Acute renal artery thrombosis after kidney transplantation

Early kidney transplant loss as a result of acute thrombosis of the renal artery remains a constant and devastating complication, with an incidence of 0.2-7.5%. While uncommon, arterial obstruction in the early postoperative period is a surgical emergency and must be ruled out if previously established diuresis ceases suddenly. Arterial thrombosis may occur as a result of injury to a diseased artery, problems with anastomoses, hypercoagulability or malpositioning of the allograft. In this study, we analyzed data on a group of 105 renal transplant recipients who presented with acute postoperative graft dysfunction between January 2006 and May 2012, to identify cases of acute renal artery thrombosis. We report on our experience of immediate re-transplantation following early kidney transplant thrombosis. Overall, two (1.9%) patients suffered early (within 48 hours of surgery) allograft renal artery thrombosis. In both patients, transplantation had not been complicated by atherosclerotic lesions or other thrombophilic states and postoperative diuresis had been successfully achieved, but diuresis ceased abruptly during the early postoperative period. Emergent duplex ultrasound scans were performed and acute renal artery thrombosis was detected in both patients. The patients were operated immediately and retransplantation procedures were conducted. We have reported our experience of immediate retransplantation following early primary graft dysfunction due to renal artery thrombosis. In conclusion, close monitoring of postoperative diuresis and, if necessary, immediate retransplantation in this situation can prove to be a successful treatment for preventing graft loss. © 2014, Sociedade Brasileira de Angiologia e Cirurgia Vascular. All rights reserved

Association of Pb, Cd, and Se Concentrations and Oxidative Damage-Related Markers in Different Grades of Prostate Carcinoma

Prostate cancer is known to be affected by the heavy metal levels and oxidative damage of the body, yet there are very few studies which look into the way it occurs. The aim of this study was to determine whether blood and tissue lead (Pb), cadmium (Cd), and selenium (Se) levels are associated with oxidative damage in the context of prostate cancer progression and development. Seventy-nine patients comprising 25 patients with benign prostatic hypertrophy (BPH), 23 patients with malignant prostatic carcinoma (malign Ca), 16 patients with low-grade prostatic intraepithelial neoplasia (LGPIN), and 15 patients with high-grade prostatic intraepithelial neoplasia (HGPIN) diagnosed on the basis of their clinical profile, transrectal ultrasonography, and histopathology were included in this study. Cd and Pb levels in whole blood were found to be increased in patients with HGPIN compared with the BPH group; also, the levels of Cd in whole blood and tissue were found to be increasing in patients with malign Ca, unlike BPH patients. Moreover, the levels of malondialdehyde (MDA) in plasma and tissue were significantly increased in malign Ca, LGPIN, and HGPIN than those in BPH. However, the levels of tissue Pb were found to be decreasing in BPH, unlike the malign Ca and HGPIN patients, and the levels of tissue protein carbonyls in malign Ca were significantly lower than those in HGPIN. The levels of tissue reduced glutathione (GSH) in malign Ca were significantly lower than those in BPH. Additionally, the levels of Se in serum and tissue in LGPIN were significantly lower than those in BPH. The serum Se levels in HGPIN were also significantly lower than those in BPH and malign Ca groups. Furthermore, the concentrations of serum Se in LGPIN were significantly lower than those in malign Ca. From the Pearson correlation analysis, there were significant positive correlations between tissue Cd and MDA levels in malign Ca, LGPIN, and HGPIN and between the tissue Pb and tissue MDA and protein carbonyl levels in malign Ca. Blood Pb and tissue Pb were also significantly positively correlated with plasma MDA and protein carbonyl levels in malign Ca. In addition, blood Pb was significantly positively correlated with tissue MDA and protein carbonyl levels in malign Ca, and a significant positive correlation was also found between blood Cd and plasma protein carbonyls and tissue MDA in LGPIN. We observed that altered prooxidant-antioxidant balance and heavy metal levels may lead to an increase in oxidative damage and may consequently play an important role in prostate carcinogenesis. These findings indicate that changes in the levels of Pb, Cd, Se, MDA, protein carbonyls, and GSH in the blood and/or tissue are related to the prostatic carcinoma development and progression, although triggering one of the mentioned changes is unknown; therefore, further study is required to determine the exact steps of the process and clarify the roles of different substances in order to obtain a more detailed explanation of the phenomenon