Increased 10-year cardiovascular disease and mortality risk scores in asymptomatic patients with calcium oxalate urolithiasis

Aydin, H. | Yencilek, F. | Erihan, I.B. | Okan, B. | Sarica, K.

Article | 2011 | Urological Research39 ( 6 ) , pp.451 - 458

Both the prevalence of cardiovascular risk factors and event rate are increased in patients with urolithiasis. Screening is recommended to all patients who have high cardiovascular risk. The aim of this study was to document 10-year risk of cardiovascular disease and mortality in asymptomatic patients with urolithiasis. Consecutive 200 patients with calcium oxalate urolithiasis were compared with 200 age- and sex-matched healthy controls. Ten-year cardiovascular disease risk was calculated with the Framingham Risk Score and mortality risk with SCORE risk score. Calcium, oxalate, and citrate excretion were studied as urinary stone ri . . .sk factors. The results indicate that patients with urolithiasis had higher total cholesterol (p < 0.0001), lower HDL-cholesterol (p < 0.0001), and higher systolic blood pressure (p < 0.0001) and hsCRP (p < 0.0001) compared with controls. Patients with urolithiasis had a higher Framingham Risk Scores [OR 8.36 (95% CI 3.81-18.65), p = 0.0001] and SCORE risk score [OR 3.02 (95% CI 1.30-7.02), p = 0.0006] compared with controls. The Framingham and SCORE risk score were significantly correlated with urinary calcium (p = 0.0001, r = 0.460, and p = 0.005, r = 0.223, respectively) and oxalate excretion (p = 0.0001, r = 0.516, p = 0.001, r = 0.290, respectively). In multiple linear regression analysis, urinary calcium and oxalate excretion, age, sex, total cholesterol, HDL-cholesterol, hsCRP and smoking were the independent predictors of 10-year cardiovascular disease risk and urinary calcium and oxalate excretion, age, sex, total cholesterol, fasting blood glucose for 10-year cardiovascular mortality. In conclusion, patients with calcium oxalate urolithiasis carry high risk of cardiovascular disease and mortality. All patients should be screened at the initial diagnosis of urolithiasis for the risk factors. © 2011 Springer-Verlag Daha fazlası Daha az

Hyperoxaluria-induced tubular ischemia: The effect of verapamil on the limitation of tissue HIF-1 alpha levels in renal parenchyma

Yencilek, F. | Sarica, K. | Eryildirim, B. | Erturhan, S. | Karakok, M. | Kuyumcuoglu, U.

Article | 2010 | International Urology and Nephrology42 ( 2 ) , pp.361 - 367

Objectives The effect of verapamil on tubular ischemia that is demonstrated by HIF-1a positivity in tubular cells following hyperoxaluria was evaluated in a rabbit model. Methods Thirty-six healthy male rabbits were randomly divided into three groups. Animals in the hyperoxaluric group were fed with 0.75% ethylene glycol. The verapamil group was fed identically to the hyperoxaluric group. Additionally, the verapamil group received verapamil orally (0.1 mg/kg). The control group received no special diet. Six animals in each group were killed on the 7th day of the experiment and the remaining six at the 28th day. Kidneys of the rabbit . . .s were examined by histopathologic and immunohistochemical analysis to detect the presence and degree of HIF-1a positivity. Results On the 7th day analysis, severe and moderate degree staining for HIF-1a in hyperoxaluric group were shown in four and two, respectively. In the verapamil group, however, three of six specimens showed nuclear staining (moderate in two and severe in one). Two of six specimens in the control group had minimal staining. The 28th day evaluation showed that two of the hyperoxaluric group had minimal degree nuclear staining but not in the remaining four. No staining was shown in the verapamil and control group animals. Conclusions Hyperoxaluria-related ischemia formation may be responsible for subsequent alterations in renal tubules. As a protective agent, verapamil was found to limit the presence of hypoxic changes as documented by HIF-1 alpha positivity in this study. These data also support the presence ischemic insult after hyperoxaluria induction in animal model. © Springer Science+Business Media, B.V. 2009 Daha fazlası Daha az

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