Background and objectives It is unclear whether the presence of albuminuria modifies the effects of intensive systolic BP control on risk of eGFR decline, cardiovascular events, or mortality. Design, setting, participants, & measurements The Systolic Blood Pressure Intervention Trial randomized nondiabetic adults ≥50 years of age at high cardiovascular risk to a systolic BP target of <120 or <140 mm Hg, measured by automated office BP. We compared the absolute risk differences and hazard ratios of ≥40% eGFR decline, the Systolic Blood Pressure Intervention Trial primary cardiovascular composite outcome, and all-cause death in those with or without baseline albuminuria (urine albumin-creatinine ratio ≥30 mg/g). Results Over a median follow-up of 3.1 years, 69 of 1723 (4%) participants with baseline albuminuria developed ≥40% eGFR decline compared with 61 of 7162 (1%) participants without albuminuria. Incidence rates of ≥40% eGFRdecline were higher in participants with albuminuria (intensive, 1.74 per 100 person-years; standard, 1.17 per 100 person-years) than in participants without albuminuria (intensive, 0.48 per 100 person-years; standard, 0.11 per 100 person-years). Although effects of intensive BP lowering on ≥40% eGFR decline varied by albuminuria on the relative scale (hazard ratio, 1.48; 95% confidence interval, 0.91 to 2.39 for albumin-creatinine ratio ≥30 mg/g; hazard ratio, 4.55; 95% confidence interval, 2.37 to 8.75 for albumin-creatinine ratio <30 mg/g; P value for interaction <0.001), the absolute increase in ≥40% eGFR decline did not differ by baseline albuminuria (incidence difference, 0.38 events per 100 person-years for albumin-creatinine ratio ≥30 mg/g; incidence difference, 0.58 events per 100 person-years for albumin-creatinine ratio <30 mg/g; P value for interaction =0.60). Albuminuria did not significantly modify the beneficial effects of intensive systolic BP lowering on cardiovascular events or mortality evaluated on relative or absolute scales. Conclusions Albuminuria did not modify the absolute benefits and risks of intensive systolic BP lowering.
|Original language||English (US)|
|Number of pages||8|
|Journal||Clinical Journal of the American Society of Nephrology|
|State||Published - Aug 7 2020|
Bibliographical noteFunding Information:
S. Beddhu reports receiving grants from Bayer, Boeringher In-gelheim, and NovoNortis outside the submitted work. P. Drawz reports receiving National Heart, Lung, and Blood Institute grant R01 HL136679 03. M. Grams reports receiving nonfinancial support from DCI outside the submitted work. M.V. Rocco reports receiving grants from Bayer, Boehringer Ingelheim, and GSK and personal fees from Abbvie, Baxter, Beacon Bioscience, and George Clinical outside the submitted work. D.E. Weiner reports serving on the SGLT2 Advisory Board for Janssen Biopharmaceuticals outside the submitted work. All remaining authors have nothing to disclose.
The SPRINT Investigators acknowledge the contribution of study medications (azilsartan and azilsartan combined with chlorthali-done) from Takeda Pharmaceuticals International, Inc. An earlier version this work was presented at the American Heart Association Epi/Lifestyle Meeting in March 2018 in New Orleans, Louisiana. All components of the SPRINT study protocol were designed and implemented by the investigators. The investigative team collected, analyzed, and interpreted the data. All aspects of manuscript writing and revision were carried out by the coauthors. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health, the US Department of Veterans Affairs, or the US Government.
The SPRINT is funded with federal funds from National Institutes of Health, including the National Heart, Lung, and Blood Institute, the National Institute of Diabetes and Digestive and Kidney Diseases, the National Institute on Aging, and the National Institute of Neurological Disorders and Stroke contracts HHSN268200900040C, HHSN268200900046C, HHSN268200900047C, HHSN268200900048C, and HHSN268200900049C and Inter-Agency Agreement A-HL-13-002-001. It was also supported in part with resources and use of facilities through the US Department of Veterans Affairs. A.R. Chang is supported by National Institute of Diabetes and DigestiveandKidneyDiseasesgrantK23DK106515.Statisticalanalyses and preparation of this manuscript are supported by National Institute of Diabetes and Digestive and Kidney Diseases grants RO1DK115814 and R21DK106574 and National Heart, Lung, and Blood Institute grant R21HL145494 (to S. Beddhu). We also acknowledge support from National Center for Advancing Translational Sciences Clinical and Translational Science Awards UL1TR000439 (to Case Western Reserve University);UL1RR02575(toTheOhioStateUniversity);UL1RR024134 and UL1TR000003 (to the University of Pennsylvania); UL1RR025771 (to Boston University); UL1TR000093 (to Stanford University); UL1RR025752, UL1TR000073, and UL1TR001064 (to Tufts); UL1TR000050 (to the University of Illinois); UL1TR000005 (to the University of Pittsburgh); 9U54TR000017-06 (to the University of Texas Southwestern); UL-1TR000105-05 (to the University of Utah); UL1 TR000445 (to Vanderbilt University); UL1TR000075 (to George Washington University); UL1 TR000002 (to the University of California, Davis); UL1 TR000064 (to the University of Florida); and UL1TR000433 (to the University of Michigan) and National Institute of General Medical Sciences Center for Biomedical Research Excellence Award P30GM103337 (to Tulane University). This work is also supported by National Institute of Diabetes and Digestive and Kidney Diseases grant R01 DK091437 and the University of Utah Study Design and Biostatistics Center (funded in part from National Center for Research Resources Public Health Services research grants UL1-RR025764 and C06-RR11234).
© 2020 by the American Society of Nephrology.