Stinghen Andréa E M, Pecoits-Filho Roberto
Basic Pathology Department, Laboratory of Experimental Nephrology, Universidade Federal do Paraná, 80531-980 Curitiba, PR, Brazil.
Int J Hypertens. 2011;2011:232683. doi: 10.4061/2011/232683. Epub 2011 Aug 14.
Chronic kidney disease (CKD) is highly prevalent and a multiplier of cardiovascular disease (CVD) and cannot be completely explained by traditional Framinghan risk factors. Consequently, greater emphasis has been placed in nontraditional risk factors, such as inflammation, endothelial dysfunction, sympathetic overactivation, protein-energy wasting oxidative stress, vascular calcification, and volume overload. The accumulation of uremic toxins (and the involvement of genetic factors) is responsible for many of the clinical consequences of a condition known as uremia. In this brief paper, we discuss mechanisms involved in the vascular damage of CKD patients, aiming to point out that important factors beyond hypertension are largely responsible for endothelial activation and increased CVD risk, with potential impact on risk stratification and development of novel therapeutic options.
慢性肾脏病（CKD）非常普遍，是心血管疾病（CVD）的倍增因素，无法完全用传统的弗明汉姆风险因素来解释。因此，人们更加关注非传统风险因素，如炎症、内皮功能障碍、交感神经过度激活、蛋白质-能量消耗、氧化应激、血管钙化和容量超负荷。尿毒症毒素的蓄积（以及遗传因素的参与）是导致尿毒症这种疾病许多临床后果的原因。在这篇简短的论文中，我们讨论了CKD患者血管损伤的相关机制，旨在指出高血压以外的重要因素在很大程度上导致了内皮激活和CVD风险增加，这可能对风险分层和新治疗方案的开发产生影响。
