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)

We studied weanling rats fed 0.06% (group 1) and 0.10% (group II) magnesium (Mg) during phosphate depletion (PD) in order to evaluate the role of Mg in the bone, soft tissue, and serum changes of PD. The following results were obtained: 1) serum Mg remained stable in the face of a negative Mg balance; 2) the hypercalcemic and hypercalciuric response to PD was the same in both groups; 3) bone Mg content was decreased with PD in both groups and was associated with a significant decrease in bone calcium and phosphorus. We conclude that: 1) the hypomagnesemia of PD is dependent mainly on the dietary intake of Mg; 2) the hypercalcemia and hypercalciuria of PD are not caused by primary changes in Mg homeostasis; 3) low-dietary Mg during PD may cause a defect in soft tissue utilization of P in the growing rat.
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PMID:Influence of dietary magnesium in experimental phosphate depletion: bone and soft tissue mineral changes. 46 91

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

Administration of gallium nitrate to rats resulted in the formation of renal precipitates which occluded tubular lumina. When analyzed with a combination of scanning electron microscopy and x-ray energy spectrometry, these precipitates were found to contain gallium complexed with calcium and phosphate. Injection of gallium nitrate also resulted in hypercalciuria, although serum calcium levels remained unaltered. Administration of an osmotic diuretic, isosorbide, prior to gallium treatment resulted in the formation of fewer renal precipitates and histopathologic changes than in the nondiuresed animals. Diuresis did not alter gallium serum pharmacokinetics, the 24 hour cumulative renal excretion of gallium or the extent of the drug-induced hypercalciuria. However, isosorbide pretreatment significantly reduced the urinary concentrations of both gallium and calcium. The data presented indicate that diuresis reduces the severity of gallium-induced renal lithiasis and subsequent renal accumulation of gallium by diluting the urinary concentration of gallium and calcium thereby lowering the incidence of interaction of these two elements within the kidney tubule.
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PMID:Gallium nitrate (NSC-15200) induced toxicity in the rat: a pharmacologic, histopathologic and microanalytical investigation. 49 44

Two siblings from a consanguineous family, suffering from nephrocalcinosis and nephrolithiasis caused by idiopathic hypercalciuria are described. The condition is associated with bilateral macular colobomata and tapeto-retinal degeneration. It is known that the latter can occur together with different nephropathies; however, until now it has never been described in combination with idiopathic hypercalciuria. Blood calcium levels were found to be normal, calcium excretion rates were, with one exception, more than 6 mg/kg/24 h corrected for 100 ml GFR. Hypomagnesemia of 1.5 and 1.2 mg/dl and hyermagnesuria of 1.9 and 2.5 mg/kg/24 h corrected for 100 ml GFR were found in both patients. Tubular phosphate reabsorption reached 87% and 84% at serum parathormone levels of 0.34 microgram/l and 0.31 microgram/l in the two patients, respectively. Under calcium and magnesium loading the clearance rates of calcium and magnesium were raised whilst there was only a small insignificant increase in the blood levels of these cations. Acid-base titrations showed normal excretion rates of acid and base in one patient and a mild proximal tubular acidosis in the other. Quantitative investigation of the renal concentrating and diluting capacity established a decrease in the formation of the medullary concentrating gradient in both patients.
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PMID:Idiopathic hypercalciuria with bilateral macular colobomata: a new variant of oculo-renal syndrome. 50 Mar 85

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

Eleven patients with kidney stone disease and idiopathic hypercalciuria (urinary calcium above 4 mg/kg/j), without phosphorus renal leak and 6 control subjects have been put for 3 days on a diet containing 1 g calcium and 1 phosphorus daily (period A), and then for 4 days on a diet containing 1 g calcium, 450 mg phosphorus and 3 g aluminium hydroxyde daily (period B). During period A, no significant difference in blood calcium, phosphorus and magnesium, not in phosphaturia, rate of phosphorus reabsorption (RPR) and ratio maximum RPR/creatinine clearance was found between the two groups. After 2 days on a low phosphate diet (period B) the blood phosphorus decreased significantly in the hypercalciuric patients but not in the control subjects, thus revealing among the forme a latent abnormality in the retention of phosphates. This abnormality could play an important role in the pathogenesis of hypercalciuria.
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PMID:[Idiopathic hypercalciuria: effects of acute phosphorus deficiency (author's transl)]. 53 14

Urinary supersaturation in respect to brushite or calcium oxalate represents the main pathogenic factor in stone formation. Of the patients with calcium oxalate stones 30 to 40% present with hypercalciuria. Herein we determine and compare the effects and side effects in the treatment of hypercalciuria with sodium cellulose phosphate or Campanyl, a potassium versus calcium ion exchanger, and thiazides alone or in combination with an ion exchanger.
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PMID:Long-term treatment of hypercalciuria with thiazides, sodium or potassium cellulose phosphate, separately or in combination. 54 17

Fifty male patients with urolithiasis (UL), associated with idiopathic hypercalciuria (IH), were studied in comparison to a group of 18 male normocalcemic patients with inactive calcium stone disease of unknown etiology. In the group of IH-UL, in addition to hypercaliuria, statistically significant hyperphosphaturia with decreased tubular reabsorption of phosphate and hyperuricemia were observed; there was a tendency to hypophosphatemia although non-significant. In 36% of the IH-UL patients the first episode of renal colic appeared at age 40 to 50. Thirty-eight per cent of the IH-UL patients had recurrent stone formation. Twenty per cent of the IH-UL patients had a family history of urolithiasis. Forty-six per cent of all stones contained oxalate in addition to calcium, and 25% of the stones contained oxalate and phosphate.
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PMID:Urolithiasis associated with hypercalciuria. 60 17

In 18 cases of sarcoidosis, 11 presented with hypercalciuria. Absorptive hypercalciuria was usually involved, but 2 patients had probably a calcium renal leak. Therapy with sodium cellulose phosphate was usually effective in lowering the amount of urine calcium, but thiazides had to be used concomitantly in three cases.
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PMID:Hypercalciuria in sarcoidosis. 61 Jan


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