Alex R Chang1, Holly Kramer2, Guo Wei3, Robert Boucher3, Morgan E Grams4, Dan Berlowitz5, Udayan Bhatt6, Debbie L Cohen7, Paul Drawz8, Henry Punzi9, Barry I Freedman10, William Haley11, Amret Hawfield10, Edward Horwitz12, Christopher McLouth13, Don Morisky14, Vasilios Papademetriou15, Michael V Rocco10, Barry Wall16, Daniel E Weiner17, Athena Zias18, Srinivasan Beddhu3,19. 1. Kidney Health Research Institute, Department of Population Health Sciences, Geisinger Health System, Danville, Pennsylvania achang@geisinger.edu. 2. Division of Nephrology, Loyola University Medical Center, Maywood, Illinois. 3. Division of Nephrology & Hypertension, University of Utah School of Medicine, Salt Lake City, Utah. 4. Division of Nephrology, Johns Hopkins School of Medicine, Baltimore, Maryland. 5. Department of Public Health, University of Massachusetts-Lowell, Lowell, Massachusetts. 6. Division of Nephrology, The Ohio State University College of Medicine, Columbus, Ohio. 7. Renal Division, University of Pennsylvania, Philadelphia, Pennsylvania. 8. Division of Renal Diseases and Hypertension, University of Minnesota, Minneapolis, Minnesota. 9. Punzi Medical Center, Trinity Hypertension and Metabolic Research Institute, Carollton, Texas. 10. Section on Nephrology, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina. 11. Division of Nephrology, Mayo Clinic, Jacksonville, Florida. 12. Division of Nephrology, MetroHealth Medical Center, Cleveland, Ohio. 13. Division of Public Health Sciences, Department of Biostatistics and Data Science, Wake Forest Health Sciences, Wake Forest School of Medicine, Winston-Salem, North Carolina. 14. Department of Community Health Sciences, University of California, Los Angeles Fielding School of Public Health, Los Angeles, California. 15. Department of Cardiology, Veterans Affairs Medical Center, Georgetown University, Washington, DC. 16. Division of Nephrology, Veterans Affairs Medical Center, Memphis, Tennessee. 17. Division of Nephrology, Tufts Medical Center, Boston, Massachusetts. 18. Stony Brook University School of Medicine, Stony Brook, New York. 19. Medical Service, Veterans Affairs Salt Lake City Health Care System, Salt Lake City, Utah.
Abstract
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% eGFR decline 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.
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% eGFR decline 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.
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