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

The authors studied the features of urolithiasis in three different geographical regions: Moscow, the Kirghiz SSR, and Berlin from the findings of examination of the composition and structure of uroliths removed by operation or passed spontaneously, (602 concrements from Moscow, 10,000 from Berlin, and 127 from Kirghizia). X-ray diffraction measurement, infrared spectrophotometry, and polarizing microscopy were conducted to analyze the composition and structure of the stones. Complex biochemical examination was carried out in patients from Moscow and Kirghizia. According to the results of the study, the following features of urolithiasis are common in the studied regions: (1) prevalence of oxalate lithiasis on the whole, which points to the principal role of metabolic factors in lithogenesis; (2) approximately similar amounts of apatite carbonate crystals in the uroliths; (3) certain similarity in composition of concrements from Berlin and Kirghizia. The most essential differences are: (1) the frequency of renal oxalate stones is highest in Berlin and lowest in Moscow. The prevalent types of calcium oxalate stones are: whewellite of concentric structure (linked with hyperuricemia) in Kirghizia; whewellite of small randomly orientated crystals (linked with hypercalciuria) and stones with signs of transformation of weddellite to whewellite in Moscow; (2) lesser distribution of phosphate lithiasis in Berlin than in Kirghizia and particularly in Moscow. Prevalence of struvite crystals in stones from Moscow, the formation of which is linked with the vital activity of Proteus and E. coli; (3) higher distribution of urate lithiasis in Moscow and particularly in Kirghizia where significant metabolic risk factors of lithogenesis were revealed.
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PMID:[The characteristics of the chemical composition and structure of urinary stones and their prevalence in the cities of Moscow, Berlin and of the Kirghiz SSR]. 214 36

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

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

Sixteen patients with medullary sponge kidney (MSK) and renal stones underwent evaluation of calcium metabolism and acid base balance. Six normal subjects and eight patients with non-MSK absorptive hypercalciuria served as control. Nine (56%) were hypercalciuric and seven (44%) were normocalciuric (N-MSK). Hypercalciuria was divided into absorptive (AH-MSK, n = 2) and renal leak hyerpcalciuria (RH-MSK, n = 7). The mean of minimal urine pH of RH-MSK group (5.28 +/- 0.09 (SE] was significantly higher than that of normal control (4.78 +/- 0.12) and of non-MSK AH (4.80 +/- 0.6) during acute acid challenge. The mean of the arterial blood HCO3 concentration of RH-MSK group was significantly lower than that of two control groups. The urine calcium and a frequency of stone passage were decreased significantly after alkali treatment in RH-MSK.
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PMID:Renal hypercalciuria and metabolic acidosis associated with medullary sponge kidney: effect of alkali therapy. 283 48

To investigate whether overall tubular dysfunction is encountered in a particular subgroup of patients with urolithiasis, the following parameters of renal tubular function have been measured in fasting morning urine in 124 male stone formers: excretion of lysozyme and gamma-glutamyl transpeptidase (gamma-GT), fractional excretion (FE) or glucose, insulin, bicarbonate after an alkali load, and theoretical phosphate threshold (TmP/GFR). The following have been diagnosed: primary hyperparathyroidism (n = 3), medullary sponge kidneys (n = 5), hyperuricemia (n = 8), cystinuria (n = 1), struvite nephrolithiasis (n = 2), idiopathic hypercalciuria of the absorptive (n = 16), dietary (n = 46) or renal (n = 5) type, and normocalciuric idiopathic urolithiasis (n = 38). Urinary excretion of lysozyme and of gamma-GT were elevated in 14% and 21% of patients respectively; FE glucose and FE insulin were elevated in 6% and 8% of patients respectively. In 62% of the patients TmP/GFR was below 0.95 mmol/l and in 52% of the patients FE HCO3 after alkali load was above normal. The findings show that a large number of stone formers have signs of renal tubular dysfunction; apparent renal leaks of phosphate and of bicarbonate are the most frequently encountered defects; while they are not specific for a given etiologic group of patients, they have been found in each group. The latter observation suggests that nephrolithiasis itself can damage renal tubular function.
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PMID:[Tubular dysfunction in renal lithiasis: cause or consequence?]. 285 24

To address whether a renal tubular dysfunction is encountered in a particular patient subgroup with urolithiasis, the following parameters of tubular function were measured in urine taken in the morning from 214 stone formers after fasting: pH, excretion of lysozyme and gamma-glutamyl transferase (gamma-GT); fractional excretion (FE) of glucose, insulin, Mg, K, and HCO3 after an alkali loading; and the renal threshold for phosphate (TmP/GFR). The following diagnoses were made in the patient group: primary hyperparathyroidism (N = 8), medullary sponge kidneys (N = 21), hyperuricemia (N = 10), cystinuria (N = 2), struvite stone disease (N = 6), idiopathic hypercalciuria of the absorptive (N = 25), dietary (N = 69) or renal (N = 7) type, and normocalciuric idiopathic urolithiasis (N = 66). In 31% of the patients TmP/GFR was below 0.80 mmole/liter and in 13% of the patients, FE HCO3 after alkali loading was above normal. Urinary excretion of lysozyme and that of gamma-GT both were elevated in 17% of the patients. FE glucose, FE insulin, FE Mg, and FE K were elevated in 8, 9, 3, and 7% of the patients, respectively. This study demonstrates that a significant number of stone formers present with signs of renal tubular dysfunction, primarily involving the proximal tubule since apparent leaks of phosphate and of bicarbonate were most frequently encountered. The defects were not specific for a given etiologic group of patients; on the other hand, occurrence was related to the presence of large stones in the pyelocaliceal system at the time data were gathered. Taken together these data suggest that the tubulopathy in nephrolithiasis is the consequence rather than the cause of the stone.
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PMID:Tubulopathy in nephrolithiasis: consequence rather than cause. 287 Dec 16

Studies in 24 recurrent oxalate stone-formers have shown that values for urinary calcium excretion for this group on at-home diets vary significantly (P less than 0.001) more than values for creatinine excretions. By placing stone-formers on controlled in-hospital diets and measuring their calcium excretions, we were able to predict probable outpatient hypercalciuria (greater than 7.5 mmol/day) with a sensitivity of 95% and a specificity of 95%. In this study, the renal loss of calcium during low-calcium diets was proportional to the absorptive hypercalciuria during high-calcium diets. Calcium loading experiments in fasted stone-formers and normal subjects indicated that citrate, at citrate:calcium molar ratios ranging from 0.12 to 1, stimulated urinary calcium excretion more than did calcium carbonate loading alone. In addition, citrate also significantly (P less than 0.05) increased the excretion of urinary oxalate by two normal subjects for a given load of calcium oxalate. Malabsorption of citrate and possibly other hydroxycarboxylic acids may thus predispose to oxalate nephrolithiasis by promoting calcium and oxalate absorption.
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PMID:Effect of citrate on the urinary excretion of calcium and oxalate: relevance to calcium oxalate nephrolithiasis. 291 May 76

Thiazides are considered to be effective in preventing recurrence of various types of nephrolithiasis, but the optimum dosage has not been established. To address this issue, 5 idiopathic stone formers with hypercalciuria on low Ca diet received chlorthalidone (CT) in 3 different oral doses and were randomly assigned either to the sequence 25-50-100 mg/day or the reverse (2 months per dose, monthly blood and urine measurements). The anticalciuric effect of CT was significant only at 50 and 100 mg/day, at the expense of a dose-dependent decrease in U-citrate excretion. We also observed a dose-dependent decrease in blood levels of K, increases in those of HCO3 and urate, as well as in U-pH, a tendency for blood levels of Mg and U-oxalate excretion to fall, and no change in U-urate excretion. Therefore, to derive the optimal CT dose the Tiselius' risk index was applied, which is based on the values of urinary [Ca], [oxalate], [Mg], [citrate] and volume. CT produced a decrement in risk index which was similar at each of the doses tested. Thus, raising CT doses beyond 25 mg/day does not hold out the prospect of improved prophylaxis. This agrees with Ettinger's preliminary data (Urol. Res., 1984) showing a similar protective effect of CT at 25 and 50 mg/day despite the absence of a significant anticalciuric effect at 25 mg/day.
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PMID:[Optimal dosage of chlorthalidone in the prevention of the recurrence of nephrolithiasis is 25 mg per day]. 396 48

The reported incidence of hypocitraturia among stone formers (SF) varies between 15 and 50%. It is not known whether this incidence depends on the subtype of SF. The recent simplification of the method of measurement of U-citrate (Boehringer-Mannheim kit) led us to address this issue in 118 male idiopathic (I) SF, with either idiopathic hypercalciuria of the renal (n = 6), absorptive (n = 19) or dietary (n = 41) type, or with normocalciuria (n = 52). Results were compared with those of 42 normal male volunteers. 9 patients had hypocitraturia (less than 215 mg/24 h), all of whom belonged to the group of normocalciuric ISF; only this group of patients had mean U-citrate X V significantly lower than controls (p = 0.025). The cause of hypocitraturia in these patients remains unknown: there were no significant correlations between U-citrate X V and U-pH or blood HCO3 or Cl. Moreover, the patients with hypocitraturia had neither urinary infection nor signs of distal tubular acidification dysfunction as assessed by fasting morning urinary pH. Extended to our whole population of ISF (250 patients) 75% of whom have idiopathic stone disease, it appears that measurement of U-citrate decreased the number of ISF without detectable disorder from 34 to 26, i.e. to 10% of the whole population of stone formers. Since hypocitraturia can easily be corrected by oral administration of citrate, routine measurement of U-citrate in normocalciuric ISF appears a promising method.
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PMID:[Indication of the urinary citrate levels in idiopathic renal calculosis]. 396 56

Antacid ingestion may lead to side-effects related to their chemical composition. Aluminum hydroxide may cause the phosphate depletion syndrome even during short-term administration of high doses in patients at high risk, such as alcoholics. Long-term intake may lead to bone demineralization and to osteomalacia. Fluoride complexing in the gut and prevention of fluoride absorption may be an additional factor. The clinical relevance of aluminum absorption in patients with normal renal function is not clear. In contrast, in patients with renal failure, aluminum hydroxide ingestion may contribute to an increasing hyperaluminemia. Hyperaluminemia and tissue deposition of aluminum in these patients may contribute to the dialysis-associated encephalopathy. Magnesium hydroxide causes an alkalinization of the urine due to magnesium absorption and urinary excretion. Thus, in renal insufficiency, a life-threatening hypermagnesemia may develop if magnesium-aluminum-containing antacids are prescribed. The milk-alkali syndrome, rarely observed nowadays, may be caused by calcium carbonate- and sodium bicarbonate-containing antacids. Hypercalciuria and alkaluria predispose to nephrolithiasis. The possibility that these disturbances in mineral metabolism will develop in patients with normal renal function is unlikely unless there is an abuse of these "over the counter" antacids.
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PMID:Antacid therapy--changes in mineral metabolism. 629 43


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