Relationship between supersaturation and calcium oxalate crystallization in normals and idiopathic calcium oxalate stone formers. (1/306)

BACKGROUND: In an earlier study on recurrent CaOx stone formers with no detectable abnormalities, we found that the urine of these subjects had a lower tolerance to oxalate load than controls and that the removal of urinary macromolecules with a molecular weight greater than 10,000 D improved their tolerance to oxalate. METHODS: The effects on CaOx crystallization of reduced urinary supersaturation of calcium oxalate (CaOx), induced by night water load, were studied in 12 normal males and in 15 male OxCa stone formers who were free from urinary metabolic abnormalities. The effect of the macromolecules, purified and retrieved from the natural and diluted urine, were analyzed in a metastable solution of CaOx. RESULTS: The water load caused an increase in urine volume (from 307 +/- 111 to 572 +/- 322 ml/8 hr, P = 0.014 in normal subjects, and from 266 +/- 92 to 518 +/- 208 ml/8 hr, P = 0.001 in the stone formers) and a concomitant reduction of the relative CaOx supersaturation (from 8.7 +/- 2.5 to 5.1 +/- 2.5 ml/8 hr, P = 0.001 in normal subjects, and from 10.4 +/- 3.5 to 5.0 +/- 2.7 ml/8 hr, P = 0.001 in the stone formers). The decrease in CaOx supersaturation was accompanied by an increase of the permissible increment in oxalate, both in normal subjects (from 43.8 +/- 10.1 to 67.2 +/- 30. 3 mg/liter, P = 0.018) and in the stone formers (from 25.7 +/- 9.4 to 43.7 +/- 17.1 mg/liter, P = 0.0001), without any significant variations of the upper limit of metastability for CaOx (from 21.6 +/- 5.3 to 20.5 +/- 4.2 mg/liter in normal subjects, and from 18.7 +/- 4.5 to 17.1 +/- 3.7 mg/liter in the stone formers). The inhibitory effect of urinary macromolecules with molecular weight greater than 10,000 Daltons did not undergo any change when the latter were recovered from concentrated or diluted urine, either in normal subjects or in the stone formers. CONCLUSIONS: Reduced CaOx supersaturation by means of water load has a protective effect with regards to CaOx crystallization in subjects who do not present any of the common urinary stone risk factors.  (+info)

Unusual case of foreign body-induced struvite urolithiasis in a dog. (2/306)

A 6-year-old, castrated male dog was presented because of inappropriate urination and hematuria. Radiographs indicated a bladder stone with a sewing needle at its center. The urolith was removed and diagnosed as predominantly struvite, most likely a result of the foreign body and a urinary tract infection.  (+info)

Calculus disease of the urinary tract at a district hospital. (3/306)

At a District General Hospital the organization of a clinic for the investigation and treatment of patients with calculus disease of the urinary tract is described. The way in which such a clinic may be orgainzed is discussed and the results presented. In patients with idiopathic hypercalciuria, sodium cellulose phosphate causes a significant reduction in urinary calcium levels when used in such a clinic.  (+info)

Urinary glycosaminoglycan excretion in urolithiasis. (4/306)

Urinary glycosaminoglycan (GAG) excretion was measured in children with idiopathic urolithiasis (15 girls and 10 boys; mean (SD) age 6.2 (2.4) years) and in healthy controls (10 girls and 14 boys; mean (SD) age 6.8 (3.8) years). GAG excretion was expressed as a GAG/creatinine (mg/g) ratio and was evaluated using dimethylmethylene blue. In healthy control children, the mean (SD) GAG/creatinine ratio was 31.67 (12.76) and it was similar in girls and boys. The children with idiopathic urolithiasis had significantly lower mean (SD) GAG/creatinine ratios than controls (22.59 (7.35)). Therefore, urinary GAG excretion may be important in the disease process in children with urolithiasis, as it is in adults.  (+info)

Inhibition of calcium oxalate crystal growth and aggregation by prothrombin and its fragments in vitro: relationship between protein structure and inhibitory activity. (5/306)

During blood coagulation, prothrombin (PT) is ultimately degraded to three fragments, thrombin, fragment 1 (F1) and fragment 2 (F2), which, collectively, contain all of the structural features of PT. One of these fragments, F1, is excreted in human urine and is the principal protein occluded into calcium oxalate (CaOx) crystals precipitated from it. This urinary form of F1, which we have named urinary prothrombin fragment 1 is present in calcium stones and is a potent inhibitor of CaOx crystallization in urine in vitro. The aim of this study was to determine whether PT itself and its other activation products, namely, thrombin, F1 and F2 also inhibit CaOx crystallization, by comparing their effects in a seeded, inorganic crystallization system. A secondary objective was to assess the relationship between the structures of the proteins and their inhibitory activities. PT was isolated from a human blood concentrate rich in vitamin K-dependent proteins. Following initial cleavage by thrombin, the resulting fragments, F1 and F2, were purified by a combination of reversed phase HPLC and low pressure column chromatography. The purity of the proteins was confirmed by SDS/PAGE and their individual effects on CaOx crystallization were determined at the same concentration (16.13 nM) in a seeded, metastable solution of CaOx using a Coulter Counter. [14C]Oxalate was used to assess deposition of CaOx and crystals were visualized using scanning electron microscopy. The Coulter Counter data revealed that the proteins reduced the size of precipitated crystals in the order F1 > PT > F2 > thrombin. These findings were confirmed by scanning electron microscopy which showed that the reduction in particle size resulted from a decrease in the degree of crystal aggregation. [14C]Oxalate analysis demonstrated that all proteins inhibited mineral deposition, in the order F1 (44%) > PT (27.4%) > thrombin (10.2%) > F2 (6.5%). It was concluded that the gamma-carboxyglutamic acid domain of PT and F1, which is absent from thrombin and F2, is the region of the molecules which determines their potent inhibitory effects. The superior potency of F1, in comparison with PT, probably results from the molecule's greater charge to mass ratio.  (+info)

National trend of the incidence of urolithiasis in Japan from 1965 to 1995. (6/306)

BACKGROUND: A nationwide survey of urolithiasis in Japan was made in order to evaluate the chronological trend of upper urinary tract stones in the Japanese. It succeeded previous studies done in 1955, 1966, 1979, and 1990. METHODS: All outpatient visits to urologists that resulted in a diagnosis of first-episode upper urinary tract stones in the years 1990 and 1995 were enumerated, irrespective of admission and treatment. The study enrolled all of the Japanese Board of Urology-approved hospitals, thereby covering nearly all urologists practicing in Japan. The annual incidence by sex and age was estimated and compared with the incidences in the previous nationwide surveys. RESULTS: The age-adjusted annual incidence of first-episode upper urinary tract stones in 1995 was estimated as 68.9 per 100,000 (100.1 in men and 55.4 in women), a steady increase from 54.2 in 1965. The annual incidence has increased in all age groups, except in those of the first three decades. The peak age for both sexes has shifted in toward the older population's direction. Estimations of longitudinal changes between 1965 and 1995 showed that the annual incidence has more than doubled for the cohort of the 1965 census population (from 43.7 in 1965 to 110.9 in 1995) and that younger generations have had progressively higher annual incidences. CONCLUSIONS: The annual incidence of upper urinary tract stones in Japan has increased steadily over the past 30 years and will continue to do so in the near future, but it still is lower than in the United States.  (+info)

The prothrombin gene is expressed in the rat kidney: Implications for urolithiasis research. (7/306)

There is considerable interest in determining the role of prothrombin fragments, especially urinary prothrombin fragment 1 (UPTF1), in the pathogenesis of calcium oxalate (CaOx) urinary calculi. This fragment is present in abundance in the matrix of CaOx crystals generated in human urine in vitro and has also been detected in human urinary stones containing calcium. More recently, prothrombin gene expression has been reported in the human kidney. However, studies examining the renal biosynthesis of prothrombin or perhaps only its fragments during experimental lithogenesis, and in consequence, the role of UPTF1 in stone formation, cannot be carried out in humans. The aim of this investigation therefore was to determine whether prothrombin gene expression is present in the rat kidney. Total RNA was isolated from the kidneys and livers of 12 rats. Using reverse transcriptase PCR, mRNAs corresponding to the thrombin and fragment 1 + 2 (F1+2) regions of prothrombin were analysed by agarose gel electrophoresis. The expression of glyceraldehyde 3-phosphate dehydrogenase was also examined to determine whether the quality of the tissue mRNAs was adequate for analyses. The amplified products were identified by sequence analysis. All kidneys displayed evidence of expression of the thrombin and F1+2 domains of the prothrombin gene. Furthermore, the sequences of these PCR-derived products from kidney were identical to those from liver. This suggests that the prothrombins secreted by these two organs are identical. The fact that prothrombin biosynthesis occurs in both the human and rat kidney presents an opportunity for using established rat models of stone disease to evaluate the influence of lithogenic conditions on prothrombin gene expression, and the potential role of UPTF1 in vivo.  (+info)

Study of urinary acidification in patients with idiopathic hypocitraturia. (8/306)

Hypocitraturia (HCit) is one of the most remarkable features of renal tubular acidosis, but an acidification defect is not seen in the majority of hypocitraturic patients, whose disease is denoted idiopathic hypocitraturia. In order to assess the integrity of urinary acidification mechanisms in hypocitraturic idiopathic calcium stone formers, we studied two groups of patients, hypocitraturic (HCit, N = 21, 39.5 +/- 11.5 years, 11 females and 10 males) and normocitraturic (NCit, N = 23, 40.2 +/- 11.7 years, 16 females and 7 males) subjects, during a short ammonium chloride loading test lasting 8 h. During the baseline period HCit patients showed significantly higher levels of titratable acid (TA). After the administration of ammonium chloride, mean urinary pH (3rd to 8th hour) and TA and ammonium excretion did not differ significantly between groups. Conversely, during the first hour mean urinary pH was lower and TA and ammonium excretion was higher in HCit. The enhanced TA excretion by HCit during the baseline period and during the first hour suggests that the phosphate buffer mechanism is activated. The earlier response in ammonium excretion by HCit further supports other evidence that acidification mechanisms react promptly. The present results suggest that in the course of lithiasic disease, hypocitraturia coexists with subtle changes in the excretion of hydrogen ions in basal situations.  (+info)