Flack John M, Peters Rosalind, Shafi Tariq, Alrefai Hisham, Nasser Samar A, Crook Errol
Department of Internal Medicine, College of Nursing, Divisions of General Internal Medicine, Wayne State University, Detroit, Michigan, USA.
J Am Soc Nephrol. 2003 Jul;14(7 Suppl 2):S92-8. doi: 10.1097/01.asn.0000070142.14843.8e.
Hypertension is a nutritional-hygienic disease. Long-term caloric intake in excess of energy expenditures, chronic supraphysiological intake of dietary sodium, excessive alcohol consumption, and psychosocial stressors all contribute to the development of hypertension throughout the world. Elevated BP, particularly systolic BP, has been linked to multiple adverse clinical outcomes including stroke, heart failure, myocardial infarction, renal insufficiency/failure, peripheral vascular disease, retinopathy, dementia, and premature mortality. These undesirable clinical outcomes are typically, although not invariably, preceded by pressure-related target-organ injury such as left ventricular hypertrophy, renal insufficiency and proteinuria. The relation of BP and CKD and, in turn, the prevention of CKD or forestalling its progression by hypertension treatment, will be the focus of this manuscript. In hypertensive persons with reduced kidney function and/or proteinuria, lowering BP with multidrug therapy that is inclusive of pharmacologic modulators of the renin-angiotensin-aldosterone-kinin system is an effective strategy to forestall the progressive loss of kidney function. The totality of data support low therapeutic BP targets for persons with proteinuria >1 g/d. Nevertheless, in persons with CKD, even those with proteinuria below the dipstick positive level (approximately 300 mg/d or urine protein to creatinine ratio of 0.22), aggressive BP control also may be warranted because of the high risk of nonrenal cardiovascular disease. Multiple antihypertensive drugs will be required in the vast majority of patients with diabetes and/or reduced kidney function to attain BP goal. Renin-angiotensin system (RAS) modulator therapy is indicated among persons with diabetes mellitus and CKD. Available data support the use of angiotensin receptor blockers in persons with type 2 diabetes and overt nephropathy for preservation of kidney function. Among persons with type I diabetes with or without overt nephropathy, type 2 diabetes without overt nephropathy and in nondiabetic CKD, the available clinical data support the use of angiotensin-converting enzyme inhibitors as the RAS modulator of choice. Low therapeutic target BP levels <130/80 mmHg in persons with type 2 diabetes mellitus also appear warranted based on available data mostly for reducing the risk of nonrenal cardiovascular disease and overall mortality.
高血压是一种营养卫生疾病。长期热量摄入超过能量消耗、长期超生理量摄入膳食钠、过量饮酒以及社会心理压力源均在全球范围内促使高血压的发生。血压升高，尤其是收缩压升高，与多种不良临床结局相关，包括中风、心力衰竭、心肌梗死、肾功能不全/衰竭、外周血管疾病、视网膜病变、痴呆和过早死亡。这些不良临床结局通常（尽管并非总是如此）之前会出现与压力相关的靶器官损伤，如左心室肥厚、肾功能不全和蛋白尿。血压与慢性肾脏病的关系，以及通过高血压治疗预防慢性肾脏病或阻止其进展，将是本手稿的重点。在肾功能减退和/或有蛋白尿的高血压患者中，采用包括肾素 - 血管紧张素 - 醛固酮 - 激肽系统的药理调节剂在内的多药联合治疗降低血压，是阻止肾功能进行性丧失的有效策略。所有数据均支持蛋白尿>1 g/d的患者采用较低的治疗血压目标。然而，在慢性肾脏病患者中，即使是蛋白尿低于试纸阳性水平（约300 mg/d或尿蛋白与肌酐比值为0.22）的患者，由于非肾性心血管疾病风险高，积极控制血压也可能是必要的。绝大多数糖尿病和/或肾功能减退的患者需要多种降压药物才能达到血压目标。糖尿病和慢性肾脏病患者适用肾素 - 血管紧张素系统（RAS）调节剂治疗。现有数据支持2型糖尿病和显性肾病患者使用血管紧张素受体阻滞剂以保护肾功能。在1型糖尿病有或无显性肾病、2型糖尿病无显性肾病以及非糖尿病慢性肾脏病患者中，现有临床数据支持使用血管紧张素转换酶抑制剂作为首选的RAS调节剂。基于现有数据，2型糖尿病患者治疗目标血压水平<130/80 mmHg似乎也是必要的，主要是为了降低非肾性心血管疾病风险和总体死亡率。
