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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the effects of dietary PO4 restriction on 25-OH-Vitamin D3 metabolism, serum iPTH levels, and mineral balances in healthy women and men. PO4 balances were progressively negative because of fecal losses without sex difference. Turnover of the plasma 25-OH-D pool was increased from 5.8 +/- 0.4 to 12 +/- 1.2 nmol/day; P less than 0.001, despite a fall in serum iPTH of -1.1 +/- 0.3 mulEq/ml; P less than 0.01. In both sexes, net intestinal calcium and magnesium absorption increased in proportion to a more rapid turnover of the plasma 25-OH-D pool, implying increased renal 1,25-(OH)2-D3 production. By contrast, there was a striking sex difference in the response of serum PO4 to dietary PO4 deprivation; the levels falling progressively in women, but remaining at control levels in men. Women demonstrated progressive hypercalciuria and negative Ca balances while in men the increments in intestinal Ca absorption were approximately matched by the increments in urinary Ca excretion so that Ca balances were not different from zero.
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PMID:Dietary phosphate deprivation in women and men: effects on mineral and acid balances, parathyroid hormone and the metabolism of 25-OH-vitamin D. 1 Dec 24

Examination of glucose kinetics, pancreatic alpha and beta cell function, plasma lipids, urinary acidification and calcium excretion has been undertaken in a patient with hereditary fructose intolerance. This case was unusual as it was associated with insulin-requiring diabetes, type IV hyperlipemia, hypercalciuria and renal calculi. He also demonstrated the previously described fructose-induced defect of urine acidification. Glucagon and C-peptide assays showed that the pancreatic alpha cells were stimulated by fructose and that the beta cells did not respond to fructose. It is not known whether the latter was due to his diabetes or to the lack of a beta cell response to this sugar. Primed 14C-glucose infusions were used for the first time to study nonsteady state glucose kinetics in man. They showed that, 24 hours after the last insulin injection and under basal conditions, the glucose concentrations increased because glucose production exceeded glucose utilization. However, after the administration of sorbitol the plasma glucose concentration decreased because glucose production decreased. After the administration of sorbitol there was no change in the metabolic clearance of glucose. This reflects the lack of a peripheral insulin effect and is consistent with the lack of any measurable C-peptide. Glucose utilization also decreased, but this decrease was less than the decrease in glucose production. Because the metabolic clearance of glucose remained unchanged, it was concluded that the change in glucose utilization was solely due to the decrease in glucose concentration. The absence of C-peptide in the plasma indicated that changes in glucose turnover were not related to any changes in endogenous plasma insulin. Furthermore, the plasma glucagon concentration increased and, hence, changes in this hormone could not account for the decrease in glucose production. Therefore, it was concluded that the sorbitol-induced decline in glucose production was due to a direct effect on hepatic metabolism.
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PMID:Studies of glucose turnover and renal function in an unusual case of hereditary fructose intolerance. 1 54

Quantitative and qualitative studies have been made of the urinary crystals from a series of normal subjects and from stone formers with idiopathic hypercalciuria with and without treatment with thiazide diuretics and/or cellulose phosphate. The results obtained from mid-morning unprepared subjects seemed more helpful than those obtained following overnight collections or after a dry breakfast. Crystalluria was more common in stone formers than in normal subjects, but was seen in both groups. The most striking difference between these 2 groups was the almost complete absence of aggregation of oxalate crystals in the normal subjects. Cellulose phosphate greatly reduced phosphate crystals but resulted in a large increase in small oxalate crystals but without change in the incidence of aggregation of oxalate crystals. Thiazides also reduced occurrence of phosphate crystals but only gave a very small increase in oxalate crystals and also without change in aggregation of oxalate crystals.
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PMID:Crystalluria in normal subjects and in stone formers with and without thiazide and cellulose phosphate treatment. 1 4

Dietary and drug treatments of calcium nephrolithiasis depend mainly on the mineral composition of renal stones: calcium oxalate, phosphate or mixed stones. The association with an hypercalciuria is an important factor which must be taken into account because oxalates and phosphates precipitate as calcium crystals in case of urinnary oversaturation. Despite many therapies have been proposed, their efficiency seems to be rather small when they are used alone. Usually, it is necessary to act on several factors with a combination of therapeutic methods. Absorptive hypercalciuria are improved with both low calcium diets and inhibitors of calcium absorption. In renal hypercalciuria, the treatment is based on the administration of thiazide diuretics which enhance calcium renal tubular reabsorption. The other therapeutic methods depend on the nature of renal stones: urinary acidification for calcium phosphate; administration of succinimide, oral phosphate or organic phosphonates for calcium oxalate stones; association with purine biosynthesis inhibitors in case of the presence of urates in renal calculi.
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PMID:[Dietary and drug treatments of calcium nephrolithiasis (author's transl)]. 3 18

Studies were performed on 12 patients with idiopathic hypercalciuria to evaluate the hypothesis that the acid load accompanying potassium acid phosphate would adversely affect renal calcium reabsorption and citrate excretion compared to the neutral form of the phosphate salt. During acute clearance studies, neutral phosphate (NP) led to a fall in FECa (2.2 +/- 0.6% to 0.8 +/- 0.1%, P less than 0.02) and no change in titratable acidity (TA) or net acid excretion (NAE). Acid phosphate (AP) did not reduce FECa acutely, and led to a rise in TA (22 +/- 4 to 62 +/- 6 muEq/min, P less than 0.02) and NAE (46 +/- 6 to 6 89 +/- 7 muEq/min, P less than 0.02). During chronic administration, AP resulted in higher urinary calcium excretion in both absorptive (187 +/- 29 vs. 141 +/- 18 mg/day, P less than 0.02) and renal hypercalciuric patients (233 +/- 24 vs. 173 +/- 190.02 mg/day, P less than 0.02). Also, TA and NAE were higher following AP, whereas citrate excretion was lower (375.4 +/- 64.6 vs. 633.4 +/- 28.8 mg/day, P less than 0.01). These data suggest that the reported ineffectiveness of AP in the therapy of nephrolithiasis may be related to the deleterious effects of the acid load on calcium and citrate metabolism.
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PMID:Differing effects of acid versus neutral phosphate therapy of hypercalciuria. 4 88

The treatment of rapidly progressive skeletal demineralisation in myelomatosis has been studied with the help of metabolic calcium balance in two patients; In one, osteoporosis accelerated during treatment with melphalan and prednisolone, although he remained normocalcaemic throughout, suggesting that osteoporosis was aggravated by corticosteroid therapy. In the other patient, who was initially hypercalcaemic, conventional treatment produced clinical remission before eventual relapse with more hypercalcaemia and skeletal dissolution. Both patients were then treated with mithramycin alone, and, although neither obtained haematological remission, bone pain was relieved, hypercalciuria and hypercalcaemia were abolished, and calcium balances proved that mithramycin was effective in restoring calcium equilibrium. The results indicate that mithramycin may abolish excessive bone resorption in myelomatosis and that severe bone dissolution may occur in the absence of hypercalcaemia. Regular determination of 24-hour urinary calcium excretion as well as of plasma-calcium is important in monitoring process. Mithramycin should be considered in the early treatment not only of hypercalcaemia but also of severe hypercalciuria, if these complications do not rapidly remit during the first course of conventional myeloma therapy, with or without steroids. Finally, these results add to evidence that a humoral factor may be responsible for osteoclast stimulation in myelomatosis.
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PMID:Treatment of osteolytic myelomatosis with mithramycin. 4 84

Urinary calcium and magnesium excretion was measured in two groups of soldiers leaving the temperate climate of the united Kingdom for service in the Persian Gulf. In one group urinary calcium levels and magnesium/calcium ratios were similar, ten days after arrival in the Gulf during the "cold season", to those found in the U.K. The other group went to the Gulf in the "hot season", and calcium excretion rose immediately to levels comparable with those found in the first group after eight months. Mg/Ca ratios fell to levels seen in stonformers, and 2 of 91 soldiers followed up for three years have had urinary calculi. Increased exposure to sunlight seems to be the most likely cause of the hypercalciuria.
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PMID:Sunlight and hypercalciuria. 4 31

Anorexia, constipation, vomiting and somnolence in a 39-year-old woman were at first misinterpreted as being of psychological and autonomic nervous system origin. Further clinical and biochemical tests revealed hyperthyroidism associated with hypercalcaemia and hypercalciuria. Thyrostatic treatment for 12 days caused regression of the hypercalcaemia and, after subtotal resection, serum calcium levels and urinary calcium excretion returned to normal for good. The hypercalcaemia syndrome must therefore be assumed to have been the direct result of the hyperthyroidism.
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PMID:[Hyperthyroidism with hypercalcaemia (author's transl)]. 5 61

A test was developed to diagnose various forms of hypercalciuria. A two-hour urine sample after an overnight fast and a four-hour urine sample after 1 g of calcium by mouth were tested for calcium, cyclic AMP and creatinine. The 24 patients with absorptive hypercalciuria had normocalcemia and normal fasting urinary calcium (less than 0.11 mg per milligram of urinary creatnine). Urinary calcium was high (greater than or equal to 0.2 mg per milligram of creatinine) after a calcium load. Of the 28 patients with primary hyperparathyroidism (resorptive hypercalciuria), 25 had hypercalcemia and 21 had high fasting urinary calcium. Urinary cyclic AMP, elevated in 30 per cent of fasting patients, was high (greater than 4.60 mu moles per gram of creatinine) in 82 per cent of cases after calcium load. Six patients with renal hypercalciuria had normocalcemia, high fasting urinary calcium, and high (greater than 6.86 mu moles per gram of creatinine) or high-normal fasting urinary cyclic AMP was normal. This simple test should facilitate the differentiation of various causes of hypercalciuria.
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PMID:A simple test for the diagnosis of absorptive, resorptive and renal hypercalciurias. 16 60

Effects of parathyroidectomy on parathyroid function and calcium (Ca) metabolism were carefully evaluated in 6 patients with primary hyperparathyroidism without symptoms normally attributed to the disease and in 7 with bone disease or nephrolithiasis. Before parathyroidectomy, both groups of patients demonstrated evidence of the sequelae of parathyroid hormone (PTH) excess, since they presented one or more of the following features: low bone density by 125I-photon absorption, hypercalciuria (urinary Ca greater than 200 mg/day on an intake of 400 mg/day), negative Ca balance (absorbed Ca less than urinary Ca), elevated fasting urinary Ca greater than 0.2 mg/mg creatinine for a night-time sample after a 6-hour fast), and decreased renal function (creatinine clearance of less than 65 ml/min). Following parathyroidectomy, most of these deleterious effects were reversed commensurate with the return of immunoreactive serum PTH, serum Ca, and urinary cyclic AMP toward normal. These quantitative non-invasive techniques may be useful for the initial evaluation and follow-up of patients with asymptomatic primary hyperparathyroidism.
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PMID:Metabolic effects of parathyroidectomy in asymptomatic primary hyperparathyroidism. 17 69


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