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

Urine excretion of magnesium (Mg), calcium (Ca) and sodium(Na) was studied in patients with renal Ca stones having normal kidney function (n= 60), and in matched controls (n= 60), on a free diet following an overnight fasting period. In some formers, Mg was lower than in normals, whereas Ca was unusually high resulting in a significantly higher molar Ca/Mg ratio (p less than 0.001). 2. In 3 out of 4 stone groups Na excretion was significantly elevated because of reduced tubular reabsorption. In normals, fractional Na excretion varied between 0.44 and 0.54% of endogenous creatinine clearance, whereas it exceeded 1% in the stone patients. Conversely, the molar ratio Na/Ca was equal in all groups. 3. Fasting urinary cyclic AMP was comparable in both populations supporting the assumption that in the majority of patients Ca- or Mg- wasting via urine may not be responsible for secondary hyperparathyroidism. In small selected groups, losses of divalent cations may act in concert, leading to stimulation of the parathyroid glands. 4. Correlations between minerals and Na reveal a close relationship between Na, Ca and Mg in terms of clearance and excretion rate in patients and controls. Fractional Na and Ca excretion are correlated in patients but not in normals. This suggests that in the absence of phosphaturia, factors other than extracellular volume expansion and/or hyperparathyroidism are operative in stone disease. 5. The origin of fasting natriuresis and relative hypercalciuria may be ascribed to a change, as yet not causally identified, in distal tubular Na reabsorption.
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PMID:Fasting urine excretion of magnesium, calcium, and sodium in patients with renal calcium stones. 18 86

Effects of oral sodium cellulose phosphate therapy (5 g three times a day with meals for 4 days) on renal excretion of oxalate and on the crystallization of calcium oxalate in urine were examined in six patients with absorptive hypercalciuria on a constant metabolic dietary regimen. During treatment, urinary oxalate increased by 9-50 mg/day. However, urinary calcium decreased by 138-225 mg/day (50%-70%). Thus, the state of saturation of urine with respect to calcium oxalate decreased or did not change significantly. There was no consistent or significant change in the formation product ratio (limit of metastability) or in the crystal growth of calcium oxalate in urine.
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PMID:Effect of sodium cellulose phosphate therapy on crystallization of calcium oxalate in urine. 24 92

The clinical peculiarities, and the etiological and pathogenetic factors of urolithiasis in 296 patients suffering from spontaneous stone elimination were studied. It was established that 209 patients eliminated stones consisting of uric acid, sodium salts and ammonium salts. Moderate hypocalcemia and hyperphosphatemia and also hyperuricemia and hyperuricuria were present. There were 39 'eliminators' of calcium stones. Their blood calcium content was higher, hypercalciuria, inorganic phosphorus and normal uric acid, were noted. Compound stones were present in 48 observations. When carrying out additional biochemical tests in 57 patients with calcium and compound stones, primary hyperparathyroidism was diagnosed in 34 observations; and parathyroidectomy was successfully performed.
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PMID:On the pathogenesis of stone formation in stone-eliminating patients. 42 6

Patients with recurrent stone disease and hypercalciuria were cleared up according to Nordin's schedule. In cases of absorptive hypercalciuria, an ion exchanger operating in the intestine, sodium cellulose phosphate (SCP), is applied under strict control of oxalate, calcium and magnesium excretion as well as ionized calcium in serum. Under treatment with SCP (27 patients), we found a reduction in the renal excretion of calcium and magnesium, and, as a side effect, a significant augmentation of the renal oxalate excretion. In cases of resorptive or resorptive/absorptive hypercalciuria, except in patients with primary HPT, 23 patients were mediated by thiazides (Esidrix). This drug effects a marked decrease of urinary calcium based on a higher rate of reabsorption of calcium in the distal tubule. No severe side effects especially primary HPT were observed.
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PMID:Resorptive and absorptive hypercalciuria. Therapy with sodium cellulose phosphate or thiazides. 42 8

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

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

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

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

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

Concentration and excretion in 24-hour urine, as well as serum concentrations of Na, K, Mg, Ca, Cl, P, uric acid and citrate were investigated in 209 calcium oxalate stone patients and 42 stone-free patients. Especially the concentration values of the urine components, except for uric acid and citrate, were found to be significantly lower for calcium oxalate stone patients. 21% of the stone patients showed hypercalciuria; hypercalciuria combined with hyperuricuria was found in only 7.1% of the cases and a solitary hyperuricuria in only 17%. As for kidney cortex, kidney papilla and muscle tissue in 10 calcium oxalate stone patients and 10 stone-free patients, the concentrations of Na, K, Ca, Mg as well as some trace elements were determined quantitatively by means of neutron activation analysis. Statistic analysis yielded a significantly lower sodium content of the kidney cortex within the stone-carrying group. Mean values of the calcium concentration in stone patients were lower for papilla and muscle tissue than in the control group. For magnesium no clear differences were found. The iron content in the papilla and muslce tissue of stone patients was significantly lower.
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PMID:Quantitative element investigations in urine, serum, kidney and muscle tissue of calcium oxalate stone patients. 65 76


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