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Diabetes was a SPRINT exclusion criterion. We defined normoglycemia and prediabetes as fasting plasma glucose &lt;100 mg\/dl and \u2265100 mg\/dl, respectively.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>Of the 9,323 participants included in this analysis, 3,898 (41.8%) had prediabetes and the rest (5,425) had normoglycemia. In participants with baseline estimated glomerular filtration rate (eGFR) \u226560 ml\/min\/1.73 m2, incident CKD was defined as a \u226530% decline in eGFR to below 60 ml\/min\/1.73 m2 with repeat confirmation. AKI events were identified clinically. In the non-CKD participants (n = 6,678), there were 164 incident CKD events. The hazard ratios (HRs) for incident CKD for intensive SBP goal (&lt;120 mm Hg) vs. standard SBP goal (&lt;140 mm Hg) in the normoglycemia (HR: 3.25, 95% CI: 2.03, 5.19) and prediabetes (HR: 3.90, 95% CI: 2.17, 7.02) groups were similar (interaction P value 0.64). In the entire analytic cohort (N = 9,323), there were 310 AKI events. AKI HRs for intensive vs. standard SBP in the normoglycemia (HR: 1.59, 95% CI: 1.17, 2.15) and prediabetes (HR: 1.74, 95% CI: 1.22, 2.48) groups were also similar (interaction P value 0.71).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS<\/jats:title>\n                    <jats:p>Prediabetes was highly prevalent, but there was no evidence that prediabetes modified the effects of SPRINT intervention on kidney events.<\/jats:p>\n                    <jats:p>CLINICAL TRIALS REGISTRATION<\/jats:p>\n                    <jats:p>NCT01206062<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/ajh\/hpz105","type":"journal-article","created":{"date-parts":[[2019,6,27]],"date-time":"2019-06-27T15:09:27Z","timestamp":1561648167000},"page":"1170-1177","source":"Crossref","is-referenced-by-count":7,"title":["Influence of Prediabetes on the Effects of Intensive Systolic Blood Pressure Control on Kidney Events"],"prefix":"10.1093","volume":"32","author":[{"given":"Naveen","family":"Rathi","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul K","family":"Whelton","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Glenn M","family":"Chertow","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Stanford University, Palo Alto, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William C","family":"Cushman","sequence":"additional","affiliation":[{"name":"VA Medical Center, Memphis, Tennessee, 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USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul L","family":"Kimmel","sequence":"additional","affiliation":[{"name":"Division of Kidney, Urologic, and Hematologic Diseases, NIDDK, National Institutes of Health, Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adam P","family":"Bress","sequence":"additional","affiliation":[{"name":"Department of Population Heath Sciences, University of Utah, Salt Lake City, Utah, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Holly J","family":"Kramer","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Loyola University, Chicago, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catreena","family":"Al-Marji","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah, 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