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 incidence of renal calculi in renal transplant recipients was reviewed. It is an infrequent problem, with an incidence less than 1%. In the pediatric population, only 8 cases had been reported in the literature since 1964. Of the 221 children transplanted at this institution from 1964 to 1989, only these 2 developed renal calculi. One case was related to hyperparathyroidism and the other to idiopathic hypercalcinuria. This represented a frequency of 0.9% which correlates closely with the reported incidence in the transplant population at large.
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PMID:Renal calculi in pediatric renal transplant recipients. 235 70

Farnolith (a dietary fibre preparation) was given to normal patients (n = 6) with absorptive hypercalciuria type I (n = 6) and to one patient with renal hypercalciuria. Farnolith binds calcium and reduces calcium absorption in the intestines. In normal subjects, the urine and serum parameters of calcium metabolism (total and ionized calcium, 1.25-dihydroxy-vitamin D) were unchanged. In absorptive hypercalciuria type I, a significant decrease in calcium excretion was achieved; oxalate excretion decreased as well. Low PTH values normalized; vitamin-D metabolites were not affected. In renal hypercalciuria, PTH and 1.25 DHCC were increased, whereas hypercalciuria persisted. Our investigations show that Farnolith is a reasonable treatment for absorptive hypercalciuria. Calcium homeostasis is rendered normal by Farnolith without producing secondary hyperoxaluria as sodium cellulose phosphate. Patients with primary renal calcium leakage and secondary hyperparathyroidism should not be treated with Farnolith.
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PMID:[Studies of calcium metabolism in normal persons and patients with hypercalciuria in relation to therapy with the dietary fiber preparation Farnolith]. 253 20

Aminoaciduria and secondary hyperparathyroidism accompany vitamin D deficiency. However, the degree of aminoaciduria and PTH elevation have not been studied relative to different calcium and phosphorus dietary intakes. Weanling rats were fed 5 vitamin D deficient diets for 4-6 weeks: very low Ca (VLC) 0.02% Ca, 0.3% P; VLC + 1,25-dihydroxyvitamin D [1,25(OH)2D3], same + 500 pmol i.p. for 2 days; low Ca (LC) 0.45% Ca, 0.3% P; very low P (VLP) 1.2% Ca, 0.1% P; high Ca (HC) 2.5% Ca, 0.3% P, and control 1.2% Ca, 0.70% P + 2.5 micrograms% vitamin D. Amino acids, serum 25-hydroxyvitamin D [25(OH)D3], 1,25(OH)2D3, and PTH, using a specific antirat PTH antibody, were measured. A significant generalized aminoaciduria (11 amino acids) was found in all vitamin D-deficient groups. Furthermore, it was independent of plasma Ca and PTH, and urinary cAMP excretion irrespective of diet. Serum 25(OH)D and 1,25(OH)2D were significantly reduced in all vitamin D-deficient groups. VLC and VLC + 1,25(OH)2D3 were associated with the highest PTH levels (10- and 13-fold increase, respectively) and urinary cAMP (2.3-fold increase in each) and the lowest serum Ca. LC rats had an 8.8- and a 1.7-fold increase in PTH and urinary cAMP, respectively. Phosphate depletion was found in VLP rats documented by insignificantly elevated PTH, normal urinary cAMP, hypercalciuria, and percent tubular reabsorption of phosphate of greater than 99%. While dietary Ca and P affect plasma and urinary Ca and P plasma PTH and urinary cAMP, it appears that dietary P affects the aminoaciduria observed in this study via mechanisms that remain unclear. The possibility that the mechanism for the tubulopathy is multifactorial should be entertained.
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PMID:Aminoaciduria of vitamin D deficiency is independent of PTH levels and urinary cyclic AMP. 254 72

The authors analyze clinical and laboratorial features of 13 patients with surgically confirmed primary hyperparathyroidism (HPT). Among them, 8 presented renal lithiasis, 7 had bone disease, and 2 had both. All patients were hypercalcemic and had elevated serum carboxyterminal levels of PTH. The aminoterminal portion of the PTH was above the normal range in 9 patients and inappropriately high for the level of serum calcium in other two. The c'AMP was elevated in 7/8 patients. Hypophosphatemia was detected in 8/11 patients. Among the lithiasic patients, hypercalciuria was found in only 3. Five patients were submitted to an oral calcium load test which detected no intestinal hyperabsorption of calcium (IH) secondary to HPT in any of them. The rate of elimination of stones/patient/year was 1.7 before the establishment of HPT diagnosis. Despite the presence of renal lithiasis, hypercalciuria and IH were not common findings in HPT patients. Serum calcium and urinary c'AMP were the best screening tests for the diagnosis of HPT in this series. The diagnosis should be further confirmed determining the PTH.
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PMID:[Primary hyperparathyroidism: clinical and laboratory spectrum]. 264 May 6

Between January 1977 and March 1988, 10 of 892 renal transplant recipients formed urinary tract calculi posttransplantation. The presenting symptoms were predominantly those of azotemia due to obstruction and/or hematuria. Factors predisposing to stone formation included a reconstructive urologic procedure at the time of transplantation (n = 4) or a surgical complication (n = 4), necessitating the placement of a ureteral stent and/or nephrostomy tube, secondary hyperparathyroidism (n = 5), hyperuricosuria (n = 4), and hypercalciuria (n = 1). Four patients passed their stones spontaneously; 1 patient underwent ureterolithotomy, 3 patients underwent endourologic stone extraction, 1 patient was treated with a combination of surgical and endourologic procedures, and 1 patient underwent extracorporeal shock wave lithotripsy as monotherapy. While the management of these patients can be challenging, awareness of predisposing factors, proper application of all currently available urologic techniques, and attention to certain guidelines of management can aid in minimizing morbidity from this rare urologic complication of renal transplantation.
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PMID:Renal transplant calculi. A reevaluation of risks and management. 266 Mar 56

Concomitance of hyperthyroidism and hyperparathyroidism is rare and only forty-nine well documented cases could be found in the literature. In the present study, only forty-three patients with adequate available clinical and laboratory data are reported. Hypercalcemia was found in all the patients and five of them (12%) had acute hyperparathyroidism. Two patients were also pregnant and had pancreatitis. Hypercalcuria was found in 73% and hypophosphatemia in 55% of the patients. Eleven patients (26%) had renal concretions. Skeletal roentgenograms showed abnormalities in 63% of the patients. Elevated serum level of alkaline phosphatase was present in 64% of the patients. However, there seemed to be no correlation with the severity of the skeletal lesions. Thyrotoxicosis commenced before that of Hyperparathyroidism in twenty-three patients (53%) whereas in the remaining twenty patients it was impossible to determine which disease began first. The etiologies of hyperparathyroidism as well as the differential diagnosis of parathyroid-related and nonparathyroid-related hypercalcemia are discussed. Microscopically, 74% of the patients had a single adenoma; 16% had hyperplasia of one to three parathyroid glands. One patient had an adenoma in combination with hyperplasia of one parathyroid gland, one had an adenoma and three hyperplastic glands, one had adenomas of two parathyroid glands in combination with hyperplasia of one parathyroid gland, and the other one had carcinoma of a parathyroid gland.2+ Finally, if a thyrotoxic patient still has hypercalcemia when becoming euthyroid after antithyroid therapy, coexisting hyperthyroidism should be considered and an operation should be performed as surgical treatment cured both diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Primary hyperparathyroidism and coexisting hyperthyroidism--review of the literature. 267 Jan 39

Some children with Bartter syndrome have hypercalciuria. To determine the mechanism for this phenomenon, we studied tubular function and calcium metabolism in six such children. All patients had hypokalemic alkalosis, normotension, hyperreninemia, growth retardation, low fractional distal chloride reabsorption (4/5), and elevated urinary prostaglandin E2 excretion (5/6). In addition, all had hypercalciuria (urinary calcium 6.5 to 25.0 mg/kg/day), with evidence of nephrocalcinosis in five. None, however, had evidence of rickets or hyperparathyroidism. There was a marked elevation in the serum concentration of 1,25-dihydroxyvitamin D in all, and four patients had a response to oral calcium loading suggestive of absorptive hypercalciuria. Five children have had long-term therapy with indomethacin. They have had improvement in hypokalemia and reduced urinary prostaglandin E2 excretion as well as reductions in the serum concentration of 1,25-dihydroxyvitamin D and in urinary calcium excretion. These data suggest that hypercalciuria in some children with Bartter syndrome is associated with an excess of 1,25-dihydroxyvitamin D. The improvement in hypercalciuria with prostaglandin synthesis inhibition may result in part from correction of this vitamin D abnormality.
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PMID:Hypercalciuria with Bartter syndrome: evidence for an abnormality of vitamin D metabolism. 267 27

The causes of impaired calcium, phosphorus and vitamin D metabolism in diabetic patients which in the long run lead to demineralization of bone can be summarized into several main groups. Above all disorders of calcium absorption from the small intestine are involved, associated with impaired absorption of vitamin D and its reduced conversion into active metabolites in the liver and kidneys. An increased elimination of calcium from the organism may also play a part (hypercalciuria, excretion in the faeces and sweat), hormonal changes (secondary hyperparathyroidism) and finally changes in the metabolism of the organic bone constituent--osteoid. Subsequent work will deal with the prevalence of osseous changes in diabetics, early diagnosis and rational treatment and possible prevention of these changes.
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PMID:[Diabetic osteopathies. 1. Etiologic factors and theoretical prerequisites for the development of bone demineralization in diabetics]. 280 Mar 64

The treatment of premature infants with the diuretic furosemide appears to be a contributory factor in the development of metabolic bone disease presumably because of furosemide-induced hypercalciuria. In this study, we measured calcium and phosphorus balance in furosemide-treated very low birth weight infants (VLBW) infants with bronchopulmonary dysplasia (BPD) who were fed a specialized premature formula containing increased amounts of calcium and phosphorus. Furosemide-treated infants received 166 +/- 37 mg/kg/day and retained 80 +/- 34 mg/kg/day of calcium, and 87 +/- 19 mg/kg/day and retained 52 +/- 14 mg/kg/day of phosphorus. The amounts retained were approximately 65% of the calcium and 72% of the phosphorus requirements for in utero mineral accretion. Compared to a group of similarly fed VLBW infants without BPD and not treated with the diuretic, the furosemide-treated infants excreted a larger percent of the calcium intake in the urine but had similar total urinary calcium and phosphorus losses (mg/kg/day) and serum calcium, phosphorus, alkaline phosphatase, and parathyroid hormone (PTH) levels. From the latter two findings, we suggest that the extra mineral content of the formula may have promoted bone mineralization and prevented the occurrence of secondary hyperparathyroidism.
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PMID:Effect of high calcium and phosphorus intake on mineral retention in very low birth weight infants chronically treated with furosemide. 280 41

The effects of glucocorticoids on calcium and bone metabolism were investigated in 11 children (aged 6 months to 13 years) who were treated with dexamethasone, prednisolone and depot-ACTH because of different disorders. Alkaline phosphatase activity and osteocalcin in serum, representing indices of osteoblastic bone synthesis, and urinary hydroxyproline in relation to creatinine in morning fasting urine specimens, an index of osteoclastic bone degradation, decreased by 53-61% from baseline (P less than 0.01), with a highly significant relationship of all 3 indices to each other. Additional influences of glucocorticoids were hyperphosphaturia due to decreased renal phosphate reabsorption not mediated by secondary hyperparathyroidism, as well as marked hypercalciuria. As the consequence of the present study the following prophylactic or therapeutic recommendations are given during steroid-treatment: 1. Approvement of the negative balance of calcium and phosphate by correcting the hypercalciuria with hydrochlorothiazide, and the hypophosphatemia with oral phosphate and 2. in elder children with osteoporosis, stimulation of the decreased osteoblastic bone formation by sodium fluoride.
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PMID:[Disorders of calcium and bone metabolism in glucocorticoid treatment]. 284 91


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