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 effects of a 2 Gm oral phosphorus load in a family with idiopathic hypercalciuria (IH) consisting of 3 symptomatic (DT, CS, DS) and 2 asymptomatic (MS, PD) members were compared with 12 normal control subjects. Biochemical parameters measured included: total and ionized calcium, phosphorus, intact and carboxyl-terminal parathyroid hormone, urinary calcium, phosphorus, and sodium. Water loading had no effect on these parameters. After the phosphorus load, serum phosphorus rose 1.60 mg/dl in the control subjects but only 1.34 mg/dl in the IH family at the end of one hour. Basal tubular reabsorption of phosphate (TRP) were comparable in the control subjects and the IH family. After the phosphorus load, the TRP in the control subjects fell (average 9.2%) accompanied by a significant (P less than 0.02) rise in the carboxyl-terminal parathyroid hormone. Except for DT who had been taking hydrochlorothiazide, the TRP fell dramatically in the rest of the IH family (DS 25%, CS 12%, PD 26%, MS 50%) in the absence of any perturbations in either the intact or carboxyl-terminal parathyroid hormone. A hypocalciuric effect was observed in the IH family but not in the control subjects after phosphorus loading. The oral phosphorus challenge unmasked a parathyroid hormone independent renal phosphate leak in both symptomatic and asymptomatic members in a family with idiopathic hypercalciuria.
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PMID:Oral phosphate load unmasks underlying renal phosphate leak in symptomatic and asymptomatic members of family with idiopathic hypercalciuria. 401 72

After discovering juvenile rheumatoid arthritis (JRA), hematuria, and urolithiasis associated with hypercalciuria in two children, urinary calcium excretion was examined in 38 patients with JRA. Fasting urine calcium/creatinine (mg/mg) (UCa/UCr) ratios were increased (greater than 0.21) in 12 patients, who had a mean UCa/UCr ratio of 0.34 +/- 0.14, compared with 0.09 +/- 0.06 in 26 normocalciuric patients with JRA. Increased UCa/UCr ratios were found more frequently in patients with systemic JRA (P less than 0.05); however, no relationship between UCa/UCr ratios and either functional classification or drug therapy was observed. Four children with increased urine calcium to creatinine ratios were examined more extensively. Twenty-four-hour urine calcium excretion ranged from 4.0 to 7.2 mg/kg/24 hours. An orally administered calcium loading test demonstrated fasting hypercalciuria after dietary calcium restriction in these four patients. Serum calcium, bicarbonate, phosphorus, and parathyroid hormone values were normal. Hematuria was found in six of 12 hypercalciuric patients with JRA but in only three of 26 normocalciuric patients (P less than 0.016). We conclude that urinary calcium excretion is frequently increased in patients with JRA and that hypercalciuria may be related to the pathogenesis of hematuria in some of them.
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PMID:Hypercalciuria in children with juvenile rheumatoid arthritis: association with hematuria. 402 May 46

Five healthy young men were studied during 24-30 wk of continuous bed rest. During the first 12 wk of bed rest, untreated subjects increased calcium excretion in the urine by 109 mg/day and in the feces by 147 mg/day. The rate of total body calcium loss was 0.5-0.7% per month. Losses of central calcaneus mineral, assessed by gamma ray transmission scanning, occurred at a tenfold higher rate, whereas the mineral content of the radius did not change. Changes in phosphorus balance resembled the calcium pattern, and increased excretion of nitrogen and hydroxyproline also occurred during bed rest. Upon reambulation, the subjects' calcium balance became positive in 1 month and recovery of their calcaneus mineral was complete within 10-20 wk. Treatment with potassium phosphate supplements (1327 mg P/day) entirely prevented the hypercalciuria of bed rest, but fecal calcium tended to increase. During the first 12 wk, calcium balance was slightly less negative (mean - 193 mg/day) than during bed rest without added phosphate (mean - 267 mg/day). This effect was not seen during the second 12 wk of bed rest. The patterns of magnesium excretion were similar to those of calcium. Fecal and urinary phosphorus excretions were doubled, and phosphorus balance became positive (+ 113 mg/day). Mineral loss from the central calcaneus was similar to that of untreated subjects. It is concluded that this form of phosphate supplementation reduces urinary calcium excretion but does not prevent bone loss during bed rest.
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PMID:The effect of supplemental oral phosphate on the bone mineral changes during prolonged bed rest. 512 4

The changes in serum calcium and the renal handling of this ion were evaluated during phosphate depletion. 96 renal clearance studies were carried out in 10 dogs before and after prolonged phosphate depletion (30-160 days) and after repletion. Depletion was produced by reducing phosphate intake and administering aluminum hydroxide gel while intakes of sodium, calcium, and magnesium were constant. With phosphate depletion, serum phosphorus fell to less than 1.0 mg/100 ml and diffusible serum calcium either remained unchanged or rose transiently. Glomerular filtration rate (GFR) fell by 15 to 53%. Despite the reduced filtered load of calcium, its fractional excretion increased in most experiments. This hypercalciuria was not dependent upon changes in sodium or magnesium excretion, or the urinary concentration of complexing anions, and persisted after sodium restriction. Phosphate repletion reversed the effects on GFR and calcium excretion. The intravenous infusion of small quantities of phosphate (0.04 mmole/min) into either intact or thyroparathyroidectomized (T-PTX), phosphate-depleted animals caused a significant reduction in fractional excretion of calcium, but the intrarenal infusion of 0.02 mmole/min of phosphate into one kidney failed to produce an ipsilateral effect. The administration of parathyroid extract reduced fractional calcium excretion, but the latter remained significantly elevated. After T-PTX, fractional calcium excretion did not increase in the phosphate-depleted animals. Furthermore, serum calcium was normal after T-PTX until serum phosphorus increased slightly, and only then did hypocalcemia develop. These observations indicate that (a) phosphate depletion produces hypercalciuria through a reduction in tubular reabsorption of calcium which is not due to changes in the tubular reabsorption of other ions; this effect is not reversed by the direct intrarenal infusion of phosphate; (b) a state of functional hypoparathyroidsm occurs during phosphate depletion which may, in part, cause reduced tubular reabsorption of calcium; (c) other extra renal mechanism(s), possibly related to events occurring in bone as a result of phosphate depletion, may have an effect on urinary calcium excretion; and (d) in the phosphatedepleted state, parathyroid hormone is not required for the maintenance of a normal level of serum calcium.
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PMID:Changes in serum and urinary calcium during phosphate depletion: studies on mechanisms. 542 13

The effects of commonly used therapeutic doses of hydrochlorothiazide and probenecid, given singly and in combination, on the urinary excretion of monovalent and divalent ions and on acid-base equilibrium were studied in four patients with idiopathic hypercalciuria.Probenecid had no effect on the urinary excretion of monovalent ions but resulted in a sustained increase in the urinary excretion of calcium, magnesium and citrate and a temporary increase in the urinary excretion of ammonium, in addition to its well-known effects on uric acid metabolism. A temporary fall in serum phosphorus levels was also observed.Probenecid also modified the response to hydrochlorothiazide in that the urinary excretion of calcium, magnesium and citrate was greater during combined therapy than when hydrochlorothiazide was administered alone. Probenecid prevented or abolished the increase in serum uric acid levels associated with the use of thiazide but did not modify the effects of hydrochlorothiazide on the urinary excretion of sodium, chloride, potassiu, phosphorus, ammonium, titratable acid and bicarbonate.
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PMID:The effects of probenecid and thiazides and their combination on the urinary excretion of electrolytes and on acid-base equilibrium. 546 17

A family of idiopathic hypercalciuria (IH), 3 symptomatic and 2 asymptomatic, plus 3 normal subjects were given the 1 Gm oral calcium challenge. Biochemical parameters measured included: serum and urinary calcium and phosphate, urinary cyclic AMP, and serum intact and carboxyl-terminal parathyroid hormone. Major differences between the normal control and the family with IH include: (1) higher calcemic response in the family with IH (0.9 vs 0.4 mg/dl); (2) a fall in carboxyl-terminal PTH and urinary cyclic AMP in the IH family in contrast to control subjects in whom there were no changes; (3) a rise in serum phosphorus in the IH family (0.8 vs 0.2 mg/dl, p less than 0.05). Urinary excretion of calcium, phosphorus, and sodium after the calcium challenge was minimal. The oral calcium challenge is a simple and useful test in demonstrating increased calcium absorption even in asymptomatic relatives of patients with idiopathic hypercalciuria.
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PMID:Altered responses in serum calcium phosphorus and parathyroid hormone to oral calcium load in symptomatic and asymptomatic members of family with idiopathic hypercalcemia. 608 33

An unusual metabolic bone disease which developed in 11 adults receiving total parenteral nutrition (TPN) for more than 3 months was characterised by the insidious onset of bone pain which became very severe and caused considerable disability. Serum levels of calcium, phosphorus, 25-hydroxy-vitamin D, and serum immunoreactive parathyroid hormone were normal. Patchy osteomalacia with impaired mineralisation and decreased bone turnover were seen on histomorphometric analysis of bone biopsy specimens. All patients receiving long-term TPN had hypercalciuria, but no biochemical features that distinguished patients with symptoms from those without. Skeletal symptoms generally resolved 1-2 months after stoppage of the TPN infusions, despite nutritional deterioration. The pathogenesis of this syndrome remains unknown.
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PMID:Bone disease associated with total parenteral nutrition. 610 76

The objectives of this study were to evaluate the effects of vitamin D(3) (D(3)) and 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) on uremic bone disease independent of their action on the intestine. The histomorphology of tibial metaphyses in uremic (5/6 nephrectomized [5/6 Nx]) rats fed a low-calcium-low-phosphorus (LCLP) diet was compared with sham-operated (SO) rats fed an LCLP diet and 5/6 Nx rats fed an LCLP diet and given 15,000 IU D(3) or 5 units (135 ng) 1,25-(OH)(2)D(3) daily for 7 days. A marked osteomalacia characterized by an increased percentage of active and inactive trabecular osteoid surface and thickened growth plates developed in proximal tibial metaphyses in 5/6 Nx rats given the placebo, compared with SO rats. These bone changes were associated with relative hypophosphatemia, hypophosphaturia, and hypercalciuria in 5/6 Nx rats. In 5/6 Nx rats treated with D(3) or 1,25-(OH)(2)D(3) the growth plates had undergone mineralization and vascular invasion and were markedly reduced in thickness. Other parameters of osteomalacia in trabecular bone were not different from 5/6 Nx rats given the placebo. There was a significant decrease in osteoclasts per millimeter of trabecular surface perimeter in D(3)- and 1,25-(OH)(2)D(3)-treated rats. These bone changes were associated with hypercalcemia, hyperphosphatemia, and hyperphosphaturia, compared with 5/6 Nx rats given the placebo. It was concluded that in uremic rats fed the LCLP diet, shortterm treatment with either pharmacologic levels of D(3) or 1,25-(OH)(2)D(3) corrected only lesions in the growth plate. Osteoid seams were not reduced in treated rats, although the serum calcium-phosphorus product was elevated. The 5/6 Nx rat fed the LCLP diet appears to be a useful model for the rapid induction of uremic osteomalacia in adult animals.
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PMID:Short-term effects of vitamin D3 and 1,25-dihydroxyvitamin D3 on osteomalacia in uremic rats fed a low calcium-low-phosphorus diet. 626 57

We have used a low-calcium diet providing only 2 mg/kg (body weight) per 24 hours of calcium to distinguish between "renal" and "absorptive" idiopathic hypercalciuria. Sixteen of 27 hypercalciuric subjects excreted calcium in excess of intake during days seven, eight and nine of he diet, suggesting some element of renal hypercalciuria; however, all patients had low or normal serum PTH and urine cAMP levels. In general, fasting urine calcium was elevated in these 16 subjects and normal in the remaining 11, who conserved calcium more normally. SErum 1,25(OH)2D3 levels were the same in patients and normal subjects, even though PTH levels of the patients were below those of he normal subjects. Urine magnesium excretion and phosphorus excretion were both increased in the patients who excreted calcium in excess of intake. Our findings suggest that renal and absorptive hypercalciuria may not be distinct entities but rather the two extremes of a continuum of behavior. A uniform elevation of intestinal calcium absorption and a variable defect of renal calcium reabsorption could explain our results far better than the hypothesis of distinct absorptive and renal forms of hypercalciuria.
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PMID:Effects of low-calcium diet on urine calcium excretion, parathyroid function and serum 1,25(OH)2D3 levels in patients with idiopathic hypercalciuria and in normal subjects. 627 90

Prolonged immobilization may result in hypercalcemia, hypercalciuria, and osteoporosis. Although bone resorption is central to this syndrome, the mechanism of resorption is uncertain. In particular, the role of systemic calcium-regulating hormones remains unclear. In 14 immobilized subjects we measured fasting calcium excretion, 24-hour urinary calcium excretion during restricted calcium intake, the renal phosphorus threshold, plasma 1,25-dihydroxyvitamin D, nephrogenous cyclic AMP, and immunoreactive parathyroid hormone. Mean serum calcium levels were normal, but fasting and 24-hour calcium excretion were markedly elevated (0.28 mg per deciliter of glomerular filtrate and 314 mg per 24 hours, respectively). The mean levels of serum phosphorus (4.8 mg per deciliter) and the renal phosphorus threshold (4.3 mg per deciliter) were elevated. Mean plasma 1,25-dihydroxyvitamin D was strikingly reduced (9.9 pg per milliliter), as were nephrogenous cyclic (0.64 nmol per deciliter of glomerular filtrate) and immunoreactive parathyroid hormone in both assays. These findings indicate that the parathyroid--1,25-dihydroxyvitamin D axis is suppressed in patients with immobilization-induced hypercalciuria, as would be predicted by a model of resorptive hypercalciuria.
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PMID:Calcium homeostasis in immobilization: an example of resorptive hypercalciuria. 628 47


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