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)

The role of parathyroid hormone (PTH) on calcium excretion during chronic metabolic acidosis was investigated in intact and thyroparathyroidectomized (TPTX) acidotic and control dogs. Intact dogs fed NH4Cl for 3 days developed marked hypercalciuria as compared to intact control animals. After thyroparathyroidectomy, calcium excretion corrected per glomerular filtration rate decreased significantly in NH4Cl-treated dogs but not in the controls. This was observed in the face of a TPTX-induced fall in filtered load of calcium in both groups. After restoration of filtered load of calcium to normal by CaCl2 infusion, fractional calcium excretion at any level of fractional sodium excretion was higher in NH4Cl-treated TPTX dogs than that of TPTX controls, indicating a calciuric effect of acidosis independent of PTH. PtH (1 U/min X 60 min) was infused to examine the effect of this hormone on calcium excretion during NH4Cl-induced acidosis. In normal dogs, PTH significantly decreased absolute and fractional calcium excretion. In contrast, PTH infusion to acidotic dogs failed to decrease absolute and fractional calcium excretion. In both groups, phosphate excretion increased significantly. The higher calcium excretion of acidotic dogs during PTH infusion resulted from failure to enhance calcium reabsorption as shown by the fact that, at any level of plasma ionizable calcium, calcium excretion was higher in acidotic dogs than in controls. These findings indicate that during metabolic acidosis PTH does not exert its normal anticalciuric effect. This may contribute to the development of hypercalciuria despite PTH excess in certain clinical conditions associated with chronic metabolic acidosis.
Kidney Int 1982 Sep
PMID:Parathyroid hormone is not anticalciuric during chronic metabolic acidosis. 717 29

Daily urinary calcium excretion in renal stone-forming subjects is shown to vary directly with moderate changes in dietary sodium intake. The changes produced are sufficient to alter the basic diagnostic classification from 'hypercalciuric' to 'normocalciuric' because dietary sodium is reduced from 200 to 80 mM/day. Similar changes were observed in fasting morning 'spot' urine samples, resulting in alteration of diagnostic subclassification between so-called 'absorptive' and 'renal' categories, in the absence of demonstrable change in parathyroid function. Diagnostic and therapeutic studies in stone-forming subjects require control of both dietary calcium and dietary sodium if misinterpretations are to be avoided. Habitual high sodium intake may be an etiological factor in the generation of excessive excretion of calcium, sodium, and phosphate--the hypercalciuria syndrome.
Kidney Int 1982 Sep
PMID:Importance of dietary sodium in the hypercalciuria syndrome. 717 31

A 51-year-old man has had absorptive hypercalciuria and corticosteroid-responsive hypercalcemia for at least 12 years. There has been no clinical or laboratory proof of primary hyperparathyroidism, hypervitaminosis D, or other known causes of hypercalcemia and absorptive hypercalciuria. Hypercalciuria as well as the elevated serum level of calcium and 1 alpha, 25(OH)2D fell to normal during treatment with corticosteroids. The disturbed calcium metabolism in this patient is characteristic of that observed in sarcoidosis, but extensive studies have failed to uncover evidence of this condition.
Ann Intern Med 1980 Sep
PMID:Corticosteroid-responsive hypercalcemia with elevated serum 1-alpha, 25 dihydroxyvitamin D. 743 65

59 children with urolithiasis were seen between 1969 and 1977 (8 1/2 years). Calculi from 50 patients were analyzed by X-ray diffraction. Half of the patients were 0-4 years old, and in this age group males greatly predominated (76%). Calculi in 26 patients were of infectious, and in 15 patients of metabolic origin (cystinuria 7, idiopathic hypercalciuria 5, primary hyperoxaluria 3), whereas 18 were idiopathic. Most infectious stones contained struvite, and most idiopathic stones contained calcium oxalate. An infectious etiology was observed in 55% of the 0-5-year-old children (n = 33), but in only 20% of the 10-16-year-old ones. In contrast, the percentage of idiopathic stones rose from 18% in the youngest to 70% in the oldest age group, although the absolute numbers were similar in all age groups, Childhood urolithiasis in Switzerland is thus primarily observed in young male patients and is usually secondary to a definable cause.
Helv Paediatr Acta 1980 Sep
PMID:Childhood urolithiasis. 745 Dec 34

The acute effects of intravenous infusions of phosphate and parathyroid hormone (PTH) upon the renal tubular handling of sodium, potassium, calcium, magnesium, and phosphate were examined in phosphate-depleted dogs using recollection micropuncture techniques. Hypercalciuria in phosphate depletion results from an impairment of calcium reabsorption between proximal and distal sampling sites, which can be partially corrected by the acute administration of PTH or by phosphate infusion. Magnesium reabsorption was normal in phosphate-depleted dogs but increased in parallel with calcium in the distal tubule following PTH and phosphate infusion. Phosphate was avidly reabsorbed in the phosphate-depleted dog so that excretion was very low even during the infusion of PTH or of neutral phosphate. Only with the infusion of both PTH and phosphate was a normal phosphaturic response observed.
Can J Physiol Pharmacol 1980 Sep
PMID:Renal tubular transport in phosphate depletion: a micropuncture study. 745 96

Although receptors for somatostatin are found in bone cells, the effect of somatostatin analogs on calcium metabolism is unknown. The authors studied, in a metabolic ward, the effect of octreotide (a long-acting somatostatin analog) and a placebo in two 6-day calcium balance periods in 8 children with Duchenne muscular dystrophy. As expected, octreotide (2 micrograms/kg, subcutaneously, every 8 hours) reduced serum growth hormone and somatomedin (IGF-1) to levels found in growth hormone deficiency. Octreotide enhanced calcium retention by 30% (96 mg daily [P < 0.04]) in 7 boys for whom complete data (diet, urine, and fecal calcium) were available. In 6 children with urinary calcium excretion (Uca) greater than 50 mg daily, octreotide markedly lowered Uca, from 114 +/- 23 mg daily to 61 +/- 9 mg daily (P < 0.03). Calcium retention occurred in patients with or without initial hypercalciuria, but the higher the basal Uca, the greater was the inhibition by octreotide (r = 0.79; P < 0.03). Inactive, nonambulatory patients had a more pronounced response of Uca to octreotide (P < 0.02). Octreotide caused a mild, nonsignificant reduction in fecal calcium, with no major changes in serum calcium, phosphorus, parathyroid hormone, urinary excretion of sodium and potassium, or in creatinine clearance. Based on the current observations and the presence of receptors for somatostatin in bone cells, this hormone may have, at least on a short-term basis, an anabolic effect on calcium, perhaps favoring its deposition in bone.
Am J Med Sci 1995 Sep
PMID:Octreotide enhances positive calcium balance in Duchenne muscular dystrophy. 766 11

Familial hypocalciuric hypercalcemia (FHH) is generally characterized by lifelong hypercalcemia without hypercalciuria and is inherited in an autosomal dominant manner. Affected individuals show abnormal parathyroid and renal responses to changes in the extracellular calcium concentration. A Japanese FHH family was screened for mutations in the Ca(2+)-sensing receptor gene by the polymerase chain reaction and single strand conformation polymorphism. The proband with hypercalcemia showed an abnormal pattern in exon 1 of the gene, whereas her two sisters with normocalcemia showed a normal pattern. The consanguineous parents with borderline serum calcium concentrations showed both patterns. Nucleotide sequence analysis identified a G-->C point mutation at nucleotide 118 that resulted in the conversion of the normal codon for proline into a codon for alanine at amino acid 40 (numbered according to the bovine complementary DNA). The proband was homozygous for the mutation, and the parents were heterozygous. These results imply that this mutation in the human Ca(2+)-sensing receptor gene causes FHH and that the dosage of the gene defect determines disease phenotype.
J Clin Endocrinol Metab 1995 Sep
PMID:Familial hypocalciuric hypercalcemia associated with mutation in the human Ca(2+)-sensing receptor gene. 767

Idiopathic osteoporosis is a syndrome appearing in adult men and women, and is different from idiopathic juvenile osteoporosis which appears in the growth period. It is characterised histomorphometrically by decreased values in bone volume, trabecular thickness, active osteoid surface, mineralization surface and bone formation rate. Hypercalciuria, which appears in many cases, is thought to reflect this depressed metabolic state of the bone. Diagnosis depends on the exclusion of all the primary endocrine disturbances and metabolic bone disease. The presence of subclinical metabolic abnormality should be carefully searched out.
Nihon Rinsho 1994 Sep
PMID:[Idiopathic osteoporosis]. 796 87

The bone mineral density of the lumbar spine was assessed in nine non-ambulant children with cerebral palsy combined with measurements of serum 25-hydroxyvitamin D, parathyroid hormone, and urinary calcium excretion. Three children with recurrent fractures received treatment with bisphosphonates for periods ranging from 12-18 months. All the children demonstrated a severe reduction in bone mineral density even when allowance was made for their body weight. There were no consistent abnormalities of vitamin D or parathyroid hormone status. Three children had gross hypercalciuria. Each of the children treated with bisphosphonates demonstrated an increment in bone density ranging from 20-40% with no apparent adverse effects.
Arch Dis Child 1994 Sep
PMID:Osteopenia in cerebral palsy. 797 97

The association between idiopathic hypercalciuria and osteopenia (OP) has been recently recognized. It is not established whether or not calcium intake plays a critical role in the loss of bone mass. Fifty-five calcium stone forming patients with either absorptive hypercalciuria (AH) or fasting hypercalciuria (FH), 29 males and 26 premenopausal females, were submitted to dual photon absorptiometry at lumbar spine. Calcium intake was assessed by a 72 hr dietary record. OP was detected in 20% (11/55) of patients, being more common among men, 9/26 (35%) than in women, 2/29 (7%), p < 0.05. Male FH patients presented lower mean bone mineral density (BMD) than sex, weight and age-matched control (1.058 +/- 0.18 vs 1.209 +/- 0.13 g/cm2, X +/- SD, p < 0.05). OP was more frequent in FH patients, 7/20 (35%) than in AH patients 4/35 (11%), albeit the difference was not statistically significant. There was no correlation between calcium intake and BMD measurement. Six osteopenic male FH patients were further submitted to histomorphometric evaluation with tetracycline double labeling. Bone volume was lower than the controls (13.2 +/- 3.0 vs 27.2 +/- 3.7%, p < 0.05). Osteoid surfaces were reduced, although not significantly (10.1 +/- 8.2% vs 15.9 +/- 6.7%). Eroded surfaces were markedly increased (23.9 +/- 13.4 vs 4.2 +/- 1.4%, p < 0.05). The bone formation rate was very low with a complete lack of tetracycline double labeling in 4 patients. These data suggest low bone volume, tendency to low bone formation, increased bone resorption and a severe mineralization defect, consistent with normal or low bone turnover osteoporosis.
Clin Nephrol 1994 Sep
PMID:Bone disease in calcium stone forming patients. 799 36


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