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

The effect of intravenous magnesium sulfate infusion on corrected serum calcium level and parathyroid function assessed by determination of nephrogenous cAMP (NcAMP) excretion were studied in normal human subjects. Significant hypermagnesemia induced by the magnesium sulfate infusion for 120 minutes was accompanied by a gradual and progressive decrease in the corrected serum calcium level. NcAMP excretion fell rapidly, reaching a nadir between 60 and 120 minutes after the infusion began, and after that rose above the baseline excretion. Urinary calcium excretion gradually increased, reaching a peak between 120 and 180 minutes after the infusion began and then gradually decreased. Since magnesium was given as the sulfate, it is not clear whether these changes were attributable to magnesium or sulfate or both. As a control study, we performed intravenous sodium sulfate infusion. The sodium sulfate infusion caused slight hypocalcemia, slight hypercalciuria, and a significant increase in NcAMP excretion. These findings indicate that the hypocalcemia and the hypercalciuria caused by the magnesium sulfate infusion is mainly due to the effect of magnesium, and that the decrease in NcAMP excretion during the infusion is due to the effect of magnesium alone. We conclude that the hypocalcemia caused by the magnesium sulfate infusion is mainly due to the renal calcium loss, and that the inhibition of parathyroid function caused by hypermagnesemia may be only partially involved in the early phase of this hypocalcemia.
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PMID:Effects of the intravenous administration of magnesium sulfate on corrected serum calcium level and nephrogenous cyclic AMP excretion in normal human subjects. 302 86

1,25-Dihydroxyvitamin D (1,25-(OH)2D) plays a crucial role in the maintenance of blood calcium and phosphorus levels and in normal skeletal mineralization. The concentration of this metabolite in the blood is, by necessity, tightly regulated. The most important stimuli for renal 1,25-(OH)2D synthesis include parathyroid hormone (PTH), its second messenger cyclic adenosine monophosphate (cAMP) and phosphate deprivation. Hypocalcemia and calcitonin, initially thought to act via stimulation of PTH release, have now been shown to directly stimulate 1-hydroxylation. Estrogens also increase 1,25-(OH)2D production, probably by upregulating renal PTH receptors. Inhibitors of the renal 25-(OH)D 1 alpha-hydroxylase include 1,25-(OH)2D itself, hypercalcemia, and phosphate loading. The PTH-vitamin D axis as modulated by the serum ionized calcium level controls adaptation to alterations in dietary calcium and sodium intake and to changes in skeletal turnover based on the level of physical activity. Although normally the renal production of 1,25-(OH)2D is tightly regulated and changes little in response to vitamin D challenge, there are certain conditions in which 1,25-(OH)2D appears to be substrate-dependent. These include hypoparathyroidism, hyperparathyroidism, vitamin D deficiency, sarcoidosis and the anephric state, conditions in which PTH is not well-modulated by alterations in serum ionized calcium or in which extrarenal synthesis of 1,25-(OH)2D occurs. In several disorders, including absorptive hypercalciuria, pseudohypoparathyroidism, hypophosphatemic rickets, and tumoral calcinosis, the regulation of the renal 1 alpha-hydroxylase appears to be altered.
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PMID:Normal and abnormal regulation of 1,25-(OH)2D synthesis. 306 16

This study was performed to assess whether treatment with prostaglandin synthesis inhibitors decreases calcium excretion in patients with idiopathic hypercalciuria. Nineteen hypercalciuric (12 with fasting hypercalciuria (FH), 7 with nonfasting hypercalciuria (NFH) and 8 control non-hypercalciuric stone formers were treated with sodium diclofenac, 50 mg t.i.d. for 2 weeks. After a washout phase, 7 FH patients received 200 mg/day of sulindac (a nonsteroidal antiinflammatory agent (NSAID) inactive on renal prostaglandin synthetase) for 14 more days. Diclofenac reduced urine calcium excretion in subjects with idiopathic hypercalciuria with either normal or elevated fasting urinary calcium (from 387 +/- 26 to 240 +/- 23 mg/day, P less than 0.001; and from 370 +/- 39 to 246 +/- 40 mg/day, P less than 0.05, respectively), whereas it was ineffective in normocalciuric stone formers. Similar antihypercalciuric effectiveness was exerted by sulindac in the seven FH patients. The antihypercalciuric action exerted by diclofenac in subjects with FH was associated with a significant increment in serum PTH (48 +/- 4 vs, 70 +/- 9 pmol/liter, P less than 0.05), whereas in NFH subjects, the antihypercalciuric effect of diclofenac on NFH was not associated with a change in parathyroid activity. Since the major effect of NSAIDs is to decrease prostaglandin synthesis, these data suggest that prostaglandins may play a pathogenetic role in idiopathic hypercalciuria. Furthermore, they suggest that PTH is suppressed in patients with FH, possibly due to stimulation of prostaglandin-mediated bone resorption process.
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PMID:Evidence for a prostaglandin-mediated bone resorptive mechanism in subjects with fasting hypercalciuria. 314 68

Abnormalities in renal tubular function have been reported in adult patients with idiopathic renal hypercalciuria. To determine if such abnormalities are present early in the natural history of renal hypercalciuria, we evaluated renal tubular function in ten children with idiopathic renal hypercalciuria, aged 5-17 years. Seven of the children presented with urolithiasis and three with hematuria. Urinary calcium excretion ranged from 4 to 9 mg/kg per day, (5.2 +/- 0.5, mean +/- SEM) with a mean fasting urinary calcium to creatinine ration of 0.31 +/- 0.03. Studies described in this report were performed after 1 week of ingesting a diet containing 1,000 mg calcium, 3,000 mg sodium, and 100 mg purine. Clearance of creatinine ranged from 84 to 159 ml/min per 1.73 m2. Tm phosphate (mg/100 ml GFR) was normal in each child (mean 4.66 +/- 0.06 mg/100 ml GFR). Fractional excretion of uric acid, sodium and beta-2-microglobulin were also normal in each child. Serum bicarbonate concentrations ranged from 21.5 to 27 mEq/l with a mean of 24.4 +/- 0.5 mEq/l and all patients lowered urinary pH to less than 5.5. Hypotonic diuresis demonstrated normal free water clearance with a mean of 12.8 ml/min per 100 ml Cin. Distal sodium delivery and fractional distal sodium reabsorption were normal with a mean of 13.6 +/- 1.2% and 92.7 +/- 0.5%, respectively. Water deprivation studies demonstrated a range of maximum urinary osmolality from 711 to 1,020 mosmol/kg H2O with a mean of 864 +/- 34 mosmol/kg H2O. Seven healthy children, ingesting an identical study diet, concentrated their urine to a mean of 1,059 +/- 31 mosmol/kg h2O.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal function in children with idiopathic hypercalciuria. 315 15

Cases of hypomagnesaemia of hereditary renal origin represent at least three different congenital disorders of tubular reabsorption of magnesium (Mg). Isolated familial hypomagnesaemia has been reported in a heterogeneous group of patients and an autosomal dominant pattern of inheritance has often been found to be present. Familial hypokalaemia-hypomagnesaemia, inherited as an autosomal recessive trait, has been reported in 17 patients and we now describe 3 additional cases. Hypomagnesaemia is accompanied by hypokalaemia, metabolic alkalosis, hypocalciuria and moderate sodium chloride wasting. Titration of renal Mg reabsorption indicates the presence of a low threshold but a normal Tm. The inherited defect is probably situated at the level of the distal convoluted tubule and mimics the therapeutic effect of thiazides. This condition is frequently confused with Bartter's syndrome. Familial hypomagnesaemia-hypercalciuria, also inherited as an autosomal recessive trait, has been reported in at least 15 patients and we now add 3 new cases. Hypomagnesaemia is always accompanied by hypercalciuria and nephrocalcinosis. Ocular abnormalities such as myopia and horizontal nystagmus are often present. Hypermagnesiuria is of a greater degree than that observed in the previous entity and reflects a low Tm of Mg reabsorption. The defect must be situated at the level of the ascending limb of the loop of Henle and affects the transport of both calcium and Mg but not of sodium and chloride. This condition has not been clearly separated from hereditary distal renal tubular acidosis in the literature.
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PMID:Hypomagnesaemia of hereditary renal origin. 315 19

1. Because urinary prostaglandin excretion could play a role in idiopathic hypercalciuria (IH), we studied the excretion of prostaglandin E (PGE), calcium and sodium at various urine flows in 21 patients (14 males) with urolithiasis and IH, seven stone formers (five males) with normal calciuria and 20 controls (11 males). Dietary composition was comparable and sodium intake was restricted to 100-120 mmol/day. 2. Analyses were performed on 30 min urine collections obtained after overnight water deprivation and during water diuresis. Male IH patients had increased levels of urinary PGE at all ranges of urine flow. PGE excretion correlated directly with urine flow in patients and controls, but the slope of this relationship in individual IH male patients was steeper than in controls (P less than 0.01). Calciuria correlated directly with urine output in patients with IH but not in controls. Calcium and sodium excretion were directly correlated (P less than 0.0001) in patients and controls. There were no significant differences between absorptive IH (seven patients) and renal IH (eight patients). There were no significant differences between stone formers with normocalciuria and control subjects. 3. The findings suggest that increased urinary PGE could play a role in the hypercalciuria syndrome, possibly by promoting natriuresis.
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PMID:Increased urinary excretion of prostaglandin E in patients with idiopathic hypercalciuria. 320 91

Among renal stone formers with idiopathic hypercalciuria, patients who remain hypercalciuric despite low calcium intake have often been regarded as having a primary renal leak of calcium, i.e. renal hypercalciuria. However, at any given intake of calcium, dietary factors other than calcium can generate hypercalciuria, e.g. high intakes of sodium, of animal protein or of carbohydrates, or obesity itself. Thus, the incidence of renal hypercalciuria among stone formers has probably been overestimated. To address this issue, the aforementioned dietary and/or metabolic factors have been evaluated in 51 stone formers with idiopathic hypercalciuria refractory (i.e. U-Ca. V greater than 250 mg/24 h) to 5 days on low calcium intake (max. 400 mg/day). In 15 patients (all had U-Na. V greater than 200 mmol/24 h), U-Ca.V was within the 95% confidence limits of a nomogram U-Ca.V versus U-Na.V, suggesting that their idiopathic hypercalciuria was related, at least in part, to the high sodium intake. 7 patients had severe hyperuricosuria (greater than 1 g/24 h) suggesting high animal protein intake. 20 patients were obese (greater than 120% ideal weight) with (7 cases) or without (13 cases) concomitant fasting hyperinsulinemia (greater than 18 microU/ml). In addition, a careful retrospective analysis of intravenous pyelograms disclosed medullary sponge kidneys in 8 cases which had remained undiagnosed so far; in one of them histological confirmation was obtained after surgical removal of a renal pole and a radiologico-histological comparison. Thus, only 14 out of 51 patients had an otherwise unexplained idiopathic hypercalciuria on low calcium intake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[So-called "renal" idiopathic hypercalciuria most often has a dietary origin]. 334 5

Effects of fixed cation-anion balance on acid-base status and calcium and phosphorus balances were examined. Pregnant and lactating goats were fed a diet of alfalfa hay, concentrate and minerals to vary the cation-anion balance [meq sodium (Na) + meq potassium (K)-meq chloride (Cl)]/100 g diet dry matter (DM) over the range found in ruminant feeds. Small but significant effects on ruminal pH, fermentation and dilution rate were observed. Metabolic acid-base status of pregnant and lactating goats was normal when (Na + K - Cl) balance was 40 to 50 meq/100 g DM. The other treatments drastically altered plasma electrolyte concentrations, causing metabolic acid-base disturbances and profound changes in calcium and phosphorus metabolism. Subclinical hypernatremic, hypochloremic metabolic alkalosis was induced by a dietary fixed cation excess (Na + K - Cl) of greater than 85 meq/100 g DM (typical of buffered, alfalfa diets) and caused hypocalciuria, diminished calcium and phosphorus absorption, and possibly diminished dietary calcium absorption and resorption of calcium from bone. Subclinical hyperchloremic, hyponatremic metabolic acidosis from a diminished dietary fixed cation-anion balance (Na + K - Cl) of less than 10 meq/100 g DM (typical of nonbuffered corn silage or grain diets) caused hypercalciuria, enhanced calcium and phosphorus absorption and apparently enhanced calcium resorption from bone. Apparent effects on absorption and resorption depended on calcium and phosphorus intakes. Alterations in goats performance were not demonstrable. Dietary excesses of fixed cations over anions (meq Na + K - Cl/100 g diet DM greater than 50) cause metabolic alkalosis in ruminants, whereas fixed anion excesses (meq Na + K - Cl/100 g diet DM less than 40) cause metabolic acidosis. Content of electrolytes in diets should be reported in all nutrition trials with ruminants for assessment of metabolic acid-base status.
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PMID:Characterization of acid-base disturbances and effects on calcium and phosphorus balances of dietary fixed ions in pregnant or lactating does. 336 4

Effects of subclinical metabolic acid-base disturbances, caused by dietary fixed ion imbalances on kinetics of calcium (Ca) metabolism were examined in eucalcemic caprine does (period 1) and does during simulated lactational Ca loss (period 2). In both experiments, Ca balance data and serial blood, fecal and urine samples were collected after an iv injection of 45Ca. In period 2, lactational Ca loss was simulated by continuous infusion of ethylene glycol-bis (beta-amino ethyl ether)N,N,N'N'-tetraacetic acid (EGTA) to standardize the loss of Ca among goats. The data were fit to a four-compartment model of Ca metabolism. In period 1, fixed anion excess, [sodium + potassium - chloride] = -2 meq/100 g diet dry matter (ANEX) increased urinary Ca excretion relative to fixed cation excess, [sodium + potassium - chloride] = 71 meq/100 g diet dry matter (CATEX). Consequently, rates of Ca absorption and resorption were elevated in goats made acidotic by dietary fixed anion excess. During period 2 (EGTA infusion), urinary Ca loss was elevated to similar levels in goats fed ANEX and CATEX, but Ca absorption remained higher in goats fed ANEX. Consequently, size of the exchangeable Ca pool, accretion rate and balance across bone were higher in these goats. Fixed anion excesses (found in corn silage and grains) cause subclinical metabolic acidosis, which elevates rates of Ca absorption but does not affect size of the exchangeable Ca pool. Fixed cation excesses (associated with diets containing alfalfa and buffers) cause subclinical metabolic alkalosis, which diminishes Ca absorption and urinary Ca excretion. Acidosis-induced hypercalciuria is the metabolic cost of maintaining high prepartum Ca absorption rates and high flux of Ca through the exchangeable Ca pool that may aid in adjustment to sudden Ca losses at parturition.
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PMID:Effects of acid-base disturbances caused by differences in dietary fixed ion balance on kinetics of calcium metabolism in ruminants with high calcium demand. 336 5

The association of various diuretic therapies with the renal handling of minerals, important factors in the development of nephrocalcinosis and osteopenia, was studied in low birth weight infants. Twenty-four-hour urine specimens (n = 65) were collected from 30 patients who were treated with (1) furosemide with or without spironolactone and hydrochlorothiazide (2) spironolactone with hydrochlorothiazide, (3) spironolactone alone, or (4) no diuretic (control; i.e., after diuretic). Hypercalciuria (urinary calcium greater than or equal to 0.15 mmol/kg/day) was observed in all but the control group. Covariate analysis demonstrated a significant effect of sodium, calcium, and vitamin D intakes (p less than 0.01) and sodium excretion (p less than 0.05) on urinary calcium excretion. Treatment with any of these diuretics in neonates may be associated with abnormal renal losses of calcium, sodium, chloride, and potassium. From a nutritional perspective, neonates requiring long-term diuretic therapy thereby require special consideration, including monitoring of mineral excretion and renal ultrasonography.
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PMID:Mineral excretion in premature infants receiving various diuretic therapies. 341 1


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