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Objective: We planned to examine the connection between serum uric acid (UA) values and prostatic calculi (PCal) presence and to evaluate the relation between PCal and other etiological factors. Methods: Patients between 20 and 60 years of age who were referred to the clinic with any reason and had non-contrast abdominal tomography (NCACT) for PCal were included in the study. While the patients were separated into 2 groups based on their serum UA level as ≥7 mg/dL (Group 1) and < 7 mg/dL (Group 2), NCACT was also divided into 2 groups as PCal presence (PCal+) and lack (PCal–) serum UA, calcium, phosphorus, sodium, prostate-specific antigen levels and urinary analysis results of the patients were evaluated and compared. Results: PCal were detected in 38 of 169 patients (22%). PCal presence was detected to be significantly high in Group 1 (p = 0.015). While Type A localization PCal were present both in Groups 1 and 2. Based on PCal presence, UA level was detected to be significantly high in PCal+ patients (p = 0.01). No significant difference was detected among the groups in biochemical parameters and urine-related parameters other than UA. Conclusion: A significant relation was found between high UA value and PCal in this study. These results may show that UA plays an active role in PCal etiology. [ABSTRACT FROM AUTHOR]

Objective: To investigate the relationship between urine pH and metabolic syndrome (MetS) and its components, while controlling for covariates.Subjects and Methods: This cross-sectional study was conducted on 5,430 Japanese subjects (4,691 without MetS; 739 with MetS) undergoing health assessments. Partial correlation analysis and analysis of covariance were used for controlling confounding parameters (age, gender, levels of serum uric acid and high-sensitivity C-reactive protein, estimated glomerular filtration rate, and smoking and drinking status). Using multiple logistic regression analyses, adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for MetS incidence were calculated across urine pH categories. Path analysis was used to determine the relationship between MetS and urine pH.Results: Subjects with MetS had significantly lower urine pH (5.9 ± 0.7) than those without MetS (6.0 ± 0.7) (p < 0.001). Partial correlation analysis showed that systolic and diastolic blood pressure, and triglyceride and fasting plasma glucose levels were negatively correlated with urine pH, while high-density lipoprotein cholesterol was positively correlated with urine pH. Analysis of covariance indicated that urine pH decreased with an increasing number of metabolic abnormalities. Adjusted ORs (95% CI) for the presence of MetS in subjects with urine pH 5.5-6.0 and pH <5.5 were 1.34 (1.04-1.73) and 1.52 (1.09-2.13), respectively (reference: subjects with a urine pH >6.0).Conclusion: The MetS and its components were independently associated with lower urine pH. [ABSTRACT FROM AUTHOR]

Background: To determine association between urine pH and OAB symptoms and to determine if urinary alkalization improves overactive bladder (OAB) symptoms. Methods: 659 patients with OAB were enrolled in this study between June 2012 and May 2014. 329 patients (group 1) were included in the final analysis. 201 adults were used as a control group (group 2). 24-hour urinary pH and the validated Turkish version of the OAB-V8 questionnaire were performed in patients. A 24-hour urine pH <6.2 was considered acidic urine. In the second part, a diet program was performed for 4 weeks in 30 participants. Urine pH values and OAB-V8 scoring results were recorded before the diet program and 2 and 4 weeks after the diet program. Results: Acidic urinary pH was determined in 61.4% of patients with OAB. There was a significant association between the presence of acidic urine and OAB. Also, the OAB-V8 scores of patients were significantly higher in patients with acidic urine than nonacidic urine. OAB-V8 scores of patients showed statistically significant improvement after diet therapy (17.87 ± 6.52 vs. 10.43 ± 7.17; p < 0.001). Conclusions: We found that acidic urinary pH was closely associated with OAB, and alkalization of urine improved lower urinary tract symptoms. We suggest that urinary pH should be considered as a parameter in treatment planning of patients with OAB. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Citrate is one of the most important inhibitors in urolithiasis. Hypocitraturia is a common risk factor in stone formers. Citrate excretion is regulated - amongst others - by acidosis and protein intake. A considerable number of stone formers, however, show hypocitraturia in the presence of normal urine pH levels. This is potentially due to defects in the renal tubular citrate carriers (NaDC 1 and 3) which may be genetically determined. Patients and Methods: 350 consecutive stone formers were examined. Exclusion criteria were urinary tract infection, hypokalemia, and steatorrhea. The following parameters were measured: serum: creatinine, calcium, potassium, and uric acid; urine: pH profiles, citrate, calcium, uric acid, ammonia, urea, and creatinine. Results: 83/350 patients were hypocitraturic (48 males, 35 females). 14/83 had low urine pH (≤6), 69/83 showed normal levels (>6). In the latter group there was a significantly higher recurrence rate (23 vs. 9%). The two groups were not different in serum parameters apart from uric acid. In urine, only pH and calcium (males) were significantly lower in the first group. Citrate did not correlate with urine pH and creatinine in the hypocitraturia-normal pH group, only with calcium in both sexes and urea and ammonia in females. In the hypocitraturia-low pH patients, there was no significant correlation between citrate and any other parameter tested. Conclusions: Hypocitraturia with normal urine pH is an entity indicating a high risk for recurrence. Since there was no correlation between citrate and pH, urea and ammonia, respectively, citrate excretion is not regulated in these patients as usual. There may be a link to calcium excretion. Potentially, these patients have defects in the renal tubular citrate carriers which may be genetically determined. Genetic examinations should be performed to elucidate a potential genetic disorder in hypocitraturia-normal pH stone formers. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Objective: The purpose of this clinical retrospective cohort study was to determine the most suitable ribavirin concentration on combination therapy of interferon (IFN)-ribavirin. Methods: Entry criteria were serum HCV-RNA level ≥100 KIU/ml, HCV-genotype 1b, chronic hepatitis, and initial combination treatment of IFN-α-2b (6 million units daily for 2 weeks and then 3 times weekly for 6 weeks) and ribavirin (600–800 mg/day) for 8 weeks without stopping or decreasing the dosage of IFN and/or ribavirin. Sixty-eight consecutive patients who satisfied the above criteria were given maintenance therapy for another 16 weeks. Results: A sustained virological response (SVR) rate of 25.0% (17/68) was seen in all subjects. The SVR rate was 44.0% (11/25) in the high ribavirin group with a serum ribavirin concentration of ≥3,000 ng/ml at 8 weeks after initiation of combination therapy. SVR was significantly dependent at a serum ribavirin level of ≥3,000 ng/ml (p = 0.005). The incidence of discontinuations and dose modifications for combination therapy in patients having a serum ribavirin concentration of ≥3,500 ng/ml 8 weeks after initiation of therapy was 57.1% (4/7). This value was statistically higher than that in patents with <3,500 ng/ml (p = 0.033). Conclusion: Our results showed that the most suitable serum ribavirin concentrations are from 3,000 to 3,500 ng/ml 8 weeks after initiation of combination therapy. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background/Aim: We recently reported that renal tubular acidosis (RTA) in Sjögren’s syndrome (SjS) is associated with high titers of an autoantibody against carbonic anhydrase (CA) II, an important enzyme in renal acid-base regulation. The purpose of this study was to determine whether a CA-II antibody could cause RTA in a mouse model of SjS. Methods: PL/J mice were immunized with human CA II to induce CA II antibody formation, whereas controls were injected with phosphate-buffered saline and adjuvant. After 6 weeks, anti-CA-II antibody titers were measured, then ammonium chloride was administered orally for 1 week to detect any acidification defect. Results: CA-II-immunized mice showed higher anti-CA-II antibody titers than control mice. Pathologically, lymphocytic and plasma cell infiltration was seen in the salivary glands and kidneys of CA-II-immunized mice, but not in controls. On acid loading, blood pH and urine pH decreased in both groups of mice, but the slope of urine pH versus blood pH was less steep in the CA-II-immunized mice, suggesting that these mice had an impaired ability to reduce their urine pH in the face of metabolic acidosis. Conclusion: CA-II-immunized mice had a urinary acidification defect, which may be similar to that seen in patients with SjS. Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]