Liu M, Li X-C, Lu L, Cao Y, Sun R-R, Chen S, Zhang P-Y
Graduate School, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China.
Eur Rev Med Pharmacol Sci. 2014 Oct;18(19):2918-26.
Cardiovascular disease (CVD), the leading cause of death, is mostly precipitated by cardiometabolic risk and chronic kidney disease (CKD). CVD and kidney disease are closely interrelated and disease of one organ cause dysfunction of the other, ultimately leading to the failure of both organs. Patients with end-stage renal disease (ESRD) are at much higher risk of mortality due to CVD. Traditional CVD risk factors viz., hypertension, hyperlipidemia, and diabetes do not account for the high cardiovascular risk in CKD patients and also standard clinical interventions for managing CVD that are successful in the general population, are ineffective to lower the death rate in CKD patients. Nontraditional factors, related to disturbed mineral and vitamin D metabolism were able to provide some explanation in terms of vascular calcification, for the increased risk of CVD in CKD. Fibroblast Growth Factor 23, a bone-derived hormone that regulates vitamin D synthesis in renal proximal tubules and renal phosphate reabsorption, has been suggested to be the missing link between CKD and CVD. Acute Kidney Injury (AKI) is strongly related to the progress of CVD and its early diagnosis and treatment has significant positive effect on the outcomes of CVD in the affected patients. Besides this, non-dialysable protein-bound uraemic toxins such as indoxyl sulfate and p-cresyl sulfate, produced by colonic microbes from dietary amino acids, appear to cause renal dysfunction. Thus, therapeutic approaches targeting colonic microbiota, have led to new prospects in early intervention for CKD patients. Intervention targets for preventing CVD events in CKD patients ideally should include control of blood pressure and dyslipidemia, diabetes mellitus, lowering proteinuria, correction of anemia, management of mineral metabolism abnormalities and life style changes including smoking cessation, decreased consumption of salt, and achievement of normal body mass index. Use of β-blockers, renin-angiotensin blockers, diuretics, statins, and aspirin are helpful in the early stages of CKD. In this review, we will address the biological, pathological and clinical relationship between CVD and CKD and their therapeutic management.
心血管疾病（CVD）是主要的死亡原因，大多由心脏代谢风险和慢性肾脏病（CKD）引发。心血管疾病和肾脏疾病密切相关，一个器官的疾病会导致另一个器官功能障碍，最终导致两个器官都衰竭。终末期肾病（ESRD）患者因心血管疾病而死亡的风险要高得多。传统的心血管疾病风险因素，即高血压、高脂血症和糖尿病，并不能解释慢性肾脏病患者心血管疾病风险高的原因，而且在普通人群中成功管理心血管疾病的标准临床干预措施，在降低慢性肾脏病患者死亡率方面无效。与矿物质和维生素D代谢紊乱相关的非传统因素，在血管钙化方面能够对慢性肾脏病患者心血管疾病风险增加作出一些解释。成纤维细胞生长因子23是一种骨源性激素，可调节肾近端小管中的维生素D合成和肾脏磷酸盐重吸收，有人认为它是慢性肾脏病和心血管疾病之间缺失的环节。急性肾损伤（AKI）与心血管疾病的进展密切相关，其早期诊断和治疗对受影响患者的心血管疾病结局有显著的积极影响。除此之外，由结肠微生物从膳食氨基酸产生的不可透析的蛋白结合尿毒症毒素，如硫酸吲哚酚和对甲酚硫酸盐，似乎会导致肾功能障碍。因此，针对结肠微生物群的治疗方法，为慢性肾脏病患者的早期干预带来了新的前景。理想情况下，预防慢性肾脏病患者心血管疾病事件的干预靶点应包括控制血压和血脂异常、糖尿病、降低蛋白尿、纠正贫血、管理矿物质代谢异常以及改变生活方式，包括戒烟、减少盐的摄入和实现正常体重指数。使用β受体阻滞剂、肾素 - 血管紧张素阻滞剂、利尿剂、他汀类药物和阿司匹林在慢性肾脏病的早期阶段是有帮助的。在这篇综述中，我们将探讨心血管疾病和慢性肾脏病之间的生物学、病理学和临床关系及其治疗管理。
