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)

To investigate the mechanisms of abnormal calcium metabolism, such as hypocalcemia, decreased intestinal calcium absorption and hypercalciuria in spontaneously hypertensive rats (SHR), we have measured the plasma concentration of calcitriol and its synthesis in 5-, 8-, 12-, 16-, and 20-week-old normotensive Wistar Kyoto rats (WKY) and SHR. Metabolic clearance rate (MCR) and production rate (PR) of calcitriol were measured by the constant isotope infusion method. Plasma concentration of calcitriol and PR of calcitriol were decreased in SHR after 12 weeks of age. MCR of calcitriol, however, was not different between WKY and SHR in any age group. Therefore, the decreased synthesis of calcitriol accounts for the lower plasma level of calcitriol in SHR after 12 weeks of age. Metabolic acidosis or decreased renal function could not account for the decreased synthesis of calcitriol, since the blood pH and pCO2 and creatinine clearance were similar between WKY and SHR at times when the calcitriol synthesis was reduced in SHR. Plasma concentration of ionized calcium was also lower in SHR after 12 weeks of age. Plasma concentration of calcitonin was significantly higher in 16-week-old SHR (41.6 +/- 1.5 pg/ml) than in age-matched WKY (30.5 +/- 1.7, P less than 0.001). The values, however, were not different between 8- and 12-week-old WKY and SHR. We believe that the decreased synthesis of calcitriol could be the pathogenetic factor for the development of abnormal calcium metabolism in SHR. Age of animals should be considered when studying the calcium metabolism in SHR.
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PMID:Calcitriol synthesis is decreased in spontaneously hypertensive rats. 318 98

The effect of mild high-calcium diet or regular-calcium diet on urinary calcium excretion, urinary oxalate excretion, urinary calcium/creatinine ratio, urinary oxalate/creatinine ratio, and the probability of being a stone former (PSF) were studied in 85 patients with idiopathic urolithiasis. Intake of high-calcium diet for 5-6 days reduced (p less than 0.01-p less than 0.001) urinary oxalate excretion, urinary oxalate/creatine ratio and PSF in patients with idiopathic hypercalciuria. Under the regular-calcium diet, administration of 60 mg/day of pyridoxal phosphate for 3 months lowered (p less than 0.05-p less than 0.01) urinary oxalate excretion, urinary oxalate/creatinine ratio and PSF in patients with idiopathic hypercalciuria alone. From these findings, intake of mild high-calcium diet appears to be beneficial to decrease the urinary oxalate excretion and PSF in patients with idiopathic hypercalciuria. Pyridoxal phosphate has all the features of suppressing such risk factors for stone formation in patients with idiopathic hypercalciuria.
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PMID:Effect of high-calcium diet on urinary oxalate excretion in urinary stone formers. 321 61

The results are presented of an oral calcium tolerance test with 1,000 mg calcium in 20 patients with recurrent renal calcium calculosis, a woman with primary hyperparathyroidism and incipient renal failure (serum creatinine 1.8 mg%), creatinine clearance 55 ml/min) and 9 healthy persons as controls. The serum osteocalcin level was determined before and after the oral test. The results show that the serum osteocalcin level alone is of no differential diagnostic value for differentiation of the various types of hypercalciuria in patients with recurrent renal calcium calculosis. As a marker of osteoblasts functional state however the determination of serum osteocalcin level is of great importance for the early diagnosis of osteoporosis. In 3 patients with renal hypercalciuria, often leading to general osteoporosis, an acute rise of serum osteocalcin level was found after the oral calcium tolerance test. High osteocalcin level was also found in the patient with primary hyperparathyroidism and incipient renal failure.
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PMID:[Serum osteocalcin level as a marker of the functional state of osteoblasts after oral calcium tolerance test]. 326 44

Osteocalcin synthesis is dependent on the influence of the renal vitamin D metabolite, 1,25(OH)2D3. This metabolite is an etiological factor in some hypercalciurias, and osteocalcin may thus be a parameter for discovering them. In turn, parathormone, which stimulates 1,25(OH)2D3 synthesis, is also implicated in the hypercalciurias. Mean molecular parathormone, osteocalcin, 24-hour calciuria and the calcium/creatinine and hydroxyproline/creatinine ratios were determined in urine samples obtained after a 12-hour fast from 18 patients with absorptive hypercalciuria and 11 patients with renal hypercalciuria out of a total of 62 patients with renal lithiasis. No changes were observed in osteocalcin or parathormone, indicating that neither is valid for the diagnosis of hypercalciuria. Significant differences were only found in the Ca/Cr ratio (p less than 0.001), which was higher (0.31 +/- 0.07 vs. 0.13 +/- 0.04 mg/mg) in renal hypercalciuria than in absorptive hypercalciuria. No changes in osteocalcin have been reported in the hypercalciurias, but variations in parathormone have been reported, therefore requiring further study and thought to understand the processes involved.
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PMID:Osteocalcin, parathormone and hypercalciuria. 326 5

Despite the frequency and morbidity of nephrolithiasis in autosomal dominant polycystic kidney disease (ADPKD), this association has not been subject to a detailed study. One hundred fifty-one of 751 ADPKD patients seen at the Mayo Clinic between 1976 and 1986 had nephrolithiasis. Seventy-four had passed calculi or had stones surgically removed. Stone analysis was available in 30 patients: uric acid, calcium oxalate, calcium phosphate, and struvite were present in 56.6%, 46.6%, 20%, and 10%, respectively. Calculi were observed in 71 of 79 patients with excretory urograms available for review. Faintly opaque and bull's eye stones, probably containing uric acid, were present in 12.7% and 14.1% of these patients, respectively. Precaliceal tubular ectasia was observed in 15.5%. Ninety-seven patients had preserved renal function (serum creatinine less than 1.5 mg/dL) at the initial evaluation. Six were excluded because they had other known causes of stone disease. The most common metabolic abnormality in the remaining 91 patients was hypocitric aciduria (ten of 15 patients with measurements). The urine pH in the first voided morning specimens (5.66 +/- 0.05) was significantly lower than that of an unselected control population (5.92 +/- 0.03, P less than 0.001). Hyperuricosuria, hyperoxaluria, and hypercalciuria were observed in six of 32 (18.8%), six of 31 (19.4%), and three of 39 (9.7%) patients with preserved renal function. The composition of the stones, the frequency of hypocitric aciduria, and the low urine pH (possibly related to the defect in excretion of ammonia described in ADPKD), suggest that metabolic, along with mechanical, factors are responsible for the frequent occurrence of nephrolithiasis in this disease.
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PMID:The association of nephrolithiasis and autosomal dominant polycystic kidney disease. 335 68

Airway, sweat-duct, and other epithelial cells in patients with cystic fibrosis display abnormal ion transport. To test whether the kidney, the organ most exquisitely adapted for ion transport, has a similar defect, we measured the levels of calcium excretion and searched for microscopic nephrocalcinosis in patients with cystic fibrosis. Thirty-eight specimens of kidney tissue were stained for calcium deposits, and 24-hour levels of urinary calcium excretion were measured in 14 patients and 15 control subjects. Microscopic nephrocalcinosis was observed in 35 of the 38 specimens (92 percent), and hypercalciuria (greater than 182 mg per gram of creatinine) in 5 of the 14 patients (36 percent). Notably, nephrocalcinosis was detected near the time of birth (in six patients under one year old, including two neonates and one stillborn infant), which supports the hypothesis that such renal calcium deposits reflect the genomic defect and are not due to longstanding pulmonary dysfunction, chronic infection, therapeutic agents, or disease progression. None of the patients with hypercalciuria or nephrocalcinosis had clinical evidence of renal dysfunction. The finding of microscopic nephrocalcinosis near the time of birth in patients with cystic fibrosis suggests a primary abnormality of calcium metabolism in the kidney. Studies of the pathophysiologic features of the kidney in cystic fibrosis may elucidate the molecular alterations observed in this disorder.
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PMID:Microscopic nephrocalcinosis in cystic fibrosis. 339 80

Calcium loading tests were performed in 21 children with hypercalciuria, haematuria and/or nephrolithiasis and 10 control subjects. Comparisons of 24-h calcium excretion before and after loading were evaluated rather than fasting urinary calcium to urinary creatinine ratio. The differences in calcium excretion before and after loading clearly distinguished absorptive from renal hypercalciuria. A difference higher than 0.035 mmol/kg indicated absorptive hypercalciuria in 6 of 21 patients, whereas in the remaining 15 much lower differences indicated renal hypercalciuria. Resorptive hypercalciuria caused by low serum values of 25-hydroxyvitamin D was considered in 6 of the 15 patients with renal hypercalciuria. These patients had low values of phosphate reabsorption (TmP/GFR) and could be clearly separated by high values of calcium reabsorption (TmCa/GFR), in contrast to patients with renal hypercalciuria who had normal values of TmP/GFR and low values of TmCa/GFR. The correct treatment and prevention of nephrolithiasis caused by hypercalciuria in children should be based on accurate diagnosis; this can be achieved by using the calcium loading test described in this report.
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PMID:The diagnosis of hypercalciuria in children. 339 95

Thirty-six patients with recurrent calcium oxalate nephrolithiasis were selected from the stone clinic. Fourteen were normocalcemic and had normal daily urinary calcium excretion. Among 22 patients with idiopathic hypercalciuria, 10 received thiazide diuretics for the prevention of new stone formation. Single-voided urine samples were collected at the outpatient clinic and 24-hour urine at the patients' homes. In hypercalciuric patients, irrespective of thiazide diuretic therapy, the mean value of the calcium/creatinine concentration ratios of postprandial single-voided urine specimens had a meaningful correlation with the man value of 24-hour urinary calcium excretion rates. Also in hypercalciuric patients with thiazide diuretics, a negative correlation was observed between the calcium/creatinine concentration ratio and the index for urinary saturation with calcium oxalate of a postprandial single-voided urine sample. Thus, in the hypercalciuric stone formers, 24-hour urinary calcium excretion rates and the degree of urinary saturation with calcium oxalate can be estimated from the calcium/creatinine concentration ratios of single-voided urinary samples.
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PMID:Significance of the calcium to creatinine concentration ratio of a single-voided urine specimen in patients with hypercalciuric urolithiasis. 345 77

The selective determination of mid-C-regional parathyroid hormone (mid-C-PTH) in combination with other laboratory parameters is a reliable tool for diagnosis and treatment of extra-renal (primary) and renal (secondary) hyperparathyroidism. Early stages, which show either high-to-normal serum calcium and elevated mid-C-PTH or increased serum calcium but normal mid-C-PTH, can be distinguished from overt hyperparathyroidism. Alkaline phosphatase (AP) activity and mid-C-regional PTH provide biochemical confirmation of histologically classified renal osteodystrophy. Since the index AP X PTH signifies osseous changes in dialysis patients at an early stage, therapeutic regimens may be altered without additional invasive procedures. After renal transplantation mid-C-PTH normalizes and serum creatinine decreases. Increased mid-C-PTH in patients with normal renal graft function reflects autonomous PTH secretion, which requires careful monitoring to prevent PTH-induced hypercalciuria.
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PMID:[Mid C regional parathyroid hormone in the clinical workup: diagnostic value in extrarenal (primary) and renal (secondary) hyperparathyroidism]. 352 Jan 30

Normocalcaemic male stone formers, 31-51 years old (n = 108) on a free diet, were divided into a hypercalciuric group (n = 47) with calcium excretion rates higher than 8.0 mmol/24 h, a normocalciuric group (n = 32) with calcium excretion rates below 6.1 mmol/24 h and an intermediate group (n = 29). There were no statistically significant differences between the hypercalciuric and the normocalciuric groups with respect to serum levels of calcium, phosphate, creatinine, urate, ALAT, albumin, PTH, 1,25-dihydroxyvitamin D or urinary excretion of cAMP. The group of patients with high calcium excretion had significantly higher serum levels of 25-hydroxyvitamin D3 (75 +/- 4 nmol/l) than the group with low calcium excretion (57 +/- 4 nmol/l) (p less than 0.002), while the group of patients with intermediate calcium excretion had 25-hydroxyvitamin D3 levels between the other two groups (69 +/- 4 nmol/l). A highly accurate method based on isotope dilution-mass spectrometry was used to assay 25-hydroxyvitamin D3. Of the patients with hypercalciuria (n = 47), seven were classified as hyperabsorbers on the basis of calcium load tests. These patients were found to have even higher serum levels of 25-hydroxyvitamin D3 (108 +/- 10 nmol/l)--significantly higher than that of the hypercalciuric patients as a whole. The above study was carried out in March 1983. In September, the group of patients with high urinary calcium excretion also had significantly higher levels of 25-hydroxyvitamin D3 than the group of patients with low calcium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High circulating levels of 25-hydroxyvitamin D3 in renal stone formers with hyperabsorptive hypercalciuria. 352 38


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