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Cast light on the elucidation of pathogenesis of AKI after AAA surgery. Recent data provide evidence bmjopen-2016-011824 that an altered ADAMTS13 activity and a tert-Butyl 4-(prop-2-yn-1-yloxy)piperidine-1-carboxylate subsequent shift in the multimeric pattern of VWF may contribute to thrombocytopenia and microcirculatory failure due to TMA, which results in organ dysfunction including AKI [8,9,31]. Several investigators postulated that ADAMTS13 deficiency was associated with AKI in patients with sepsis [7]. Martin et al. also demonstrated that 50 2-Chloro-5-aminomethylthiazole of patients with severe sepsis suffered from AKI in whom the median ADAMTS13 activity was 43.2 [26]. This value is similar to the result in the current study, whereas none of the patients was diagnosed as AKI based on AKIN criteria. Such discrepancy between sepsis and AAA patients might be attributed to the difference in severity and persistence of systemic inflammatory response. Thrombocytopenia due to abnormal platelet aggregation is usually recognized in patients with high VWF/ADAMTS13 ratio. We found a trend of decrease in platelet count with higher VWF/ADAMTS13 ratio in the current study although it was not significant. Because bleeding during the surgery also decreases platelet count, it might be difficult to prove statistically significant correlation between VWF/ADAMTS13 ratio and platelet count in patients undergoing major aortic surgery. Furthermore, decrease in platelet count due to bleeding during the surgery might mask clinical manifestation or development of TMA in spite of high VWF/ADAMTS13 ratio. There are several limitations to interpret the data herein. First, this study enrolled 14 patients and only 10 patients were accepted for the statistical analysis. We could not exclude the contribution of this small sample size on the detection of AKI. We estimated the incidence of AKI after AAA surgery as 40 and calculated thesample size to show statistical significance as 24 cases when we made the study protocol. However, we had to cease the study after including 14 cases because the elective open AAA surgery was almost replaced by endovascular surgery in our institute. Second, we did not directly measure UL-VWF level which is the most important factor that induces abnormal platelet aggregation. An ideal method was to examine both VWF antigen level and distribution of VWF multimers using electrophoresis analysis to prove existence of UL-VWF as shown in previous studies [7,32]; however, electrophoresis analysis is not always feasible in clinical diagnosis PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/9282946 and therapeutic monitoring. VWF activity assays are also useful to evaluate contribution of VWF to platelet adhesion or PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/12113769 aggregation. Claus et al. investigated qualitative and quantitative variations of VWF and ADAMTS13 in patients with inflammation of varying severity, but they could not find a significant correlation between VWF activity and TMA or severity of organ dysfunction [8]. They concluded that VWF antigen/ADAMTS13 ratio could be a helpful parameter to identify patients with high risk of TMA or organ dysfunction due to systemic inflammation. Recent investigations also indicated that high VWF antigen level accompanied by decreased ADAMTS13 activity (high VWF antigen/ADAMTS13 ratio) could be a good parameter to evaluate prothrombotic properties or severity of diseases [15,33,34]. Third, the current study could not demonstrate the direct link between high VWF/ ADAMTS13 ratio and TMA in the kidney. We did not examine histological change in the kidney because it is too invasive in the clinical setting.