Jafar Tazeen H, Stark Paul C, Schmid Christopher H, Landa Marcia, Maschio Giuseppe, de Jong Paul E, de Zeeuw Dick, Shahinfar Shahnaz, Toto Robert, Levey Andrew S
Tufts-New England Medical Center, Boston, Massachusetts 02111, USA.
Ann Intern Med. 2003 Aug 19;139(4):244-52. doi: 10.7326/0003-4819-139-4-200308190-00006.
Angiotensin-converting enzyme (ACE) inhibitors reduce blood pressure and urine protein excretion and slow the progression of chronic kidney disease.
To determine the levels of blood pressure and urine protein excretion associated with the lowest risk for progression of chronic kidney disease during antihypertensive therapy with and without ACE inhibitors.
11 randomized, controlled trials comparing the efficacy of antihypertensive regimens with or without ACE inhibitors for patients with predominantly nondiabetic kidney disease.
MEDLINE database search for English-language studies published between 1977 and 1999.
Data on 1860 nondiabetic patients were pooled in a patient-level meta-analysis. Progression of kidney disease was defined as a doubling of baseline serum creatinine level or onset of kidney failure. Multivariable regression analysis was performed to assess the association of systolic and diastolic blood pressure and urine protein excretion with kidney disease progression at 22 610 patient visits.
Mean duration of follow-up was 2.2 years. Kidney disease progression was documented in 311 patients. Systolic blood pressure of 110 to 129 mm Hg and urine protein excretion less than 2.0 g/d were associated with the lowest risk for kidney disease progression. Angiotensin-converting enzyme inhibitors remained beneficial after adjustment for blood pressure and urine protein excretion (relative risk, 0.67 [95% CI, 0.53 to 0.84]). The increased risk for kidney progression at higher systolic blood pressure levels was greater in patients with urine protein excretion greater than 1.0 g/d (P < 0.006).
Although reverse causation cannot be excluded with certainty, a systolic blood pressure goal between 110 and 129 mm Hg may be beneficial in patients with urine protein excretion greater than 1.0 g/d. Systolic blood pressure less than 110 mm Hg may be associated with a higher risk for kidney disease progression.
血管紧张素转换酶（ACE）抑制剂可降低血压、减少尿蛋白排泄，并减缓慢性肾脏病的进展。
确定在使用或不使用ACE抑制剂进行抗高血压治疗期间，与慢性肾脏病进展风险最低相关的血压和尿蛋白排泄水平。
11项随机对照试验，比较了含或不含ACE抑制剂的抗高血压方案对主要为非糖尿病肾病患者的疗效。
检索MEDLINE数据库中1977年至1999年发表的英文研究。
在一项患者水平的荟萃分析中汇总了1860例非糖尿病患者的数据。将肾脏病进展定义为基线血清肌酐水平翻倍或出现肾衰竭。进行多变量回归分析，以评估在22610次患者就诊时收缩压和舒张压以及尿蛋白排泄与肾脏病进展之间的关联。
平均随访时间为2.2年。311例患者记录有肾脏病进展。收缩压110至129 mmHg且尿蛋白排泄小于2.0 g/d与肾脏病进展风险最低相关。在对血压和尿蛋白排泄进行校正后，血管紧张素转换酶抑制剂仍然有益（相对风险，0.67 [95% CI，0.53至0.84]）。尿蛋白排泄大于1.0 g/d的患者，收缩压水平较高时肾脏病进展风险增加更大（P < 0.006）。
虽然不能完全排除反向因果关系，但收缩压目标在110至129 mmHg之间可能对尿蛋白排泄大于1.0 g/d的患者有益。收缩压低于110 mmHg可能与肾脏病进展风险较高相关。
