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)

1,25 dihydroxyvitamin D (1,25(OH)2 D) is the active metabolite of vitamin D and has an essential role in bony metabolism on the regulation of the calcium-phosphorus balance. The circulating level of 1,2(OH)2 D is normally between 25 and 45 pg/ml. Isolation of the fraction to be titrated requires sophisticated purification techniques using high performance chromatography (HPLC). In osteomalacia secondary to a deficiency the mean level of 1,25(OH)2 D is low (14.1 +/- 6.9 pg/ml) because of substratum deficiency. Administration of vitamin D supplements is quickly followed by a supraphysiological increase of the level of active metabolite. The role of the parathyroid hormone on the activity of 1-hydroxylase is illustrated by the results of the titration in parathyroid dysfunctions: decrease of the mean level in hypoparathyroidism (18 +/- 6.9 pg/ml), and on the contrary, a significant increase in hyperparathyroidism (56.6 +/- 15.4 pg/ml) despite of a spread of the individual values. In 18 cases of idiopathic hypercalciuria, we have only observed an increase of 1,25(OH)2 D level, in two cases. Titration of 1,25(OH)2 D complements the calcium-phosphorus evaluation to precise the physiopathogenic mechanism of the disorders observed in various diseases. Its interpretation requires the joint measurement of the substratum level, 25-hydroxyvitamin D, and the evaluation of the parathyroid function.
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PMID:[Serum concentrations of 1,25-dihydroxyvitamin D in cases of osteomalacia, parathyroid dysfunction and idiopathic hypercalciuria]. 356 83

Acidosis induced increase in renal calcium excretion was produced by means of ammonium chloride load in 12 control persons and in 76 patients with recurrent oxalate lithiasis. This increase is more marked in stone patients - even in those with normocalciuria - than in control persons. The calcium excretion is especially increased in patients with renal hypercalciuria. This might result from the primary nature of the renal defect. The acid load did not prove useful in the diagnosis of hyperparathyroidism.
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PMID:[Calcium excretion in patients with calcium oxalate calculi in acid administration]. 360 99

The relation between signs and symptoms of Paget's disease of bone was studied in 180 patients consecutively submitted for treatment. In these patients 826 lesions were identified by scintigraphy. The intensity of scintigraphic uptake was correlated with long-term calcium uptake in bone. The frequency distribution of lesions over the patients was compatible with a 65 per cent chance of local disease once the patient had been exposed to an extraneous agent. The spatial distribution within a skeleton was related to the local density of the osteoclast population. The particular frequency distribution resulted in a log-normal distribution diagram for anatomical spread. Within lesions, increases in numbers of osteoclasts and osteoblasts were proportional and these too had a log-normal distribution. Increases of alkaline phosphatase levels and hydroxyproline excretion were closely related and reflected anatomical spread on the one hand and local activity on the other. They were also closely correlated with overall calcium fluxes. It was shown that alkaline phosphatase is the more sensitive and hydroxyproline the more accurate of the biochemical signs. Maximum values, corresponding to total skeletal disease, were approximately 25 times the upper limit of normal. Equilibrium between bone formation and resorption was not always maintained. There were, indeed, wide variations of urinary calcium, which were significantly related to the difference between bone formation and resorption, but the extracellular calcium homeostasis was generally maintained. This may explain the frequent occurrence of normocalcaemic and hypercalcaemic hyperparathyroidism. The hypercalciuria constitutes an additional risk for urolithiasis in men. The most frequent complaint was pain (86 per cent). Extent of lesions was important, but a major decisive factor was the specific nature of the bone affected. The findings allowed assessment of the relative importance of the various signs, symptoms and locations as criteria of disease severity and as indications for treatment.
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PMID:Relation between signs and symptoms in Paget's disease of bone. 371 67

To clarify the mechanism for the impaired mineral metabolism in Cushing's syndrome, the clinical features, biochemical parameters before and after oral calcium load, and vitamin D metabolism were compared between two groups of patients of endogenous Cushing's syndrome (17 cases) with and without osteopenia. The patients with osteopenia [OP (+): 7 cases, all female] were older (42.7 +/- 8.3 y. o.) and had a longer duration (117 +/- 75 M) of the syndrome than those without osteopenia [OP (-): 33.8 +/- 8.9 y. o., 36 +/- 25 M]. OP (-) showed a blunted hypercalciuria after oral calcium load (63.7 +/- 20.4 to 90.9 +/- 36.1 mg/g X Cr), while OP (+) had higher levels of urinary excretion of calcium (fasting: 120.4 +/- 37.5, and after oral calcium load: 235.6 +/- 72.6 mg/g X Cr), of cyclic AMP (7.6 +/- 1.1 nmol/dl X GF), and of plasma 1.25(OH)2D (76.6 +/- 34.0 pg/ml) than OP (-) (u-cAMP: 3.2 +/- 2.0 nmol/dl X GF, 1,25(OH)2D: 27.9 +/- 16.3 pg/ml). These results indicate that 1) elderly female patients with Cushing's syndrome of long duration are susceptible to OP, 2) during the early phases of the syndrome, reduced intestinal calcium absorption with sustained calciuria (probably through the inhibition of calcium reabsorptive effect of PTH by glucocorticoid) induces negative calcium balance, leading to 3) a development of secondary hyperparathyroidism which stimulates 1,25(OH)2D synthesis. Thus, the mechanism involving bone resorption stimulated by excess PTH along with the direct inhibition of bone formation by glucocorticoid seems to play an important role in a progressive development of OP in Cushing's syndrome.
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PMID:Impaired mineral metabolism in Cushing's syndrome: parathyroid function, vitamin D metabolites and osteopenia. 375 23

The high incidence of renal lithiasis in hyperparathyroidism (55 p. 100) suggests that PTH plays a causal role in stone production. It also motivates a systematic search for primary hyperparathyroidism in all patients with renal stones although it is only found in about 7 p. 100 of cases. PTH acts through the stimulation of 1.25(OH)2 vitamin D production and therefore, the absorption of calcium from the intestine, which in turn increases the filtrable calcium, hence the calciuria. In renal stones, in general, hypercalciuria represents one of the major metabolic disturbances, besides the hyperoxaluria, hyperuricosuria and the reduction of the inhibitors of crystallization. However, hypercalciuria is rarely the indirect result of excess PTH. It is usually caused by increased dietary ingestion of NaCl, meat, calcium and possibly carbohydrates.
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PMID:[Renal lithiasis in idiopathic hypercalciuria and primary hyperparathyroidism]. 376 88

The case of a 11 year old boy with medullary sponge Kidney and nephrolithiasis discovered because of abdominal pain is described. Functional tubular impairment (concentrating defect, distal tubular acidosis) was present. No hypercalciuria nor hyperparathyroidism was detected. The diagnosis of medullary sponge Kidney was confirmed histopathologically. The pediatric cases described in the literature are characterized by a higher incidence of concentrating defect and acidosis, while the adults subjects often show hypercalciuria and or hyperparathyroidism. The careful study of tubular functions in the pediatric cases appears to be very useful to understand which are primary tubular disturbances and which are only secondary.
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PMID:[Medullary sponge kidney. Description of a pediatric case]. 378 97

The effect of two doses of Phosphorus (P) supplementation to pooled breast milk (BM): 0.48 and 0.800 mmol/kg/24 h given during the second month of life was evaluated in 22 very low birthweight infants. The concentration of calcium and phosphorus in serum and urine, the serum concentration of immunoreactive parathyroid hormone (iPTH) and the plasma 1,25-dihydroxy-vitamin D concentration (1,25-OH-D) were compared to the values in 19 control infants. The mean +/- SD concentrations in control infants and adults are 63 +/- 18 microliters Eq/ml for serum iPTH and 85 +/- pmol/l for plasma 1,25-OH-D. With 0.48 P supplementation, urinary Ca (UCa) excretion (median and range) 0.238 mmol/kg/24 h (0.105-0.520) was lower than in the control group 0.288 (0.205-0.679) (p less than 0.05); the reduction of UCa was larger with 0.8 P supplementation: 0.047 (0.023-0.163) (p less than 0.01). P supplementation induced no change in serum Ca concentration but a slight and significant increase in serum iPTH was observed only with the 0.8 P supplementation: 55 microliters Eq/ml (less than 25-80) (p less than 0.05). With 0.8 P supplementation there was no significant change of plasma 1,25-OH-D concentration: 173 pmol/l (106-271) vs. 255 (132-293) in the control group. These data show that with 0.8 P supplementation, the hypercalciuria in BM-fed infant disappears without secondary hyperparathyroidism, but without any change in plasma 1,25-OH-D concentration.
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PMID:Effect of phosphate supplementation to breast fed very low birthweight infants on urinary calcium excretion, serum immunoreactive parathyroid hormone and plasma 1,25-dihydroxy-vitamin D concentration. 384 Mar 17

A 52-year-old man with an acromegalic appearance of prolonged duration suffered abdominal colic attacks and hematuria during the middle of the course of the disease. The patient was diagnosed as having urolithiasis caused by increased urinary calcium. The calcium metabolic disorder was not considered to be due to hyperparathyroidism because serum calcium and PTH levels were within the normal range and no abnormality was observed in a parathyroidal scintigraph. The serum 1,25-dihydroxyvitamin D (1,25-(OH)2D) levels (55.0 and 73.0 pg/ml) were higher than the normal range (27.2-53.8 pg/ml). A selective adenomectomy by the transsphenoidal route (Hardy's method) was performed, resulting in an improvement in the hypercalciuria and urolithiasis, and a decrease in the levels of serum 1,25-(OH)2D (23.0 and 23.0 pg/ml). These findings suggest that GH may promote the activation of vitamin D in the kidney in acromegaly, resulting in an acceleration of calcium absorption in the intestine through the action of activated vitamin D and the induction of increased urinary calcium excretion by the urinary excretion of excessive blood calcium.
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PMID:An acromegalic patient with recurrent urolithiasis. 384 20

The stimulation of cyclic AMP production by human renal cortical membranes in the presence of the GTP analogue 5'-guanylimidodiphosphate and a calcium chelator represents a homologous assay system for the evaluation of biologically active parathyroid hormone (bioPTH) in human serum. Bioactive PTH was raised above normal (normal range: undetectable to 4.6 pmol human PTH(1-34) per 1) in 13/17 (76%) patients with primary hyperparathyroidism, in 5/6 (83%) patients with surgically proven hyperparathyroidism secondary to chronic renal failure, in 4/5 (80%) patients with hyperparathyroidism secondary to hypocalcaemia, in all three patients with pseudohypoparathyroidism, in 5/17 (29%) patients with osteoporosis and in 1/9 (11%) patients with renal stones and/or hypercalciuria. Bioactive PTH correlated positively with immunoreactive PTH (iPTH) measured with a radioimmunoassay predominantly recognizing the middle- and carboxyl-terminal region of the PTH molecule (r = 0.503, P less than 0.001). A positive correlation (r = 0.572, P less than 0.05) was found between values of serum calcium and bioPTH in the group with primary hyperparathyroidism. Immunoreactive PTH did not correlate significantly with calcium in this group. In the other patients except those who had chronic renal failure, a negative correlation between serum calcium and both bioPTH and iPTH was observed (P less than 0.01). When alkaline phosphatase was compared with bioPTH in all patients, the correlation was positive (r = 0.390, P less than 0.01); no significant correlation existed between iPTH and alkaline phosphatase in the patients studied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal adenylate cyclase assay for biologically active parathyroid hormone: clinical utility and physiological significance. 394 39

The clinical records of ten premature infants with nephrolithiasis were reviewed. The probable mechanism of stone formation was hypercalciuria due to furosemide therapy (nine patients) and congenital hyperparathyroidism (one patient). The relatively high rates of urinary excretion of calcium from immature kidneys predisposed these neonates to the development of calcium stones. Renal calculi in neonates are complications of distinct, treatable conditions, and premature babies receiving furosemide treatment should be screened by ultrasonography for renal calcifications.
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PMID:Nephrolithiasis in premature infants. 396 25


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