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

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

Idiopathic hypercalciuria is a common disorder whose inheritance suggests an enzyme abnormality in calcium transport. We measured calcium-magnesium-ATPase activity in erythrocytes from 38 patients (mean age [+/- SEM], 40 +/- 2.1 years) with idiopathic hypercalciuria (24-hour urinary calcium excretion greater than or equal to 0.1 mmol per kilogram of body weight) and a history of multiple calcium oxalate kidney stones. As compared with 41 healthy controls, the patients with hypercalciuria had increased erythrocyte-membrane calcium-magnesium-ATPase activity (64.2 +/- 2.19 vs. 51.6 +/- 1.91 nmol of ATP split per milligram per minute; P less than 0.01) and increased sodium-potassium pump activity (6866 +/- 233 vs. 6096 +/- 228 mumol of sodium per liter of red cells per hour; P less than 0.05). No significant difference between the two groups was found in erythrocyte sodium-potassium cotransport, sodium-lithium countertransport, or potassium content. In 66 patients with kidney stones (38 with hypercalciuria and 28 with normal calcium excretion), 24-hour urinary calcium excretion correlated with calcium-magnesium-ATPase activity (r = 0.46, P less than 0.001). Erythrocyte calcium-magnesium-ATPase activity remained unchanged in eight subjects studied after four months on a low-calcium diet. A study of 30 healthy families found significant correlations between mean values in parents and those in offspring for calcium-magnesium-ATPase (r = 0.68, P less than 0.001) and urinary calcium excretion (r = 0.45, P less than 0.02), with no significant correlations between parents with respect to these measures (r = 0.27 and r = 0.08, respectively). We conclude that abnormalities in erythrocyte calcium-magnesium-ATPase activity may represent an inherited defect in calcium transport related to the cause of idiopathic hypercalciuria.
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PMID:Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria. 297 Nov 39

The clinical and laboratory findings in 14 infants, 2 children and 42 adults with RTA-1 have been retrospectively analyzed and the patients classified as having the hereditary (14%), acquired (31%), or idiopathic (55%) form. In 7 of the 8 hereditary cases, RTA-1 appeared to be a complication of hereditary hypercalciuria. The majority of acquired cases (61%) were secondary to immune-mediated diseases. All of the 14 infants with RTA-1 were classified as idiopathic. All of the idiopathic cases in children and adults were associated with nephrolithiasis and/or nephrocalcinosis, 33% of which had a family history of nephrolithiasis. The 14 infants presented with failure to thrive. Seventy-seven percent of children and adults with RTA-1 had nephrolithiasis and/or nephrocalcinosis and usually presented with symptoms related to this problem. Adults without nephrolithiasis or nephrocalcinosis usually presented with electrolyte disturbances or acidosis. Hypokalemia, the most common electrolyte disturbance, was present in 28% of the entire series. Acidosis was present in all infants and in 70% of children and adults. Clinically apparent bone disease was observed in 3 infants, and in 1 adult with nephrolithiasis. Glomerular function was normal in infants and in the 2 children, but depressed in 40% of adults. Recurrent urinary tract infection was a contributing factor but was not the sole cause of renal failure. Surprisingly, kidney stone number, the number of surgical procedures, and the presence of nephrocalcinosis had no apparent effect on the development of renal failure. Glomerular filtration rate was significantly higher in patients with incomplete RTA-1, and serum total CO2 was significantly correlated with creatinine clearance and minimum urinary pH. Hypercalciuria was present in 32% of patients with nephrolithiasis and/or nephrocalcinosis, and urinary citrate excretion was low in all of 16 patients in whom it was measured. Hypocitraturia appeared to be due in most cases to potassium depletion and renal failure, but may have occurred as a primary defect in 1 patient with hereditary RTA. Urinary uric acid excretion was elevated in 23% of patients with stones in whom it was measured. The mean number of stone-forming events was 51 +/- 14. Although a weak correlation between urinary calcium excretion and stone number was observed, the cause for prodigious stone formation could not be explained. This series emphasizes the variable degree to which the common clinical manifestations of RTA-1 (metabolic acidosis, hypercalciuria, nephrolithiasis, nephrocalcinosis, and potassium depletion) are expressed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The syndrome of distal (type 1) renal tubular acidosis. Clinical and laboratory findings in 58 cases. 312 50

Growth from birth to the age of 19 years was studied in a patient with the neonatal form of Bartter syndrome. The initial modes of therapy (extra fluid, potassium supplements and triamterene) resulted in satisfactory but not optimal growth. Treatment with spironolactone together with potassium led to impressive catch-up growth. When the patient reached the age of 9 years, indomethacin therapy was started, which resulted in a second growth acceleration and was also accompanied by a significant reduction of both polyuria and hypercalciuria. Puberty developed normally, menarche occurred at 12 years 4 months and a normal adult height of 162 cm was reached at the age of 14 years. Treatment with prostaglandin synthetase inhibitors seems to be the best therapy for children with the neonatal form of Bartter syndrome.
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PMID:Growth from birth to adulthood in a patient with the neonatal form of Bartter syndrome. 315 13

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

We describe a patient who initially formed calcium-containing renal stones owing to gouty diathesis and hypocitraturia. On therapy with 300 mg. allopurinol and 60 mEq. potassium citrate daily serum uric acid decreased from 9.2 to 5.8 mg. per dl., urinary pH increased from less than 5.5 to 6.6 and urinary citrate increased from 223 to 1,005 mg. per day. Four months later while still on this medical regimen, the patient presented with hypercalcemia (13.4 mg. per dl.), high serum 1,25-dihydroxyvitamin D (65 pg. per ml.) and hypercalciuria (598 mg. per day), which subsequently were found to result from sarcoidosis. Prednisone therapy normalized the disturbances in calcium metabolism. During 33 months of combined treatment with 7.5 to 10 mg. prednisone a day, allopurinol and potassium citrate, the patient was free of stones and he had normal urinary calcium, pH and citrate. However, a calcium stone formed 1 month after discontinuation of prednisone therapy, although treatment with allopurinol and potassium citrate was continued. The patient had marked hypercalciuria of 447 to 465 mg. per day, despite normal urinary pH, citrate and uric acid. This case represents calcium stone formation in a patient with 2 separate etiologies for stone disease, that is gouty diathesis and sarcoidosis. Therapeutic regimens directed at the correction of both metabolic disturbances were required to control renal stone formation.
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PMID:Gouty diathesis and sarcoidosis in patient with recurrent calcium nephrolithiasis. 337 3

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

We describe our experience in 14 children with idiopathic hypercalciuria and hematuria who received a finite course of thiazide diuretics. Thiazides reduced urinary calcium excretion and resolved hematuria in all cases. Serum calcium concentration was not altered with treatment. Serum potassium concentration decreased, and total carbon dioxide content and uric acid concentrations increased in response to therapy but these changes did not necessitate discontinuation of treatment. Thiazides were discontinued electively after 16 +/- 15 months of treatment (range 3 to 40 months). Six children maintained normal urinary calcium excretion, while 8 displayed excessive calcium excretion for 16 +/- 4 months after treatment was stopped. Renal calculi were not detected in any patient during this interval but hematuria recurred in 4 children. These findings suggest that thiazides are safe and effective for resolving hypercalciuria and hematuria. Thiazides may be discontinued safely in some children, while others will require further treatment courses or prolonged continuous therapy.
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PMID:Thiazide diuretics for the treatment of children with idiopathic hypercalciuria and hematuria. 366 71

The long-term effects of potassium citrate therapy (usually 20 mEq. 3 times daily during 1 to 4.33 years) were examined in 89 patients with hypocitraturic calcium nephrolithiasis or uric acid lithiasis, with or without calcium nephrolithiasis. Hypocitraturia caused by renal tubular acidosis or chronic diarrheal syndrome was associated with other metabolic abnormalities, such as hypercalciuria or hyperuricosuria, or occurred alone. Potassium citrate therapy caused a sustained increase in urinary pH and potassium, and restored urinary citrate to normal levels. No substantial or significant changes occurred in urinary uric acid, oxalate, sodium or phosphorus levels, or total volume. Owing to these physiological changes, uric acid solubility increased, urinary saturation of calcium oxalate decreased and the propensity for spontaneous nucleation of calcium oxalate was reduced to normal. Therefore, the physicochemical environment of urine following treatment became less conducive to the crystallization of calcium oxalate or uric acid, since it stimulated that of normal subjects without stones. Commensurate with the aforementioned physiological and physicochemical changes the treatment produced clinical improvement, since individual stone formation decreased in 97.8 per cent of the patients, remission was obtained in 79.8 per cent and the need for surgical treatment of newly formed stones was eliminated. In patients with relapse after other treatment, such as thiazide, the addition of potassium citrate induced clinical improvement. Thus, our study provides physiological, physicochemical and clinical validation for the use of potassium citrate in the treatment of hypocitraturic calcium nephrolithiasis and uric acid lithiasis with or without calcium nephrolithiasis.
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PMID:Long-term treatment of calcium nephrolithiasis with potassium citrate. 389 44


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