Beddhu Srinivasan, Rocco Michael V, Toto Robert, Craven Timothy E, Greene Tom, Bhatt Udayan, Cheung Alfred K, Cohen Debbie, Freedman Barry I, Hawfield Amret T, Killeen Anthony A, Kimmel Paul L, Lash James, Papademetriou Vasilios, Rahman Mahboob, Rastogi Anjay, Servilla Karen, Townsend Raymond R, Wall Barry, Whelton Paul K
From University of Utah School of Medicine, Salt Lake City, Utah; Wake Forest School of Medicine, Winston-Salem, North Carolina; University of Texas Southwestern Medical Center, Dallas, Texas; Ohio State University, Columbus, Ohio; University of Pennsylvania, Philadelphia, Pennsylvania; University of Minnesota, Minneapolis, Minnesota; National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland; University of Illinois at Chicago, Chicago, Illinois; VA Medical Center, Washington, DC; Case Western Reserve University, Cleveland, Ohio; University of California, Los Angeles, Los Angeles, California; VA Medical Center, Albuquerque, New Mexico; VA Medical Center, Memphis, Tennessee; and Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana.
Ann Intern Med. 2017 Sep 19;167(6):375-383. doi: 10.7326/M16-2966. Epub 2017 Sep 5.
The public health significance of the reported higher incidence of chronic kidney disease (CKD) with intensive systolic blood pressure (SBP) lowering is unclear.
To examine the effects of intensive SBP lowering on kidney and cardiovascular outcomes and contrast its apparent beneficial and adverse effects.
Subgroup analyses of SPRINT (Systolic Blood Pressure Intervention Trial). (ClinicalTrials.gov: NCT01206062).
Adults with high blood pressure and elevated cardiovascular risk.
6662 participants with a baseline estimated glomerular filtration rate (eGFR) of at least 60 mL/min/1.73 m2.
Random assignment to an intensive or standard SBP goal (120 or 140 mm Hg, respectively).
Differences in mean eGFR during follow-up (estimated with a linear mixed-effects model), prespecified incident CKD (defined as a >30% decrease in eGFR to a value <60 mL/min/1.73 m2), and a composite of all-cause death or cardiovascular event, with surveillance every 3 months.
The difference in adjusted mean eGFR between the intensive and standard groups was -3.32 mL/min/1.73 m2 (95% CI, -3.90 to -2.74 mL/min/1.73 m2) at 6 months, was -4.50 mL/min/1.73 m2 (CI, -5.16 to -3.85 mL/min/1.73 m2) at 18 months, and remained relatively stable thereafter. An incident CKD event occurred in 3.7% of participants in the intensive group and 1.0% in the standard group at 3-year follow-up, with a hazard ratio of 3.54 (CI, 2.50 to 5.02). The corresponding percentages for the composite of death or cardiovascular event were 4.9% and 7.1% at 3-year follow-up, with a hazard ratio of 0.71 (CI, 0.59 to 0.86).
Long-term data were lacking.
Intensive SBP lowering increased risk for incident CKD events, but this was outweighed by cardiovascular and all-cause mortality benefits.
National Institutes of Health.
强化收缩压（SBP）降低与慢性肾脏病（CKD）发病率升高相关，但其对公共卫生的意义尚不清楚。
研究强化降低SBP对肾脏和心血管结局的影响，并对比其明显的有益和有害作用。
收缩压干预试验（SPRINT）的亚组分析。（ClinicalTrials.gov：NCT01206062）。
患有高血压且心血管风险升高的成年人。
6662名基线估计肾小球滤过率（eGFR）至少为60 mL/min/1.73 m²的参与者。
随机分配至强化或标准SBP目标组（分别为120或140 mmHg）。
随访期间平均eGFR的差异（采用线性混合效应模型估计）、预先设定的新发CKD（定义为eGFR下降>30%至<60 mL/min/1.73 m²），以及全因死亡或心血管事件的复合终点，每3个月进行一次监测。
强化组与标准组调整后的平均eGFR差异在6个月时为-3.32 mL/min/1.73 m²（95%CI，-3.90至-2.74 mL/min/1.73 m²），18个月时为-4.50 mL/min/1.73 m²（CI，-5.16至-3.85 mL/min/1.73 m²），此后保持相对稳定。在3年随访时，强化组3.7%的参与者发生新发CKD事件，标准组为1.0%，风险比为3.54（CI，2.50至5.02）。死亡或心血管事件复合终点在3年随访时的相应百分比分别为4.9%和7.1%，风险比为0.71（CI，0.59至0.86）。
缺乏长期数据。
强化降低SBP增加了新发CKD事件的风险，但心血管和全因死亡率获益超过了这一风险。
美国国立卫生研究院。
