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)

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

Seventeen patients who recurrently formed idiopathic calcium kidney stones (SF) and 25 age- and sex-matched healthy blood donors (H) were challenged by an oral calcium load (1 g) after an overnight fast. Their usual diet was not changed before the test. Urine samples were taken before, 2 1/2, and 4 h after the calcium load. A blood sample was drawn 3 3/4 h after calcium loading. Before and 2 1/2 h after calcium dosage urinary measurements of calcium, magnesium, phosphate, oxalate, uric acid, and creatinine did not reveal any differences between SF and H. According to the calciuria after 4 h SF were separated in normocalciurics (NCSF) and hypercalciurics (HCSF). Nine-tenths of the NCSF had higher serum ionic calcium levels than H after calcium load (P less than 0.001), whereas HCSF were not different from H. Serum phosphate in SF was lower than in H (P less than 0.001). Carboxy-terminal parathormone, measured in 3 NCSF and 2 HCSF, was normal. Depending on the calciuria or calcemia 4 h after an oral calcium load, 16 of 17 SF showed a metabolic abnormality (hypercalcemia or hypercalciuria). It is concluded that intestinal calcium absorption in SF might be increased to variable rates.
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PMID:[Peroral calcium administration test with free diet in idiopathic calcium nephrolithiasis--possibilities and limits]. 378 54

An increased calcium excretion in 24-hour urine was found in 32 of 42 out-patients with recurrent calcium nephrolithiasis (calcium excretion > 300 mg in males, > 250 mg in females). Subsequent hospitalization of the 32 patients revealed the following diagnosis after a calcium tolerance test: absorptive hypercalciuria in 18, renal hypercalciuria in 4, primary hyperparathyroidism in 2 and dietary hypercalciuria in 7. Normocalciuria in 10 out-patients was confirmed in 6; in one instance there was, however, primary hyperparathyroidism, in 3 there was absorptive hypercalciuria. In one patient it was not possible to classify the hypercalciuria. Total as well as nephrogenic cAMP showed wide scatter and was unsuitable, therefore, in differential diagnosis. In 2 of 3 cases of hyperparathyroidism the serum level of parathormone was distinctly elevated.
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PMID:[Diagnosis of hypercalciuria in calcium nephrolithiasis (author's transl)]. 625 Jul 84

Ninety-seven male patients with idiopathic calcium urolithiasis and 17 normal male subjects were studied to evaluate the mechanism of idiopathic hypercalciuria with an oral calcium tolerance test, which has been useful in differentiating hypercalciuria. The changes in parathyroid function, such as parathormone and urinary cyclic AMP, and calcium after calcium load differed between absorptive hypercalciuria and renal hypercalciuria. We have confirmed that the change in serum calcitonin after calcium load was also different in these two hypercalciurias. The increase in serum calcium was sufficient to reduce parathyroid function but serum calcitonin was unchanged after calcium load in the control group, in patients with normocalciuria, and those with renal hypercalciuria. Although serum and urinary calcium were more elevated in absorptive hypercalciuria than in the other three groups, parathyroid function was not significantly reduced after loading in absorptive hypercalciuria. In this group only, the serum calcitonin was significantly elevated after calcium load. It is reasonable to suggest that, in this group, because parathyroid function is usually suppressed by intestinal hyperabsorption of calcium, parathyroid function may not be further suppressed by even calcium load. Possibly the significant stimulation of calcitonin may compensate for the lack of suppression of parathyroid function and maintain normal serum calcium levels in absorptive hypercalciuria. These results suggest that the change in serum calcitonin is also useful to differentiate abnormalities of calcium metabolism in patients with hypercalciuria.
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PMID:Oral calcium tolerance test and serum calcitonin in calcium stone formers. 630 68

The authors propose to study parathyroid hormone receptors in humans by means of a test "inspired by the Ellsworth-Howard test" using the active synthetic 1-34 fragment of the hormone PTH-1-34. The use of this test in 44 patients (29 healthy subjects, 7 patients with idiopathic hypercalciuria 5 cases of Paget's disease, 1 patient with idiopathic hypoparathyroidism, 2 cases of basal cell nevus syndrome) who received different doses of this substance intravenously, revealed a marked dose-dependent stimulation of adenyl-cyclase as objectified by an increase in urinary excretion of cyclic AMP (AMPcU). Distal tubular calcium reabsorption was also significantly affected as demonstrated by a decrease in urinary calcium in the first hours following administration of the 1-34 fragment even in the case of idiopathic hypercalciuria. In comparison to the "classical" Ellsworth-Howard test, however, no significant urinary phosphate response was observed during the present test. Similarly, urinary hydroxyproline and phosphate and calcium blood levels remained stable. As the results obtained for the case of hypoparathyroidism demonstrate, this easily performed test is useful for valuating parathormone receptors in kidney by means of two sensitive parameters (AMPcU and the ratio of fractional urinary calcium to urinary creatinine). In addition to its action, synthetic fragment h PTH-1-34 offers the advantage of being totally innocuous.
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PMID:[The effects of synthetic 1-34 fragment of human PTH on kidney and bone receptors in man. Use of the Ellsworth-Howard test]. 631 80

In 25 cases of spasmophilia the parathyroid function was assessed by complete exploration of the P-Ca metabolism and radioimmunoassay (RIA) of parathormone (PTH). Concomitantly the bone mineralization status was assessed by induced hypercalciuria tests and administration of 30 mg vitamin D2. RIA of PTH revealed increased values in 50% of the cases. The values fall within the range of secondary hyperparathyroidism, but this percentage varies with the values of the parathyroid function obtained by P-Ca metabolism explorations. The increased PTH values do no correlate with the level of plasma total calcium, ionic calcium, and magnesemia. Nor do they correlate with the bone mineralization disorders or the duration of the disease and the age of the patients.
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PMID:The functional status of the parathyroid in adult spasmophilia patients estimated by plasma parathormone assay. 732 51

1. Inorganic fluoride concentrations were determined in serum and urine specimens of 24 subjects receiving a standardized low fluoride intake. Serum fluoride was directly correlated with previous intake and appeared to reflect bone fluoride stores. 2. A positive correlation between creatinine and fluoride clearance was found. However, striking reductions in fluoride clearance, which resulted in increases in serum fluoride, were not usually seen until the creatinine clearance was below 25 ml/min. 3. Parathormone produced an increase in serum fluoride and thyrocalcitonin a decrease, probably by their action on bone. 4. Six patients with chronic increased bone resorption had elevated fluoride concentrations. In five, when treatment was successful, serum fluoride fell. Interpretation of the data from this group of patients is complicated by initially low filtration rates associated with hypercalcaemia and hypercalciuria. 5. The sensitivity of the serum fluoride concentration to previous intake, glomerular filtration and the intensity of bone resorption suggests that the human organism exerts no direct homeostatic control over this ion.
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PMID:Serum inorganic fluoride: changes related to previous fluoride intake, renal function and bone resorption. 735 34

The authors analyse the results obtained during 54 radioisotope investigations using 45Ca in 13 cases of idiopathic hypercalciuria, 12 cases of osteoporosis, 3 cases of Paget's disease, and 2 cases of osteomalacia including one of Fanconi's disease in an adult. In 12 patients, repetition of the radio-isotope test two, three or four times; permitted the authors to study the effects of the treatments administered: calcitonin, phosphate, vitamin D, parathormon, oestrogen. Calcitonin increases intestinal absorption and reduces bone reabsorption and also accretion. Phosphate greatly increases accretion and bone reabsorption in vitamin-resistant osteomalacia of adults. The synthetic fragment 1--34 of human parathormone increases accretion and reabsorption but does not modify the calcium balance. The addition of estrogen reduces reabsorption and slightly increases accretion in two osteoporotic patients producing a positive calcium balance. This method of investigation is of great interest to assess the effects of a drug on calcium metabolism and on the two processes of bone remodelling.
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PMID:[Calcium metabolism study performed by means of Ca-45 in bone diseases and idiopathic hypercalciuria]. 745 4

Very few patients with familial hypomagnesemia, hypercalciuria and nephrocalcinosis have been described. Information about clinical course, familial studies or evolution after renal transplantation is very scant. We have studied eight patients with this syndrome who belong to five different families. The mean age at diagnosis was 15 +/- 7 years (5 to 25 years). The primary clinical data were polyuria-polydipsia (8 cases), ocular abnormalities (5), recurrent urinary tract infections (5) and recurrent renal colics with stone passage (2). Bilateral nephrocalcinosis was observed in all cases. Every patient showed hypomagnesemia (1.1 +/- 0.2 mg/dl) with inappropriately high urinary magnesium (Mg) excretions (70 +/- 17 mg/day), Mg clearances (4.4 +/- 1.2 ml/m) and Mg fractional excretions (16.2 +/- 7.1%). Hypercalciuria was present in every case except in those with advanced renal insufficiency. Serum parathormone levels were abnormally high. Serum calcium (Ca), phosphorus and potassium, and urinary excretions of uric acid and oxalate were normal. Neither chronic oral Mg administration nor thiazide diuretics normalized serum Mg levels or urinary Ca excretions, respectively. Follow-up was 6 +/- 4.5 years. Renal function worsened in every case with six patients starting on chronic dialysis after 4.3 +/- 3.8 years. The progression rate of renal insufficiency correlated with the severity of nephrocalcinosis. Five patients have received a kidney graft, and their serum Mg and urinary Ca have always been within normal values after transplantation. Twenty-six members of four of the affected families were studied: none of them showed hypomagnesemia, renal insufficiency or nephrocalcinosis. However, eleven cases (42%) had hypercalciuria and four of them presented with recurrent renal stones. Two family members had medullary sponge kidneys. In conclusion, progression to renal insufficiency is common in this syndrome; oral Mg and thiazide diuretics are ineffective to correct abnormalities. After kidney graft, tubular handling of Mg and Ca was normal. A striking incidence (42%) of hypercalciuria was found in the familial study.
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PMID:Familial hypomagnesemia with hypercalciuria and nephrocalcinosis. 763 71

Rapid immobilization after acute spinal cord injury (SCI) leads to increased bone resorption, net calcium efflux from the bone, hypercalciuria, depressed parathormone (PTH) and increased calcitonin release. However, the effects, if any, of long-standing SCI on calcium regulatory system is not well understood. We measured plasma concentrations of 25 hydroxy (OH) vitamin D, 1,25(OH)2 vitamin D (calcitriol), intact PTH molecule, calcitonin, ionized calcium [Ca++] and phosphorus in 40 clinically stable men with long-standing SCI of 3-year to 50-year duration (22 persons with paraplegia and 18 persons with quadriplegia). The results were compared with those obtained in 14 able-bodied control men. Plasma PTH concentration in the SCI group was significantly lower than that found in the able-bodied controls despite virtually identical concentrations of ionized calcium. Likewise, plasma calcitriol concentration in the SCI group was significantly lower than the value found in the able-bodied control group and lower in persons with quadriplegia than in those with paraplegia. In contrast, plasma calcitonin concentration in the quadriplegic group was significantly higher than that in persons with paraplegia and insignificantly higher than that in the control group. No significant difference was noted in serum ionized calcium between the study groups. PTH and calcitriol levels were positively related to one another (r = 0.35, p < .01) and negatively related to the level of injury (r = -0.43, p < .002 and r = -0.54, p < .001, respectively). In conclusion, long-standing SCI is associated with significant depression of calcitriol and PTH concentrations despite normal ionized calcium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vitamin D, parathormone, and calcitonin profiles in persons with long-standing spinal cord injury. 802 22


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