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

The authors report on the clinical, biological and radiological anomalies observed in a series of 42 cases of idiopathic hypercalciuria. An histological bone study showed "osteomalacia" type changes (an increase in the osteoid volume and a decrease in the mineralization speed). The Ca45 isotope studies showed that there was an exchangable pool of calcium and a turnover, which was generally low. A study of the kidney functions revealed a decrease in the tubular reabsorption of calcium, while that of phosphorous remained within normal limits. There was no case of hyperparathyroidism in this series. The authors pose the question of whether the failure of calcium to settle on the tissues and the lack of tubular reabsorption of calcium, does not result from the relatively ineffective action of the endogenous circulating parathyroid hormone.
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PMID:[Idiopathic hypercalciuria. Correlative study of bone tissue and phosphocalcium investigations]. 44 70

We have studied 83 patients with recurrent calcium stone formation in an attempt to determine an approximate incidence of metabolic disturbances associated with stone disease. Male veterans (n = 42), male non-veterans (n = 13), and women (n = 28) composed the group. We divided the groups in such fashion because they represented generally two distinct socioeconomic groups. Primary hyperparathyroidism was present in 19 per cent of the subjects; a marked predominance of women (15/16) was noted. Hypercalciuria of renal or intestinal origin was present in 23 per cent of the group. Of interest was a group of male veterans (17/83) in whom normocalciuria, normocalcemia, and normal serum phosphate were associated with high values of immunoreactive parathyroid hormone. These subjects had low urine phosphate. This set of findings indicates that these patients may be a new subgroup of stone-forming patients. Metabolic abnormalities could not be detected in 38 per cent of the patients. Classification of stone subjects is essential for rational management.
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PMID:Some characteristics of recurrent calcium stone formers in Puerto Rico. 45 11

Mechanisms involved in the hypercalciuria caused by high levels of protein intake were investigated. Six healthy males participated in a 20-day metabolic study. During the first 10-day period, all subjects were given a 47 g protein diet and during the second 10-day period, a 142 g protein diet. Calcium, magnesium and phosphorus intakes were kept constant at 515, 320 and 1,110 mg daily, respectively. Urinary calcium was elevated significantly when the protein intake was increased. Glomerular filtration rate and calcium clearance were increased significantly when the high protein diet was fed; the fractional tubular reabsorption of calcium was decreased from 98.4 to 97.4%. Thus, the increase in urinary calcium caused by the high protein diet appears to be due in part to an increase in the filtered load of calcium by the glomeruli and in part to a decrease in calcium reabsorption by the renal tubules. The level of protein intake had no effect on the fasting serum concentrations of parathyroid hormone, total calcium, magnesium or inorganic phosphorus or plasma ultrafiltrable calcium.
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PMID:Effect of level of protein intake on calcium metabolism and on parathyroid and renal function in the adult human male. 45 94

A 9 year old girl with idiopathic Fanconi syndrome and hypercalciuria is described. In order to determine whether the increased calcium excretion was directly or indirectly due to the disturbed phosphate metabolism, the behavior of the calcium excretion during therapy, the serum levels of 1,25-dihydroxyvitamin D and parathyroid hormone, and the effect of parathyroid hormone on the renal tubules were investigated. Normal serum 1,25-dihydroxyvitamin D and parathyroid hormone levels, lack of a correlation between the serum phosphate concentration and the degree of hypercalciuria, as well as unsuccessful therapy of the hypercalciuria with oral phosphate indicate that the increased calcium excretion cannot be explained by impaired renal phosphate reabsorption. The hypercalciuria in the patient was therefore regarded as being due to a primary decrease of tubular calcium reabsorption.
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PMID:Hypercalciuria in idiopathic Fanconi syndrome. 47 82

The safety and effectiveness of sodium cellulose phosphate (SCP) in the treatment of calcium urolithiasis of absorptive hypercalciuria was explored. Eighteen patients with absorptive hypercalciuria with intestinal hyperabsorption of calcium, normal or suppressed parathyroid function, and active stone disease received 10 to 15 Gm SCP daily (2.5 to 5 Gm with meals) and 2 to 3 Gm magnesium gluconate daily (1 to 1.5 Gm twice daily orally separately from SCP) for eight to 54 months, while maintained on a moderate calcium and oxalate restriction. During treatment, serum calcium, immunoreactive parathyroid hormone, and urinary cyclic AMP remained within the normal range. Serum alkaline phosphatase and bone density (measured by photon absorptiometry) did not change significantly or remained within normal limits. Serum concentrations of magnesium, copper, zinc, and iron and blood hematocrit were not significantly altered by therapy. However, urinary calcium returned toward normal, and incidence of renal stone formation markedly decreased. The results suggest that SCP is a safe and an effective drug for absorptive hypercalciuria.
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PMID:Clinical pharmacology of sodium cellulose phosphate. 48 64

The handling of an acute oral calcium load in 22 men with recurrent calcium stone disease was studied before and after diuretic therapy. As a group, the patients had marginal hypercalciuria (150 mg calcium per gram of creatinine in a 24-hr urine collection). Metolazone, a diuretic with an action in the cortical thick ascending limb of Henle's loop, was given in oral daily doses of 5.0 mg for periods of 9 to 34 mo. An oral calcium load induced a rapid rise in urine calcium exeretion, which was blunted markedly by metolazone. Further analysis of the subjects revealed that one group (11 subjects) had higher baseline 24-hr calcium excretion levels and higher parathyroid hormone (PTH) than the others. The effect of metolazone in reducing the calciuric response was significant only in this group. Thus, while long-term treatment with metolazone inhibited the rise in urinary calcium excretion elicited by an oral calcium load, the effect was significant only in patients who had high baseline urinary calcium and PTH values. The reduction in calcium excretion in response to an acute calcium challenge may explain in part the beneficial effects of cortical diluting segment diuretics in recurrent stone formers.
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PMID:Changes in calcium excretion after prolonged metolazone therapy in recurrent stone formers. 49 17

Increased calcium (Ca) excretion is characteristic of chronic phosphate (PO(4)) depletion (PD). To study the changes in tubular transport and the site of the hypocalciuric effect of PO(4) administration, clearance and micropuncture experiments were performed in intact rats pair fed either a control diet (0.5% PO(4)) or a PO(4)-depleted (PD) diet (0.01% PO(4)) plus Al(OH(3)) and in parathyroidectomized (PTX) PD rats, infused either with saline or with neutral sodium PO(4). Intact PD rats, compared with intact rats on a control diet, exhibited a lower plasma ultrafiltrable (UF) PO(4) (5.8+/-0.5 vs. 7.8+/-0.3 mg/dl), higher fractional excretion (FE) of Ca (4.1+/-1.2 vs. 0.6+/-0.1%), and reduced FE PO(4) (0.1+/-0.01 vs. 10.2+/-1.8%). Tubular fluid/plasma inulin was lower in the late proximal tubule of PD rats, associated with increases in fractional delivery (FD) from the proximal tubule of Na and Ca.The%FD of Ca to the early distal tubule of PD rats was increased (20+/-3 vs. 11+/-2%), but this difference was abolished by the late distal tubule (5.1+/-1.2 vs. 3.3+/-0.9%). In PTX-PD rats, PO(4) infusion increased plasma UF PO(4) (13.8+/-0.7 vs. 7.8+/-0.7 mg/dl). FE of Ca was reduced (1.08+/-0.35 vs. 4.59+/-1.57%) without correcting the increased Ca delivery to the late distal tubule. These data indicate that PD impairs Ca reabsorption in tubular segments before but not within the distal convoluted tubule, so that hypercalciuria is ultimately a result of decreased Ca transport either in the terminal nephron or in deeper nephrons where PO(4) infusion stimulates Ca transport independent of parathyroid hormone or changes in the filtered load of Ca.
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PMID:Renal tubular sites of altered calcium transport in phosphate-depleted rats. 50 Aug 33

Chronic administration of lithium salts is associated with hypercalciuria in the rat. To study the renal and extrarenal mechanisms of this phenomenon, we utilized balance and clearance techniques in rats pair-fed diets with or without Li2CO3 (0.5 meq/day per rat). Lithium induced hypercalcemia (mean +/- SE: 5.40 +/- 0.09 VS. 5.06 +/- 0.05 meq/liter) and hypercalciuria (Ca/creatinine = 0.28 +/- 0.04 vs. 0.13 +/- 0.03) only during feeding. When CaCO2 supplement to a calcium-deficient diet was abruptly withdrawn, hypercalciuria was abolished. However, polyuria and polydipsia persisted. No significant changes in serum phosphate, urine phosphate, sodium, pH, or citrate were observed. Chronic parathyroidectomy (PTX) also abolished this effect. During clearance studies, fasting excretion of calcium was similar between treated and control animals. Superimposed acute PTX resulted in comparable changes, hence arguing against primary changes in renal calcium reabsorption or changes in parathyroid hormone effects on the renal tubule. Thus, lithium produces absorptive hypercalciuria by a mechanism dependent on intact parathyroid glands and adequate diet calcium, but independent of urine sodium, phosphate, or pH. The active component of gut calcium transport may be involved, possibly via alterations of vitamin D metabolism.
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PMID:Mechanism of lithium-induced hypercalciuria in rats. 62 44

Fifteen patients, 13 women and 2 men (mean age 60 years) with osteoporosis of different types have been under treatment with 1 alpha-hydroxyvitamin D3 and calcium. The responses were observed clinically and by the use of roentgen morphometry, photon absorptiometry and by blood and urine chemical analyses. The treatment had beneficial clinical effect in all but 3 patients. The intestinal calcium absorption rate increased significantly. Slight hypercalcemia and a significant hypercalciuria occurred during treatment. Serum and urine phosphate levels, alkaline phosphatase and parathyroid hormone values were within normal ranges. The bone mineral content increased significantly during treatment. 1 alpha-hydroxyvitamin D3 and calcium was well tolerated by the patients. Three patients had coincidental acute attacks of spinal pain and 2 had further vertebral crush fractures. A period of time longer than one year is necessary to further evaluate the effects of 1 alpha-hydroxyvitamin D3 therapy on the clinical course of severe osteoporosis.
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PMID:Interim report on treatment of osteoporotic patients with 1 alpha-hydroxyvitamin D3 and calcium. 70 36

The effects of chronic phosphate depletion on renal tubular function were evaluated by micropuncture and free water clearance studies in the dog. Proximal tubular punctures demonstrated that chronic hypophosphatemia led to a reduction in ratio of tubular fluid to plasma inulin in late superficial tubular from 1.59+/-0.08 in control animals to 1.29+/-0.06 in phosphate-depleted dogs, with proportional inhibition of calcium and sodium reabsorption. The chronic decrease in proximal tubular fluid reabsorption was confirmed by the analysis of sustained water diuresis in conscious, phosphate-depleted dogs, before and after repletion of body PO4 stores, and in control animals. Urine flow rate/100 ml glomerular filtration rate (V/GFR) was significantly higher in PO4 DEPLETION THAN CONTROL (15.8+/-1.1 VS. 10.7+/-0.82). In addition, acetazolamide infusion did not increase V/GFR in phosphate-depleted dogs (15.8+/-1.1 vs. 17.16+/-0.9), supporting the conclusion that inhibition of proximal tubular fluid reabsorption was responsible for the elevated urine flow rate. PO4 repletion over 5 days reduced V/GFR to 9.2+/-0.7 despite no change in urine osmolality and no change in GFR, further suggesting a specific reversible alteration in proximal tubular reabsorption in phosphate depletion. Although hypercalciuria was a constant finding in phosphate depletion (fractional excretion of calcium of 2.04+/-0.4% vs. 0.47+/-0.13% in controls), the enhanced distal delivery of calcium was not a crucial factor; acute phosphate infusion reduced urinary calcium excretion to control values without affecting the reduced proximal tubular reabsorption in either intact or thyroparathyroidectomized phosphate-depleted dogs the change in distal nephron calcium reabsorption was independent of parathyroid hormone (PTH) levels since infusion of PTH failed to alter urinary calcium excretion. We conclude that chronic phosphate depletion leads to a reversible, sustained inhibition in proximal tubular reabsorptive fuction as well as a specific decrease in distal nephron calcium reabsorption. This latter reabsorptive defect is sensitive to phosplate infusion but not corrected by PTH.
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PMID:Renal tubular effects of chronic phosphate depletion. 85 68


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