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

Magnesium absorption was studied in the normal human jejunum and ileum by in vivo intestinal perfusion, using test solutions containing from 0 to 20 mM Mg (as MgCl2). As luminal Mg concentration was increased, the rate of absorption in the jejunum rose progressively with a tendency towards saturation at the higher concentrations. The kinetics and rates of Mg absorption in the ileum were comparable to those in the jejunum, with the exception that at higher luminal concentrations the ileal absorptive process was fully saturated. Using test solutions containing various combinations of Ca and Mg, we found that Ca had little or no influence on Mg absorption, even through Mg depressed Ca absorption to a modest extent. Patients with end-stage renal disease, who had a reduced rate of Ca absorption (presumably due to deficiency of 1,25-dihydroxycholecalciferol) were found to have a severe depression of Mg absorption. On the other hand, patients with absorptive hypercalciuria and nephrolithiasis, who had an increased rate of Ca absorption, were found to absorb Mg normally. These results suggest that Mg absorption in the human is mediated by a transport process different from that which facilitates Ca absorption, and that normal Mg absorption may be dependent on vitamin D. Our results do not establish whether or not the normal intestine can absorb Mg against an electrochemical gradient.
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PMID:Magnesium absorption in the human small intestine. Results in normal subjects, patients with chronic renal disease, and patients with absorptive hypercalciuria. 93 89

A young man, investigated because of tetanic convulsions and arthritic pains, was shown to have hypomagnesemia, hypermagnesuria, hypokalemia, hypercalciuria, progressive nephrocalcinosis and chondrocalcinosis. In this syndrome, renal function was normal except for the abnormal excretion of electrolytes. Renal sodium conservation was normal. Light and electron microscopic studies of renal biopsy specimens showed the presence of several abnormal tubules. Immunofluorescent staining showed deposits of immunoglobulins in the glomeruli and tubules. Magnesium therapy was started under balance study conditions and resulted in decreased calciuria and complete remission of subjective symptoms. The progression of nephrocalcinosis was halted, and there was some decrease in the intra-articular calcium deposits after two years of continuous oral magnesium therapy. The administration of spironolactone decreased urinary magnesium but did not normalize it, whereas triamterene administration was without effect in this respect. The results of the morphologic and electrolyte balance studies are discussed. The patient was found to exhibit several features which have not been described before in connection with hypomagnesemia of unknown origin.
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PMID:Hypomagnesemia due to renal disease of unknown etiology. 119 Feb 59

In a group of 327 normal children, aged 4 to 11, we measured Calcium (Ca) and Creatinine (Cr) in the second morning urine. In 226 of them, Magnesium (Mg) and Uric Acid (UA) were also calculated. Means and SD were respectively Ca/Cr: 0.11 +/- 0.09, Mg/Cr: 0.10 +/- 0.03, Mg/Ca: 1.56 +/- 1.48 and UA/Cr: 0.093 +/- 0.29. Distribution was not normal, so we used the 97.5 centile for the upper acceptable limit. This value was higher for Ca/Cr (0.37) and different for Mg/Cr (0.17), compared to the previous reports. Our values of Mg/Ca were related to age (p less than 0.01). These results suggest the need for local establishment of normal ranges and a better definition of hypercalciuria and hypermagnesiuria.
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PMID:[Urinary calcium, magnesium and uric acid in normal children]. 159 79

Adult cats with normal renal function were fed a nutritionally balanced, vitamin A-replete, experimental dry diet with or without ammonium chloride (NH4Cl) for 6 mo to study the effects of chronic dietary acidification on acid-base parameters and the metabolism of selected minerals. Dietary balance studies were performed monthly. Blood and urine samples were collected monthly to evaluate acid-base parameters, plasma parathyroid hormone (PTH) and 1.25-dihydroxycholecalciferol levels. Ammonium chloride-treated cats had significantly lower blood and urinary pH, and lower blood bicarbonate concentrations. Treated cats also had higher blood ionized calcium concentrations, hypercalciuria and lower intestinal calcium absorption relative to baseline (prior to feeding the experimental diet) and to control cats. This resulted in the development of lower calcium balance in the first several months. PTH levels were unaffected by dietary acidification; however, 1.25-dihydroxycholecalciferol levels were significantly decreased in treated cats. Treated cats had negative potassium balance during 5 mo of dietary acidification. Magnesium, sodium, and phosphorus balances were lower, but positive, in treated cats compared to control cats. Cats consuming the NH4Cl-supplemented diet had increased chloride balance. Thus, chronic dietary acidification with 1.5% NH4Cl produced chronic metabolic acidosis and lower or negative, calcium and potassium balance.
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PMID:The effect of chronic dietary acidification using ammonium chloride on acid-base and mineral metabolism in the adult cat. 274 72

Fifty-two cases of urinary tract calculus disease were investigated for dietary habits, routine chemical and microscopic urinalysis, bacterial culture, quantitative analysis of 24 h urine sample and qualitative analysis of the stones. 54 out of the 56 stones analysed were of mixed type. Magnesium ammonium phosphate was present in 78.2% stones. Dietary habits revealed principal dependence on cereals, lack of animal proteins, consumption of oxalate rich vegetables and widespread consumption of tea. Urinary tract infection was present in 63.7% of the cases. Significant calcium oxalate crystalluria (2+ to 4+) was present in 34.6% of the cases. Hyperoxaluria, hypercalciuria associated with hyperoxaluria-lower excretion of magnesium and citric acid were important urinary risk factors in the local population. These observations strongly suggest the multifactorial etiology of stone disease in this region. Imbalanced nutrition and urinary tract infection were the principal risk factors for urolithiasis in this study.
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PMID:The etiology of urolithiasis in Udaipur (western part of India). 372 15

To reduce urinary calcium excretion, 50 mg of hydrochlorothiazide per day was given to 35 patients with hypercalciuria. Urinary calcium decreased significantly after 4 weeks of drug administration, but urinary magnesium did not change. Magnesium calcium ratio increased significantly. Although serious side effects were not seen, serum potassium decreased and serum uric acid increased significantly. From these results thiazide seems to be a useful and safe medicine to reduce urinary calcium excretion. The dose and method of administration require further examination because the patients have to take the drug for a long time.
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PMID:[Treatment of hypercalciuria found in urolithiasis patients]. 399 93

The acute effects of intravenous infusions of phosphate and parathyroid hormone (PTH) upon the renal tubular handling of sodium, potassium, calcium, magnesium, and phosphate were examined in phosphate-depleted dogs using recollection micropuncture techniques. Hypercalciuria in phosphate depletion results from an impairment of calcium reabsorption between proximal and distal sampling sites, which can be partially corrected by the acute administration of PTH or by phosphate infusion. Magnesium reabsorption was normal in phosphate-depleted dogs but increased in parallel with calcium in the distal tubule following PTH and phosphate infusion. Phosphate was avidly reabsorbed in the phosphate-depleted dog so that excretion was very low even during the infusion of PTH or of neutral phosphate. Only with the infusion of both PTH and phosphate was a normal phosphaturic response observed.
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PMID:Renal tubular transport in phosphate depletion: a micropuncture study. 745 96

The aetiology of nephrolithiasis was investigated in 32 north Indian children (25 boys, 7 girls, mean age 7.9 +/- 3.3 years). An underlying disorder was detected in 16 (50%) patients and included idiopathic hypercalciuria (8 patients), hyperoxaluria (3 patients) and renal tubular acidosis, primary hyperparathyroidism and hyperuricosuria (1 patient each). Magnesium ammonium phosphate calculi were found in 2 patients with recurrent urinary tract infections, 1 of whom had a duplex pelvic collecting system. In 16 patients (50%) a cause for renal calculi was not identified. Our findings suggest that an underlying disorder is present in a large proportion of children with nephrolithiasis where appropriate treatment may be beneficial.
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PMID:Aetiology of nephrolithiasis in north Indian children. 757 12

The normal fractional urinary excretion of filtered magnesium is about 5%. In magnesium deficiency in man, the kidneys can normally reduce the 24-hour urinary magnesium excretion to less than 1 mmol (24 mg) via unknown mechanisms, and initially without a fall in plasma magnesium concentration. Renal magnesium wasting may be defined as a urinary excretion greater than 1 mmol/day in the presence of hypomagnesemia (plasma magnesium < 0.7 mmol/l). Congenital renal magnesium wasting occurs in several syndromes including Bartter's syndrome in which it is associated with hypercalciuria, and the defect may be in the thick ascending limb of Henle's loop, and Gitelman's syndrome in which there is hypocalciuria, and the defect may be in the distal convoluted tubule. Other causes of renal magnesium wasting include diabetes mellitus, hypercalcemia and diuretics. Magnesium wasting may also result from various toxicities including those of cis-platinum, in which the biochemical features resemble Gitelman's syndrome, and those of aminoglycosides, pentamidine and cyclosporin. Calcitriol deficiency may also contribute to renal magnesium wasting in some circumstances. Mild hypermagnesemia may occur in familial hypocalciuric hypercalcemia and may reflect abnormal sensitivity of the loop of Henle to calcium and magnesium ions. By contrast, the hypermagnesemia that occurs in chronic renal failure results from the reduced glomerular filtration of magnesium.
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PMID:Abnormal renal magnesium handling. 826 9

Population based data on urinary excretion of various metabolites of pathological importance, Calcium, Magnesium, Sodium, Potassium, Oxalates, Citrates, Phosphates, Uric acid and urea have been collected from around three hundred children of the Quetta valley. The body weight was in the range of 11-50 kg and the age was in between 4-16 years. The urine excretion average was 987.5 +/- 452.5 ml per 24 hours. There was 11.5% incidence of hypercalciuria, 8.5% incidence of hyperuricosuria, 2.0% hyperphosphaturia, 2.5% hypomagnesuria, 3.5% hypocitraturia, 6.5% hypernatriuria, 43.5% hypokaliurea and 2.1% hyperoxaluria. Urea excretion average was 23.11 +/- 14.99 g per 24 hours. The study provided the basis for childhood reference pattern in urinary excretion of compounds related to various pathological conditions, in particular stone formation in this region.
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PMID:Population based data on urinary excretion of various metabolites in children of north western region of Pakistan. 1006 40


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