercalciuria. The pathogenesis of IH is controversial. Our data suggest that disordered 1,25 (OH)2 vitamin D metabolism with excessive urinary phosphate excretion occurs in absorptive hypercalciuria.
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PMID:Screening for hypercalciuria. 208 73


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