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)

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

To clarify the mechanism of development of hypercalcemia in adult T-cell leukemia/lymphoma (ATLL), ten patients with a serum creatinine level less than 177 mumol/L (2 mg/dL) were examined. Although hypercalcemia was seen in only four (40%) of these patients, four of six normocalcemic patients showed hypercalciuria (greater than 5 mmol/d [greater than 200 mg/24 h]). All hypercalcemic patients exhibited high nephrogenous cyclic adenosine monophosphate (NcAMP) levels in the face of low-normal immunoreactive parathyroid hormone and reduced serum 1,25-dihydroxyvitamin D [1,25(OH)2D] concentration. Half of the hypercalciuric patients with normocalcemia also showed high NcAMP and reduced serum 1,25(OH)2D levels. Furthermore, the changes in NcAMP and serum 1,25(OH)2D concentration closely paralleled the development of hypercalcemia and hypercalciuria in two patients. These results are reminiscent of the syndrome of humoral hypercalcemia of malignancy and suggest that derangements in calcium metabolism develop by a similar mechanism in patients with ATLL. The present data also indicate the importance of the measurement of urinary calcium excretion for early detection and prevention of fatal hypercalcemia in patients with ATLL.
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PMID:Clinical evaluation of calcium metabolism in adult T-cell leukemia/lymphoma. 289 17

Studies in 24 recurrent oxalate stone-formers have shown that values for urinary calcium excretion for this group on at-home diets vary significantly (P less than 0.001) more than values for creatinine excretions. By placing stone-formers on controlled in-hospital diets and measuring their calcium excretions, we were able to predict probable outpatient hypercalciuria (greater than 7.5 mmol/day) with a sensitivity of 95% and a specificity of 95%. In this study, the renal loss of calcium during low-calcium diets was proportional to the absorptive hypercalciuria during high-calcium diets. Calcium loading experiments in fasted stone-formers and normal subjects indicated that citrate, at citrate:calcium molar ratios ranging from 0.12 to 1, stimulated urinary calcium excretion more than did calcium carbonate loading alone. In addition, citrate also significantly (P less than 0.05) increased the excretion of urinary oxalate by two normal subjects for a given load of calcium oxalate. Malabsorption of citrate and possibly other hydroxycarboxylic acids may thus predispose to oxalate nephrolithiasis by promoting calcium and oxalate absorption.
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PMID:Effect of citrate on the urinary excretion of calcium and oxalate: relevance to calcium oxalate nephrolithiasis. 291 May 76

To elucidate the pathophysiology of mixed stone formation in cystinuria, 27 patients with documented cystine nephrolithiasis underwent an inpatient evaluation under a constant dietary regimen. All patients had homozygous cystinuria, since the daily urinary cystine excretion exceeded 250 mg. per gm. creatinine. Hypercalciuria was noted in 5 patients (18.5 per cent), 4 of whom had fasting hypercalciuria. Hyperuricosuria was found in 6 patients (22.2 per cent) and it was not caused by a consumption of a diet rich in animal proteins, since urinary pH was higher and urinary sulfate lower than in control subjects. Serum uric acid was slightly lower and uric acid clearance was higher in hyperuricosuric patients than in control subjects. Hypocitraturia was found in 12 patients (44.4 per cent) and it was associated with defective renal acidification in 4 of 5 patients in whom it was tested. Thus, hypercalciuria, hyperuricosuria and hypocitraturia frequently accompany cystinuria in patients with cystine nephrolithiasis. These conditions might be renal in origin, rather than a result of dietary or environmental aberrations. They may contribute to the formation of calcium and uric acid stones, which sometimes complicate cystine nephrolithiasis.
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PMID:The spectrum of metabolic abnormalities in patients with cystine nephrolithiasis. 292 71

The renal response to low and high phosphate intake was studied in weanling, young and adult rats. Weanling rats were started on experimental diets containing 0.37%, 0.7%, or 1.7% phosphate at 24 days and adult rats at 60 days of age. After 21 days, clearance studies were done in anaesthetized animals. Urine was collected during basal conditions and following a phosphate infusion. Urinary excretion of calcium, phosphate and creatinine, and plasma levels of phosphate and creatinine were determined. Plasma phosphate was slightly higher in the younger rats in all dietary groups but was not influenced by phosphate intake in either age group. Urinary phosphate excretion and fractional phosphate excretion increased significantly in both age groups with increasing phosphate intake. After high phosphate intake, both net and fractional phosphate excretions were significantly higher in younger rats (0.97 +/- 0.08 and 0.24 +/- 0.06 mumol min-1 100 g-1, P less than 0.01, and 47.5 +/- 3.84 and 18.15 +/- 5.59%, P less than 0.01, respectively). The urinary excretion of calcium related to creatinine was higher in younger rats in all dietary groups with the highest value found after low phosphate intake. During an acute phosphate infusion, fractional phosphate excretion increased significantly in both age groups after normal phosphate intake but remained unchanged after low or high phosphate intake. Plasma phosphate increased significantly only in younger rats with high phosphate intake (2.9 +/- 0.18, 3.88 +/- 0.43, P less than 0.05). It is suggested that hypercalciuria reflects early stages of phosphate depletion and that in young rats stabilized on a high phosphate intake, phosphate retention may occur during an acute phosphate load.
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PMID:Renal response to low and high phosphate intake in weanling, adolescent and adult rats. 292 72

Urinary excretions of calcium and cyclic AMP were studied in male recurrent stone-formers after an overnight fast and following an oral calcium load. The results from eight patients with established hypercalciuria (greater than 7.5 mmol Ca/24 h) were compared with those from eight age matched normocalciuric stone-formers. The urinary calcium/creatinine ratio was higher in the hypercalciuric group both when fasting and calcium loaded whilst their urinary cyclic AMP was lower in both 24-h and calcium-loaded collections. Five of the eight hypercalciuric patients exhibited an increased urinary calcium/creatinine ratio whilst fasting. These findings support the view that renal calcium wasting, in association with suppression of parathyroid activity, is common among men with idiopathic hypercalciuria. Dietary calcium restriction may lead to bone loss in patients with obligatory renal calcium wasting and enteric adsorption is rarely applicable to the treatment of stone disease. Therefore, the demonstration of a high fasting urinary calcium/creatinine ratio is a strong indication for therapeutic agents which act to suppress renal calcium loss to treat hypercalciuria.
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PMID:Renal calcium conservation in recurrent stone-formers with idiopathic hypercalciuria. 298 70

The circadian rhythm of urinary total hydroxyproline (THP) excretion was determined in matched groups of ten male idiopathic calcium stoneformers and ten normal subjects in order to determine whether enhanced resorption of bone might contribute to hypercalciuria in these patients. THP increased progressively in normal subjects in successive eight-hour urine collections from period 1 (8 AM to 4 PM) to period 3 (12 midnight to 8 AM), the nocturnal high level in period 3 being significantly greater than in period 1 (P less than 0.01) and in period 2 (P less than 0.05). By contrast, no significant circadian rhythm was observed in THP excretion in the stoneformers. Their THP excretion was similar to that of normal subjects in period 3, but was significantly higher than that of normal subjects in period 1 (THP/creatinine ratio(mg/mg): 0.026 +/- 0.003 v 0.017 +/- 0.001; P less than 0.05. Indices of parathyroid hormone activity were not significantly different between stoneformers and normal subjects; mean serum 1,25(OH)2 vitamin D levels were higher in the stoneformers than the normal subjects (44 v 37 pg/mL) but the difference was not significant (P greater than 0.05). These studies suggest that increased bone turnover may contribute to hypercalciuria in these calcium stoneformers.
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PMID:Bone resorption and hypercalciuria in calcium stoneformers. 301 44

109 patients with calcium-containing nephrolithiasis and 10 normal controls underwent oral calcium load test. After thorough examination, 6 of the 109 patients were diagnosed as having primary hyperparathyroidism (PHPT) and the remainder as having normocalcemic nephrolithiasis without PHPT. Following the oral calcium load test, the latter were operationally divided into 3 groups - normocalciuric nephrolithiasis (NN), n = 78; absorptive hypercalciuria (AH), n = 10, and renal hypercalciuria (RH), n = 15 - according to the criteria reported by Pak et al. Before the oral calcium load test, nephrogenous adenosine 3',5'-monophosphate (NcAMP), urinary adenosine 3'-5'-monophosphate (urinary cAMP), and plasma immunoreactive parathyroid hormone (iPTH) were determined to evaluate parathyroid function. This function, as assessed by mean basal NcAMP in the NN, AH and RH groups as well as the PHPT group, was significantly increased as compared with that in the normal controls. Within the NcAMP-elevated 4 groups, the mean basal NcAMP was highest in the PHPT group followed by the RH, AH and NN groups. In view of the mean basal NcAMP, disregarding the PHPT group, the NN and AH groups seemed to be intermediate types between the normal controls and the RH groups. Similar, but less distinctive results were obtained in the determination of urinary cAMP and plasma iPTH. On the other hand, when leaving the PHPT group out, the mean basal urinary calcium creatinine ratio (Ca/Cr) was highest in the RH group followed by the AH and NN groups, and lowest in normal controls, suggesting that the NN and AH groups were intermediate between normal controls and the RH group. The mean basal urinary Ca/Cr ratio in the PHPT group was moderately elevated but not remarkable. Almost similar tendencies were observed in 24-hour urinary calcium excretions on a calcium-restricted diet. A weakly positive correlation (r = 0.232, p less than 0.05) between basal NcAMP and basal urinary Ca/Cr ratio was observed in accumulated cases of the NN, AH and RH groups, whereas a negative correlation (r = -0.664, p less than 0.05) was obtained in normal controls. It is concluded that a possible abnormal calcium metabolism is suggested in stone formers without PHPT. Additionally, it is speculated that 'relative hypercalciuria' in NN and hypercalciuria in AH and RH might be accounted for in a single line of a primary renal leak of calcium.
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PMID:Possibility of elevated parathyroid function in patients with calcium-containing nephrolithiasis as compared with normal controls. 303 19

The clinical and laboratory findings in 14 infants, 2 children and 42 adults with RTA-1 have been retrospectively analyzed and the patients classified as having the hereditary (14%), acquired (31%), or idiopathic (55%) form. In 7 of the 8 hereditary cases, RTA-1 appeared to be a complication of hereditary hypercalciuria. The majority of acquired cases (61%) were secondary to immune-mediated diseases. All of the 14 infants with RTA-1 were classified as idiopathic. All of the idiopathic cases in children and adults were associated with nephrolithiasis and/or nephrocalcinosis, 33% of which had a family history of nephrolithiasis. The 14 infants presented with failure to thrive. Seventy-seven percent of children and adults with RTA-1 had nephrolithiasis and/or nephrocalcinosis and usually presented with symptoms related to this problem. Adults without nephrolithiasis or nephrocalcinosis usually presented with electrolyte disturbances or acidosis. Hypokalemia, the most common electrolyte disturbance, was present in 28% of the entire series. Acidosis was present in all infants and in 70% of children and adults. Clinically apparent bone disease was observed in 3 infants, and in 1 adult with nephrolithiasis. Glomerular function was normal in infants and in the 2 children, but depressed in 40% of adults. Recurrent urinary tract infection was a contributing factor but was not the sole cause of renal failure. Surprisingly, kidney stone number, the number of surgical procedures, and the presence of nephrocalcinosis had no apparent effect on the development of renal failure. Glomerular filtration rate was significantly higher in patients with incomplete RTA-1, and serum total CO2 was significantly correlated with creatinine clearance and minimum urinary pH. Hypercalciuria was present in 32% of patients with nephrolithiasis and/or nephrocalcinosis, and urinary citrate excretion was low in all of 16 patients in whom it was measured. Hypocitraturia appeared to be due in most cases to potassium depletion and renal failure, but may have occurred as a primary defect in 1 patient with hereditary RTA. Urinary uric acid excretion was elevated in 23% of patients with stones in whom it was measured. The mean number of stone-forming events was 51 +/- 14. Although a weak correlation between urinary calcium excretion and stone number was observed, the cause for prodigious stone formation could not be explained. This series emphasizes the variable degree to which the common clinical manifestations of RTA-1 (metabolic acidosis, hypercalciuria, nephrolithiasis, nephrocalcinosis, and potassium depletion) are expressed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The syndrome of distal (type 1) renal tubular acidosis. Clinical and laboratory findings in 58 cases. 312 50

Abnormalities in renal tubular function have been reported in adult patients with idiopathic renal hypercalciuria. To determine if such abnormalities are present early in the natural history of renal hypercalciuria, we evaluated renal tubular function in ten children with idiopathic renal hypercalciuria, aged 5-17 years. Seven of the children presented with urolithiasis and three with hematuria. Urinary calcium excretion ranged from 4 to 9 mg/kg per day, (5.2 +/- 0.5, mean +/- SEM) with a mean fasting urinary calcium to creatinine ration of 0.31 +/- 0.03. Studies described in this report were performed after 1 week of ingesting a diet containing 1,000 mg calcium, 3,000 mg sodium, and 100 mg purine. Clearance of creatinine ranged from 84 to 159 ml/min per 1.73 m2. Tm phosphate (mg/100 ml GFR) was normal in each child (mean 4.66 +/- 0.06 mg/100 ml GFR). Fractional excretion of uric acid, sodium and beta-2-microglobulin were also normal in each child. Serum bicarbonate concentrations ranged from 21.5 to 27 mEq/l with a mean of 24.4 +/- 0.5 mEq/l and all patients lowered urinary pH to less than 5.5. Hypotonic diuresis demonstrated normal free water clearance with a mean of 12.8 ml/min per 100 ml Cin. Distal sodium delivery and fractional distal sodium reabsorption were normal with a mean of 13.6 +/- 1.2% and 92.7 +/- 0.5%, respectively. Water deprivation studies demonstrated a range of maximum urinary osmolality from 711 to 1,020 mosmol/kg H2O with a mean of 864 +/- 34 mosmol/kg H2O. Seven healthy children, ingesting an identical study diet, concentrated their urine to a mean of 1,059 +/- 31 mosmol/kg h2O.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal function in children with idiopathic hypercalciuria. 315 15


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