TY - JOUR
T1 - Incident Type 2 Diabetes Among Individuals With CKD
T2 - Findings From the Chronic Renal Insufficiency Cohort (CRIC) Study
AU - Chronic Renal Insufficiency Cohort (CRIC) Study Investigators
AU - Jepson, Christopher
AU - Hsu, Jesse Y.
AU - Fischer, Michael J.
AU - Kusek, John W.
AU - Lash, James P.
AU - Ricardo, Ana C.
AU - Schelling, Jeffrey R.
AU - Feldman, Harold I.
AU - Appel, Lawrence J.
AU - Feldman, Harold I.
AU - Go, Alan S.
AU - He, Jiang
AU - Kusek, John W.
AU - Ojo, Akinlolu
AU - Rahman, Mahboob
AU - Townsend, Raymond R.
N1 - Funding Information:
Support: Funding for the CRIC Study was obtained under a cooperative agreement from the National Institute of Diabetes and Digestive and Kidney Diseases (U01DK060990, U01DK060984, U01DK061022, U01DK061021, U01DK061028, U01DK060980, U01DK060963, and U01DK060902). In addition, this work was supported in part by the Perelman School of Medicine at the University of Pennsylvania Clinical and Translational Science Award (CTSA) National Institutes of Health (NIH)/National Center for Advancing Translational Sciences (NCATS) UL1TR000003, Johns Hopkins University UL1 TR-000424, University of Maryland General Clinical Research Center M01 RR-16500, Clinical and Translational Science Collaborative of Cleveland, UL1TR000439 from the NCATS component of the NIH and NIH Roadmap for Medical Research, Michigan Institute for Clinical and Health Research UL1TR000433, University of Illinois at Chicago CTSA UL1RR029879, Tulane COBRE for Clinical and Translational Research in Cardiometabolic Diseases P20 GM109036, Kaiser Permanente NIH/National Center for Research Resources UCSF-CTSI UL1 RR-024131. Dr Kusek, who was Project Scientist for the CRIC Study at the time this research took place, is a co-author. The funding agencies had no role in study design; collection, analysis, and interpretation of data; or decision to submit the report for publication.
Publisher Copyright:
© 2018 National Kidney Foundation, Inc.
PY - 2019/1
Y1 - 2019/1
N2 - Rationale & Objective: Few studies have examined incident type 2 diabetes mellitus (T2DM) in chronic kidney disease (CKD). Our objective was to examine rates of and risk factors for T2DM in CKD, using several alternative measures of glycemic control. Study Design: Prospective cohort study. Setting & Participants: 1,713 participants with reduced glomerular filtration rates and without diabetes at baseline, enrolled in the Chronic Renal Insufficiency Cohort (CRIC) Study. Predictors: Measures of kidney function and damage, fasting blood glucose, hemoglobin A1c (HbA1c), HOMA-IR (homeostatic model assessment of insulin resistance), demographics, family history of diabetes mellitus (DM), smoking status, medication use, systolic blood pressure, triglyceride level, high-density lipoprotein cholesterol level, body mass index, and physical activity. Outcome: Incident T2DM (defined as fasting blood glucose ≥ 126 mg/dL or prescription of insulin or oral hypoglycemic agents). Analytical Approach: Concordance between fasting blood glucose and HbA1c levels was assessed using κ. Cause-specific hazards modeling, treating death and end-stage kidney disease as competing events, was used to predict incident T2DM. Results: Overall T2DM incidence rate was 17.81 cases/1,000 person-years. Concordance between fasting blood glucose and HbA1c levels was low (κ for categorical versions of fasting blood glucose and HbA1c = 13%). Unadjusted associations of measures of kidney function and damage with incident T2DM were nonsignificant (P ≥ 0.4). In multivariable models, T2DM was significantly associated with fasting blood glucose level (P = 0.002) and family history of DM (P = 0.03). The adjusted association of HOMA-IR with T2DM was comparable to that of fasting blood glucose level; the association of HbA1c level was nonsignificant (P ≥ 0.1). Harrell's C for the models ranged from 0.62 to 0.68. Limitations: Limited number of outcome events; predictors limited to measures taken at baseline. Conclusions: The T2DM incidence rate among individuals with CKD is markedly higher than in the general population, supporting the need for greater vigilance in this population. Measures of glycemic control and family history of DM were independently associated with incident T2DM.
AB - Rationale & Objective: Few studies have examined incident type 2 diabetes mellitus (T2DM) in chronic kidney disease (CKD). Our objective was to examine rates of and risk factors for T2DM in CKD, using several alternative measures of glycemic control. Study Design: Prospective cohort study. Setting & Participants: 1,713 participants with reduced glomerular filtration rates and without diabetes at baseline, enrolled in the Chronic Renal Insufficiency Cohort (CRIC) Study. Predictors: Measures of kidney function and damage, fasting blood glucose, hemoglobin A1c (HbA1c), HOMA-IR (homeostatic model assessment of insulin resistance), demographics, family history of diabetes mellitus (DM), smoking status, medication use, systolic blood pressure, triglyceride level, high-density lipoprotein cholesterol level, body mass index, and physical activity. Outcome: Incident T2DM (defined as fasting blood glucose ≥ 126 mg/dL or prescription of insulin or oral hypoglycemic agents). Analytical Approach: Concordance between fasting blood glucose and HbA1c levels was assessed using κ. Cause-specific hazards modeling, treating death and end-stage kidney disease as competing events, was used to predict incident T2DM. Results: Overall T2DM incidence rate was 17.81 cases/1,000 person-years. Concordance between fasting blood glucose and HbA1c levels was low (κ for categorical versions of fasting blood glucose and HbA1c = 13%). Unadjusted associations of measures of kidney function and damage with incident T2DM were nonsignificant (P ≥ 0.4). In multivariable models, T2DM was significantly associated with fasting blood glucose level (P = 0.002) and family history of DM (P = 0.03). The adjusted association of HOMA-IR with T2DM was comparable to that of fasting blood glucose level; the association of HbA1c level was nonsignificant (P ≥ 0.1). Harrell's C for the models ranged from 0.62 to 0.68. Limitations: Limited number of outcome events; predictors limited to measures taken at baseline. Conclusions: The T2DM incidence rate among individuals with CKD is markedly higher than in the general population, supporting the need for greater vigilance in this population. Measures of glycemic control and family history of DM were independently associated with incident T2DM.
KW - Diabetes
KW - chronic kidney disease (CKD)
KW - chronic kidney insufficiency
KW - fasting blood sugar (FBS)
KW - glycemic control
KW - hemoglobin A (HbA)
KW - insulin resistance (HOMA-IR)
KW - kidney function
KW - prediabetes
KW - renal damage
KW - type 2 diabetes mellitus (T2DM)
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U2 - 10.1053/j.ajkd.2018.06.017
DO - 10.1053/j.ajkd.2018.06.017
M3 - Article
C2 - 30177484
AN - SCOPUS:85052753808
SN - 0272-6386
VL - 73
SP - 72
EP - 81
JO - American Journal of Kidney Diseases
JF - American Journal of Kidney Diseases
IS - 1
ER -