Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prophylactic treatment with alkaline citrate in patients with recurrent calcium oxalate (CaOx) stone disease results in reduced CaOx supersaturation and increased urinary citrate. The effects of a single evening dose were compared with those of two and three daily doses in six recurrent CaOx stone formers with hypercalciuria, hypocitraturia or raised calcium/citrate quotients. While on a standardized hospital diet the patients were given 7.5 g (28 mmol) of sodium potassium citrate (URALYT-U) in one, two, and three doses. Fractional urine collections during 24 hours were analyzed for pH, composition, and crystallization risk (CR). All dosage regimens had favourable effects on urinary calcium, citrate, calcium/citrate quotients, and CaOx-CR. The most sustained effect was recorded with three divided doses. Single evening doses resulted in the most pronounced effects between 22.00-06.00 h, thereby counteracting the increased risk of CaOx crystallization during that period. In terms of 24h urine composition the best effect was recorded with alkaline citrate administered three times daily, but because of the favourable response by a single evening dose between 22.00-06.00 h the assumption was made that this dosage regimen might be sufficient to reduce the risk of CaOx crystallization and stone formation. However, the validity of such an assumption can only be established by long-term clinical studies.
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PMID:Effects of different doses of alkaline citrate on urine composition and crystallization of calcium oxalate. 231 66

The case of a 7-year-old boy with the normotensive form of "chloride-shunt" syndrome is described. An unusual feature was the clinical presentation with lithiasis, caused by marked hypercalciuria of renal origin. The present studies were carried out to investigate the nature of the renal tubular defect. Indices for proximal and distal sodium chloride reabsorption were increased during hypotonic saline diuresis. Baseline sodium chloride excretion was low but increased above the range of control values after acute furosemide administration. Baseline potassium excretion was low, was not modified by the infusion of sodium chloride and increased significantly during infusions of sodium sulphate or sodium bicarbonate. Calcium excretion remained unchanged during sodium chloride, sodium sulphate or sodium bicarbonate infusions, but increased after furosemide administration. Nasal insufflation of 1-desamino-8-D-arginine-vasopressin induced both an increase in potassium excretion and a decrease in calcium and magnesium excretion. Plasma atrial natriuretic peptide was increased and was not significantly modified by infusion of hypertonic saline or acute administration of furosemide. These findings indicate that the primary renal abnormality appears to be an enhanced tubular reabsorption of sodium chloride, apparently present in the proximal tubule and the ascending loop of Henle. The associated presence of hypercalciuria also suggests a transport defect in the distal tubule. Decreased potassium excretion probably depends on a voltage-shunting defect in the cortical collecting tubule, which can be reversed by increasing the delivery of non-reabsorbable anions or by enhancing the conductance of the luminal membrane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:"Chloride-shunt" syndrome: an overlooked cause of renal hypercalciuria. 253 69

Farnolith (a dietary fibre preparation) was given to normal patients (n = 6) with absorptive hypercalciuria type I (n = 6) and to one patient with renal hypercalciuria. Farnolith binds calcium and reduces calcium absorption in the intestines. In normal subjects, the urine and serum parameters of calcium metabolism (total and ionized calcium, 1.25-dihydroxy-vitamin D) were unchanged. In absorptive hypercalciuria type I, a significant decrease in calcium excretion was achieved; oxalate excretion decreased as well. Low PTH values normalized; vitamin-D metabolites were not affected. In renal hypercalciuria, PTH and 1.25 DHCC were increased, whereas hypercalciuria persisted. Our investigations show that Farnolith is a reasonable treatment for absorptive hypercalciuria. Calcium homeostasis is rendered normal by Farnolith without producing secondary hyperoxaluria as sodium cellulose phosphate. Patients with primary renal calcium leakage and secondary hyperparathyroidism should not be treated with Farnolith.
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PMID:[Studies of calcium metabolism in normal persons and patients with hypercalciuria in relation to therapy with the dietary fiber preparation Farnolith]. 253 20

Various studies have shown that a high protein (HP) diet, compared to a low protein (LP) diet, leads to hypercalciuria and alterations in renal and systemic hemodynamics. The authors compared the effects of HP diet to those of normal protein diet (NP) to determine the possible mechanisms by which changes in systemic hemodynamics and hypercalciuria occurred. The studies were conducted in awake rats; the effects of dietary sodium content on the changes induced by HP also were evaluated. The relationship of prostaglandins (PG), renin (PRA), and aldosterone (PA) to changes in blood pressure (BP) was assessed. Two weeks after HP and normal sodium feeding (40%), glomerular filtration rate (GFR) and urine flow (V) were not different from the same values in a group on an NP diet (23%). When HP was fed with low sodium, there was a rise in V as a consequence of greater fluid intake. Although plasma calcium remained constant, the hypercalciuria correlated with high protein and sodium content. Alterations in 1,25(OH)2 vitamin D3 or PTH (cyclic AMP excretion) function did not explain the hypercalciuria induced by HP. This suggests that HP leads to inhibition of tubular calcium reabsorption by mechanism(s) yet to be elucidated. Although HP did not alter GFR, it led to an increase in BP, a fall in renal vascular resistance, and an increase in RPF, regardless of sodium intake. PRA and urine PGE2 excretion were significantly higher in the rats on HP diet, whereas PA remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal and systemic effects of short-term high protein feeding in normal rats. 254 89

Urinary uric acid excretion was assessed in 38 children to determine whether hyperuricuria was a risk factor in children with urolithiasis. Uric acid excretion (measured per deciliter glomerular filtration rate), and fractional excretion of uric acid were similar in 27 children with hypercalciuria and calcium oxalate urinary stones, in six children with idiopathic calcium oxalate urolithiasis, and in five with uric acid urolithiasis, of whom four were white boys and one was an Asian girl. One boy with a urate stone had cystinosis. Serum uric acid concentrations exceeded 6.0 mg/dl (360 mumol/L) in two children with hypercalciuria and in two patients with idiopathic calcium oxalate urolithiasis. None of the children with calcium urolithiasis had excessive urinary excretion of uric acid. In children with hypercalciuria, uric acid excretion did not change significantly when dietary sodium was increased from 1.0 to 5.0 gm/1.73 m2. We conclude that excessive urinary uric acid excretion is seldom an additional risk factor in children with calcium urolithiasis and that dietary sodium chloride does not have a strong influence on urinary excretion of uric acid in children with hypercalciuria.
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PMID:Uric acid excretion in children with urolithiasis. 258 28

This study was conducted to determine the effect of a high protein diet on calcium metabolism in rat. Wistar strain male rats (50 days old) were divided into 5 groups (day 0): control diet (18% casein); high protein diet (18% casein +20% lactalbumin); high protein and 0.1% sodium bicarbonate diet; high protein and 0.2% sodium bicarbonate diet; and high protein and 0.4% sodium bicarbonate diet. On days 0, 1, 3, 5, 7, 9, urine samples were collected and, at the same time, feces were collected from half of the animals in each group. Urinary titratable acidity (TA-HCO3-), ammonium ion (NH4+), and net acid excretion (NAE) were measured as an index of acid-base balance in rat body. Urinary volume was rapidly increased and the increase of urinary volume continued throughout the study in rats fed the high protein diet. Urinary excretions of calcium and phosphorus were increased after day 3 and day 1, respectively, in rats fed the high protein diet. The high protein diet depressed calcium absorption and elevated phosphorus absorption from the digestive tract in rats fed the high protein diet. The high protein diet decreased TA-HCO3-, which was closely correlated with the decrease of NAE. Sodium bicarbonate supplementation to the high protein diet had little effect on urinary calcium excretion and NAE. This study suggested that there was no relationship between metabolic acidosis and hypercalciuria in rats fed the high protein diet.
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PMID:Effects of high protein diet and sodium bicarbonate supplementation on calcium metabolism in rats. 263 82

We studied, by dietary recall, the calcium and magnesium intake in 1109 adolescents aged 14-18 years; from 128 we collected a 24-h urine sample to determine electrolyte excretion. Subjects with blood pressure greater than 90th percentile (211) did not consume less calcium or magnesium than those with blood pressure less than 50th (597). Urinary calcium excretion tended to be higher in the adolescents with the highest blood pressure, the difference being statistically significant in males. Urinary sodium excretion also tended to be higher in those adolescents with blood pressure above the 90th percentile than in those with blood pressure below the 50th percentile, the differences being statistically significant in females. A positive significant correlation was found between systolic blood pressure and both calcium and sodium excretion. Our results suggest that hypercalciuria is present in the early phase of hypertension and demonstrate that adolescents at high risk of developing hypertension consume the same amounts of calcium and magnesium as those with low blood pressure.
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PMID:Calcium intake, calcium excretion and blood pressure in adolescents in the upper decile of the distribution: the Torrejon study. 263 23

In normal individuals, 1,25-dihydroxyvitamin D (1,25-D) levels regulate calcium (Ca) absorption according to Ca intake; its synthesis is stimulated by low Ca intake, probably via increased parathyroid hormone (PTH) secretion, to increase Ca absorption, and suppressed during high intake to reduce Ca absorption. The body also adapts Ca absorption in response to renal Ca excretion, and phosphate absorption in response to phosphate intake. These adaptations may fail or be impaired in certain diseases. In disorders of overadaptation, the intestinal tract absorbs excessive amounts of Ca due to overproduction of 1,25-D, as in absorptive hypercalciuria, sarcoidosis, primary hyperparathyroidism, and tumoral calcinosis. Intestinal hyperabsorption and hypercalciuria may occur on both low- and high-Ca diets. Primary hyperparathyroidism and hypoparathyroidism are bihormonal, related to over- and underproduction, respectively, of both 1,25-D and PTH. Underadaptation disorders are typically related to low 1,25-D synthesis or resistance to this metabolite; examples include postmenopausal osteoporosis, chronic renal failure, and osteomalacia. Many of these adaptational disorders can be relieved or improved by manipulating Ca, phosphate, sodium, or protein intake or by administering exogenous 1,25-D. Overabsorption of Ca and other substances, such as oxalate, may be responsible for Ca nephrolithiasis. Hypocitraturia (which may be a complication of certain diseases or the result of unbalanced diet or excessive exercise), diets high in readily metabolizable sugars and purine-rich proteins (meat, poultry, and fish), and low fluid intake can all contribute to stone formation. Various regimens may reduce the risk of Ca nephrolithiasis.
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PMID:Calcium metabolism. 268 27

The mechanism of stone formation in the urinary tract is reviewed. Diet, urinary tract infection and metabolic disorders account for the different epidemiological patterns of stone formation. The diagnosis and management of renal tract calculi are discussed. Calcium stones are associated with hypercalciuria, urine acidification defects, the use of furosemide in premature babies, hypercalcaemia, hyperoxaluria, hyperuricosuria, an alkaline urine and hypocitraturia. Uric acid stones occur in acid urine, from increased purine synthesis with lympho- or myeloproliferative disorders or from several inborn errors of purine metabolism which can also cause xanthine or dihydroxyadenine stones. Cystinuria, inherited as an autosomal recessive disorder is best treated with a low sodium diet, a fluid intake exceeding 40 ml/kg per day maintaining urine pH between 7.5 and 8 and, if necessary, with oral penicillamine. Oxalate stones occur in relation to diet, bowel disease and primary inherited defects in oxalate metabolism. Urinary tract infection causing struvite and carbonate apatite formation is the commonest cause of stones in Europe.
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PMID:Urolithiasis in children: current medical management. 270 15

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


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