Sodium Intake, ACE Inhibition, and Progression to ESRD
Sodium Intake, ACE Inhibition, and Progression to ESRD
复制标题
DOI：
10.1681/asn.2011040430
复制
发表时间：
2012-01-01
影响因子：
13.6
通讯作者：
Ruggenenti, Piero
中科院分区：
文献类型：
--
作者：
Vegter, Stefan;Perna, Annalisa;Ruggenenti, Piero
High sodium intake limits the antihypertensive and antiproteinuric effects of angiotensin-converting enzyme (ACE) inhibitors in patients with CKD; however, whether dietary sodium also associates with progression to ESRD is unknown. We conducted a post hoc analysis of the first and second Ramipril Efficacy in Nephropathy trials to evaluate the association of sodium intake with proteinuria and progression to ESRD among 500 CKD patients without diabetes who were treated with ramipril (5 mg/d) and monitored with serial 24-hour urinary sodium and creatinine measurements. Urinary sodium/creatinine excretion defined low (4.25 years, 92 individuals (18.4%) developed ESRD. Among those with low, medium, and high sodium intakes, the incidence of ESRD was 6.1 (95% confidence interval [95% Cl], 3.8-9.7), 7.9 (95% Cl, 6.1-10.2), and 18.2 (95% Cl, 11.3-29.3) per 100 patient-years, respectively (P14 g daily) seems to blunt the antiproteinuric effect of ACE inhibitor therapy and increase the risk for ESRD, independent of BP control.
