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)

Our primary objective was to test the hypothesis that a defect in acidification is more common in patients who have idiopathic calcium phosphate kidney stones than in those whose stones are formed mainly of calcium oxalate. Additionally, other risk factors might differ for these 2 stone types. Urine pH was measured serially over 24 hours, and along with ammonium and titratable acid, it was measured before and serially after ingestion of ammonium chloride in 3 groups of subjects: 24 patients with predominantly calcium phosphate stones, 30 patients with calcium oxalate stones, and 15 health non-stone-formers. Twenty-six parameters potentially related to stone formation and acidification were assayed on urines collected over 24 hours, and 15 parameters on blood. The data base was a computerized list of 5900 analyses of stones from patients living in Newfoundland. Patients not known by their physician to have had urinary tract infection, anatomical abnormality, hyperparathyroidism, or renal tubular acidosis were asked to participate in the study. Differences between means were considered significant if p values were less than 0.05 for F by analysis of variance and also less than 0.01 by t-test. In all patients with calcium oxalate stones and all non-stone-formers, urine acidified to pH less than 5.25, but in 8 of the 23 phosphate stone formers who completed the ammonium chloride study urine failed to acidify to pH less than 5.25. As all 8 had normal values for venous pH, total CO2, and chloride, they were considered to have incomplete renal tubular acidosis (IRTA). The 8 phosphate stone formers with IRTA had greater mean values for urine pH on all 9 specimens collected serially over 24 hours (all means greater than 6.2), and after administration of ammonium chloride (p less than 0.01), as well as lower mean values for urine titratable acid excretion (p less than 0.01), both after administration of ammonium chloride and in 24-hour urine samples, compared with the remaining phosphate stone formers whose urine acidified and the oxalate and non-stone-forming control groups. Nearly all the phosphate stone formers had 1 or more risk factors for stone formation, but with frequencies not significantly higher than those found in the oxalate group. Hypercalciuria and hypocitruria were the commonest, but increased oxalate or urate also occurred. Thus, idiopathic calcium phosphate stone formation can be associated with 1 or more of several risk factors, and, with the possible exception of those with IRTA, treatment should be similar to that given to patients with calcium oxalate stones.
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PMID:Comparison of patients with idiopathic calcium phosphate and calcium oxalate stones. 195 78

It is currently believed that the two chronic acidemic disorders exert disparate effects on urinary calcium excretion: chronic metabolic acidosis induces consistent hypercalciuria, but no appreciable change or even a decrease in calcium excretion is reported to attend chronic respiratory acidosis. Whereas the effect of metabolic acidosis is well documented, little work has been carried out in chronic hypercapnia. In fact, most of the studies on chronic respiratory acidosis were short in duration, had employed only mild hypercapnia, or had failed to control carefully the prevailing metabolic conditions. We have carried out balance observations in nine dogs exposed to a 10% CO2 atmosphere in an environmental chamber for a period of two weeks. Chronic respiratory acidosis led to a significant increase in urinary calcium excretion from a mean control value of 0.4 +/- 0.1 mmol/day to 0.6 +/- 0.1 mmol/day during both week 1 and 2 of hypercapnia (P less than 0.05). Hypercalciuria occurred even though filtered load of calcium fell. Mean fractional excretion of calcium increased significantly during each week of hypercapnia averaging 0.60 +/- 0.12% during control, 1.05 +/- 0.13% during week 1, and 1.26 +/- 0.17% during week 2 of hypercapnic exposure (P less than 0.05). There were no changes in plasma levels of immunoreactive parathyroid hormone or 1,25-dihydroxyvitamin D3. These findings suggest that chronic respiratory acidosis, just like chronic metabolic acidosis, augments urinary calcium excretion by a direct depressive effect on the tubular reabsorption of calcium.
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PMID:Effect of chronic respiratory acidosis on urinary calcium excretion in the dog. 223 83

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

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

Chronic metabolic acidosis typically results in hypercalciuria and negative calcium balance. The impact of chronic respiratory acidosis on calcium metabolism has been less well studied. To address this issue, metabolic balance and static bone histomorphometric data were obtained during a 14-day exposure of rats to 10% CO2 (blood pH 7.33, PaCO2 83 mm Hg) and were compared with pair-fed controls. All rats were fed a 0.8% calcium diet. Urinary calcium excretion (mg/period, mean +/- SEM) was increased during both week 1 and week 2 (16 +/- 3 vs 9 +/- 1 and 16 +/- 2 vs 9 +/- 1, CO2 group vs controls, respectively [p < 0.05]). Net intestinal calcium absorption (intake minus fecal excretion) was increased throughout the period of hypercapnia (week 1, 213 +/- 19 mg vs 135 +/- 15 mg; week 2, 135 +/- 16 mg vs 43 +/- 14 mg; and cumulatively, 344 +/- 27 mg vs 178 +/- 20 mg, CO2 group vs controls [p < 0.01]). As a consequence of the marked increment in intestinal calcium absorption during hypercapnia, mean net calcium balance was more positive than that of controls throughout the study (week 1, 197 +/- 18 mg vs 126 +/- 15 mg; week 2, 120 +/- 15 mg vs 34 +/- 15 mg; and cumulatively, 317 +/- 25 mg vs 159 +/- 20 mg, CO2 group vs controls, respectively [p < 0.01]). There were no significant differences in calcium intake, plasma total calcium, immunoreactive parathyroid hormone, 25-hydroxyvitamin D, or creatinine clearance between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of chronic respiratory acidosis on calcium metabolism in the rat. 760 39

Distal renal tubular acidosis is frequently associated with hypercalciuria. To further investigate the cause-and-effect relationships between the two conditions, we examined 20 children (5 to 18 years of age) with idiopathic hypercalciuria for evidence of renal tubular acidosis. Serum electrolytes and urine citrate levels were normal in all subjects. After a single dose of furosemide, 1 of the 20 subjects did not show a decrease in urine pH < 5.5, which suggests an acidification defect in the cortical collecting duct. Three other patients failed to show an increase in urine-minus-blood partial pressure of carbon dioxide > 20 mmHg after urine alkalinization with orally administered acetazolamide, a finding compatible with a rate-dependent distal renal tubular acidosis. These four subjects underwent acute acid loading with arginine hydrochloride. In all four subjects urine pH decreased < 5.5 but urinary ammonium excretion failed to increase normally; this supports the diagnosis of a defect in distal acidification. Four of six patients with nephrolithiasis had evidence of distal renal tubular acidosis, in contrast to none of the 14 patients without stones (p = 0.003). We conclude that distal acidification abilities seem to be intact in children with hypercalciuria in the absence of nephrolithiasis. We speculate that calcium precipitation may lead to tubular damage, including distal renal tubular acidosis.
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PMID:Renal acidification in children with idiopathic hypercalciuria. 815 65

The relationship between bone mineral status and hypercalciuria is controversial. The effect on bone composition of different forms of hypercalciuria was studied in female rats made hypercalciuric by 7-week administration of oral furosemide (F, n=12), intraperitoneal 1,25-dihydroxy vitamin D (VD, n=11), or oral ammonium chloride (AC, n=12). Seven untreated rats served as controls (C). Hypercalciuria (mg/100 g per 24 h, mean +/-SEM) of F (4.3+/-0.2), VD (4.1+/-0.4), and AC (3.9+/-0.3) groups was of similar intensity (C rats 1.3+/-0.1, P<0.01). Weight and length gains and serum CO2, sodium, potassium, calcium, and phosphate were no different among the four groups. Bone was studied by dual-energy X-ray absorptiometry of left tibiae. AC rats had significantly less bone area (1.505+/-0.018 cm2) than VD and C (1.602+/-0.020 and 1.587+/-0.019 cm2). Bone mineral content was decreased in F (0.357+/-0.007 g) and AC (0.362+/-0.006 g) compared with VD (0.407+/-0.008 g) and C (0.389+/-0.009 g) groups. Bone mineral density was different between F (0.231+/-0.002 g/cm2) and VD and C rats (0.254+/-0.004 and 0.245+/-0.003 g/cm2), and also between AC (0.240+/-0.003 cm2) and VD rats. In these rat models, hypercalciuria of renal origin (F) and hypercalciuria caused by acid load (AC) adversely impaired bone mass.
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PMID:Influence of three different types of hypercalciuria on bone. An experimental study. 1041 59

Even small losses of gastrointestinal secretions when combined with reduced intake of electrolytes may seriously disturb electrolyte balance. Knowledge of the ionic composition of secretions lost is essential in planning therapy. Loss of gastric contents usually results in excessive loss of chloride; in achlorhydria this is not the case. Loss of sodium and potassium may be large in either case and is often underestimated. Small bowel obstruction results in a more balanced loss of electrolyte which may not affect acidbase balance greatly. In diarrhea loss of base predominates, and may result in a large potassium deficit. Steatorrhea due to nontropical sprue results in large fecal losses of sodium, potassium and chloride, in addition to the large calcium and phosphorus loss. In chronic peptic ulcer excessive ingestion of milk and absorbable alkalies may result in hypercalcemia, azotemia and alkalosis, without hypercalciuria. Since renal function is usually adequate in the milder gastrointestinal disturbances, electrolyte and fluid replacement should be started early, and can be guided by generally available laboratory tests, the carbon dioxide combining power and serum chloride levels, provided the predominate ionic loss is known and potassium deficiency remedied. If this is done, development of serious fluid and electrolyte deficits can usually be prevented.
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PMID:Electrolyte balance in gastrointestinal disease. 1326 Sep 27