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

Dual-energy x-ray absorptiometry and single-photon absorptiometry were used to determine bone density at the lumbar spine and radial shaft in 62 patients with absorptive hypercalciuria, 27 patients with fasting hypercalciuria, and 31 nonhypercalciuric stone formers. Lumbar bone density was significantly lower in patients with absorptive (-10%) as well as in those with fasting hypercalciuria (-12%), with 74 and 92% of patients displaying values below the normal mean, whereas only 48% of the nonhypercalciuric stone formers had bone density values below the normal mean. In contrast, radial bone density was similar in all three groups of renal stone formers investigated. The comparison of urinary chemistry in patients with absorptive hypercalciuria and low normal bone density compared to those with high normal bone density showed a significantly increased 24 h urinary calcium excretion on random diet and a trend toward a higher 24 h urinary uric acid excretion and a higher body mass index in patients with low normal bone density. Moreover, among the patients with absorptive hypercalciuria we found a statistically significant correlation between the spinal bone density and the 24 h sodium and sulfate excretion and the urinary pH. These results gave evidence for an additional role of environmental factors (sodium and animal proteins) in the pathogenesis of bone loss in absorptive hypercalciuria. In conclusion, our data suggest an osteopenia of trabecular-rich bone tissues in patients with fasting and absorptive hypercalciurias.
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PMID:Reduced vertebral bone density in hypercalciuric nephrolithiasis. 148 24

With 2 groups of 10 patients the influence of an additional therapy with 1 g magnesium sulfate/h during i.v. tocolysis with the betamimetic fenoterol (2 micrograms/min) upon parameters of water and electrolyte balance has been investigated. The whole of the magnesium administered during the 24 hours investigational period has been eliminated via the kidneys. Most probably due to a competition within the distal tubulus hypermagnesemia was associated with hypocalcemia and hypercalciuria, followed by a rise in parathyroid hormone. As PTH is able to compensate hypocalcemia not only by means of bone mobilisation but also by an increase in enteral Ca absorption, estimated losses of calcium are minimal. These may be neglected, as additional therapy with magnesium sulfate--besides the advantages yet known (cardioprotection, saving of betamimetic dosage, reduction of drug tolerance development)--reduces betamimetic induced water retention, thus significantly diminishing lung edema hazard during tocolytic therapy.
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PMID:[Effect of co-medication with magnesium sulfate in beta-mimetic tocolysis on parameters of water-electrolyte balance]. 231 70

To elucidate the pathophysiology of mixed stone formation in cystinuria, 27 patients with documented cystine nephrolithiasis underwent an inpatient evaluation under a constant dietary regimen. All patients had homozygous cystinuria, since the daily urinary cystine excretion exceeded 250 mg. per gm. creatinine. Hypercalciuria was noted in 5 patients (18.5 per cent), 4 of whom had fasting hypercalciuria. Hyperuricosuria was found in 6 patients (22.2 per cent) and it was not caused by a consumption of a diet rich in animal proteins, since urinary pH was higher and urinary sulfate lower than in control subjects. Serum uric acid was slightly lower and uric acid clearance was higher in hyperuricosuric patients than in control subjects. Hypocitraturia was found in 12 patients (44.4 per cent) and it was associated with defective renal acidification in 4 of 5 patients in whom it was tested. Thus, hypercalciuria, hyperuricosuria and hypocitraturia frequently accompany cystinuria in patients with cystine nephrolithiasis. These conditions might be renal in origin, rather than a result of dietary or environmental aberrations. They may contribute to the formation of calcium and uric acid stones, which sometimes complicate cystine nephrolithiasis.
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PMID:The spectrum of metabolic abnormalities in patients with cystine nephrolithiasis. 292 71

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

The possibility that hypercalciuria could cause calcium stone formation through a mechanism other than by increasing urinary saturation of stone-forming calcium salts was explored. The effect of increasing calcium concentration on the inhibitor activity against the spontaneous precipitation of calcium oxalate was examined in whole urine (in the presence of naturally occurring inhibitors) and in synthetic media (with added inhibitors). In 11 patients with calcium nephrolithiasis, the induced hypercalciuria from calcium supplementation (600 mg/day) caused a significant fall in the urinary inhibitory activity against calcium oxalate precipitation, as shown by a decline in the formation product ratio from 12.6 +/- 1.1 SEM to 9.6 +/- 1.4 (P less than 0.005). In order to more fully explore this observation, the effect of increasing calcium concentration on the inhibitory activities of citrate (2 mM), chondroitin sulfate (0.05 mg/liter) and a heterogeneous group of naturally-occurring urinary inhibitors (1.0 mg/liter) against calcium oxalate precipitation was examined in vitro in synthetic solutions. The inhibitory actions of both citrate and chondroitin sulfate were significantly attenuated by increasing calcium concentration from 0.25 mM to 6.0 mM (P less than 0.01). However, raising the calcium concentration in synthetic media containing a mixture of partially purified urinary inhibitors produced a significant rise in the urinary inhibitory activity of this macromolecular mixture (P less than 0.01). We conclude that hypercalciuria can attenuate the inhibitory activities of citrate and chondroitin sulfate against calcium oxalate precipitation while at the same time accentuating the inhibitory activity of naturally-occurring urinary inhibitors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation by calcium of the inhibitor activity of naturally occurring urinary inhibitors. 313 70

Urinary glycosaminoglycans are thought to be macromolecular inhibitors of calcium stone formation. The 24-hour excretion of urinary glycosaminoglycans was measured quantitatively in 24 normal subjects and 206 patients with different etiologies of stone disease. In both groups a positive correlation was found between urinary glycosaminoglycans and total urinary volume and urinary sulfate. In normal subjects total urinary volume was r equals 0.716, p less than 0.001 and urinary sulfate was r equals 0.813, p less than 0.001, while in patients with stones these values were r equals 0.338, p less than 0.001 and r equals 0.326, p less than 0.001, respectively. The only significant difference in excretion of urinary glycosaminoglycans between the groups was found in the subgroup of patients with type I absorptive hypercalciuria. The type I absorptive hypercalciuria value of 33.4 +/- 14.9 mg. per day in patients with stones was significantly higher than the 25.8 +/- 8.3 mg. per day detected in normal subjects (p less than 0.05). Urinary glycosaminoglycan excretion in all other subgroups of nephrolithiasis as well as in a combined group of all patients with stones showed no significant difference when compared to that of normal subjects. Thus, no major quantitative relationship could be demonstrated between urinary glycosaminoglycan excretion and calcium stone formation in this study.
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PMID:Urinary glycosaminoglycans in normal subjects and patients with stones. 175 Aug 87

Dietary protein exerts a significant calciuretic effect. A twofold increase in protein at constant levels of calcium and phosphorus intakes causes a 50% increase in urinary calcium. The protein-induced hypercalciuria results primarily from decreased fractional renal tubular reabsorption of calcium associated with catabolism of excess sulfur amino acids and the resultant urinary excretion of acid and sulfate. A protein-induced elevation in glomerular filtration rate also contributes to the calciuresis. Dietary phosphorus also modifies the calciuretic effect of proteins, as it increases renal tubular reabsorption of calcium and thereby exerts a hypocalciuretic effect. Consequently, a soy-based diet was able to maintain calcium balance at a calcium intake of 457 mg/day in spite of a protein intake of 90 g, presumably due to the lower level of sulfur amino acids in the soy diet and to the 1450 mg phosphorus which accompanied the soy protein.
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PMID:Calcium utilization: effect of varying level and source of dietary protein. 341 94

From the analysis of various urinary constituents and the estimation of urinary saturation of stone-forming salts, it is now possible to identify risk factors responsible for or contributing to stone formation. Metabolic factors included calcium, oxalate, uric acid, citrate and pH. Environmental factors were total volume, sodium, sulfate, phosphate and magnesium. Physicochemical factors represented saturation of calcium oxalate, brushite, monosodium urate, struvite and uric acid. A scheme for graphic display of risk factors was developed to allow ready visual recognition of important risk factors presumed to cause stone formation. This graphic display had diagnostic use as well as practical value in following response to treatment. For example, a low urinary pH and high urinary concentration of undissociated uric acid could be discerned readily in cases of uric acid lithiasis, as were high urinary pH and exaggerated urinary supersaturation of struvite in cases of infection lithiasis. In a patient with absorptive hypercalciuria and hypocitraturia treatment with thiazide and potassium citrate could be shown to abolish high risks (hypercalciuria, hypocitraturia and relative supersaturation of calcium oxalate) displayed before treatment.
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PMID:Graphic display of urinary risk factors for renal stone formation. 405 68

Ingestion of protein is known to increase urinary calcium excretion. By studying the effect of intravenous amino acid infusion on calcium excretion, the variables of diets and intestinal absorption are avoided. Five patients on total parenteral nutrition with otherwise constant nutrient infusions containing 240 mg of calcium were randomized to two different levels of amino acid infusion. On 1 g/kg ideal body weight amino acid infusion, two patients excreted more than 240 mg of calcium in the urine, while on 2 g/kg ideal body weight amino acid infusion all five patients lost more calcium in urine than was infused. Mean urinary calcium excretion was increased from 287 to 455 mg/day. On the higher amino acid dose, mean glomerular filtration rate increased from 102 to 143 ml/min. There was no effect of amino acid dose on serum calcium, ionized calcium, parathyroid hormone, and 25 (OH) vitamin D. Calcium excretion corrected for the glomerular filtration rate was increased at the higher amino acid dose, indicating a decrease in renal calcium reabsorption. Daily urinary excretion of sulfate, ammonia, and titratable acidity were increased during the high amino acid infusion. Hypercalciuria induced by high levels of amino acid infusion during total parenteral nutrition may contribute to the development of metabolic bone disease.
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PMID:Amino acid-induced hypercalciuria in patients on total parenteral nutrition. 641 Aug 98

45Ca-labeled adult male rats were fed diets high in protein to determine long-term effects on calcium metabolism and bone status. Factors influencing renal excretion of calcium were examined for their involvement in protein-induced hypercalciuria. Control rats were fed a 6% casein diet. Test diets contained 6% casein plus 24% protein as lactalbumin, beef, casein, soy, egg white or gelatin. All diets were equal in Mg, P, and Ca. Collections made during the 20-week feeding regimen indicated a transient but marked calciuria (greater than or equal to 200% of control) occurring at or prior to days 56-59 by rats fed the lactalbumin, egg white, gelatin (P less than or equal to 0.001) and 30% casein (P less than or equal 0.01) diets. Soy and beef diets were not calciuric. At days 56-59, rats fed lactalbumin, 30% casein, soy and egg white exhibited significantly depressed urinary specific activity of calcium (P less than or equal to 0.001), and all rats fed test diets produced higher fecal endogenous calcium, suggesting an increased absorption. No compositional differences indicative of bone resorption were present in the femur or mandibles of any rat fed test protein, dismissing bone as the source of calciuria. End-products of protein metabolism known to chelate calcium or compete with its renal reabsorption were significantly correlated with urinary calcium; these included sulfate, oxalate and sodium.
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PMID:Effect of protein-induced calciuria on calcium metabolism and bone status in adult rats. 709 53


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