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Impaired Fasting Glucose and Chronic Kidney Disease, Albuminuria, or Worsening Kidney Function: a Secondary Analysis of the SPRINT.
PURPOSE: Diabetes mellitus is a risk factor for the development and progression of chronic kidney disease (CKD). However, the association of prediabetes with adverse kidney outcomes is uncertain.
METHODS: We performed a secondary analysis of the Systolic Blood Pressure Intervention Trial (SPRINT), including 9,361 participants without diabetes at baseline. We categorized participants according to fasting glucose as having impaired fasting glucose (≥100 mg/dL [(≥5.6 mmol/L]) or normoglycemia (<100 mg/dL [(<5.6 mmol/L]). Unadjusted and adjusted proportional hazards models were fit to estimate the association of impaired fasting glucose (versus normoglycemia) with a composite outcome of worsening kidney function (≥30% decrease in eGFR to <60 ml/min/1.73 m2 in participants without baseline CKD; ≥50% decrease in eGFR or need of long-term dialysis/kidney transplantation in participants with CKD) or incident albuminuria (doubling of urinary albumin to creatinine ratio from <10 mg/g to >10 mg/g). These outcomes were also evaluated separately, and according to CKD status at baseline.
RESULTS: The mean age was 67.9 ± 9.4 years, 35.5% were female, and 31.4% were black. The median follow-up was 3.3 years and 41.8% had impaired fasting glucose. Impaired fasting glucose was not associated with higher rates of the composite outcome (HR 0.97; 95%CI 0.81-1.16), worsening kidney function (HR 1.02; 95%CI 0.75-1.37), or albuminuria (HR 0.98; 95%CI 0.78-1.23). Similarly, there was no association of impaired fasting glucose with outcomes according to baseline CKD status.
CONCLUSIONS: Impaired fasting glucose at baseline was not associated with the development of worsening kidney function or albuminuria in participants of SPRINT.
METHODS: We performed a secondary analysis of the Systolic Blood Pressure Intervention Trial (SPRINT), including 9,361 participants without diabetes at baseline. We categorized participants according to fasting glucose as having impaired fasting glucose (≥100 mg/dL [(≥5.6 mmol/L]) or normoglycemia (<100 mg/dL [(<5.6 mmol/L]). Unadjusted and adjusted proportional hazards models were fit to estimate the association of impaired fasting glucose (versus normoglycemia) with a composite outcome of worsening kidney function (≥30% decrease in eGFR to <60 ml/min/1.73 m2 in participants without baseline CKD; ≥50% decrease in eGFR or need of long-term dialysis/kidney transplantation in participants with CKD) or incident albuminuria (doubling of urinary albumin to creatinine ratio from <10 mg/g to >10 mg/g). These outcomes were also evaluated separately, and according to CKD status at baseline.
RESULTS: The mean age was 67.9 ± 9.4 years, 35.5% were female, and 31.4% were black. The median follow-up was 3.3 years and 41.8% had impaired fasting glucose. Impaired fasting glucose was not associated with higher rates of the composite outcome (HR 0.97; 95%CI 0.81-1.16), worsening kidney function (HR 1.02; 95%CI 0.75-1.37), or albuminuria (HR 0.98; 95%CI 0.78-1.23). Similarly, there was no association of impaired fasting glucose with outcomes according to baseline CKD status.
CONCLUSIONS: Impaired fasting glucose at baseline was not associated with the development of worsening kidney function or albuminuria in participants of SPRINT.
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