Department of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA; Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia, PA.
Department of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA; Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia, PA.
Am J Kidney Dis. 2019 Jan;73(1):72-81. doi: 10.1053/j.ajkd.2018.06.017. Epub 2018 Sep 1.
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.
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.
Measures of kidney function and damage, fasting blood glucose, hemoglobin A (HbA), 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.
Incident T2DM (defined as fasting blood glucose ≥ 126mg/dL or prescription of insulin or oral hypoglycemic agents).
Concordance between fasting blood glucose and HbA 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.
Overall T2DM incidence rate was 17.81 cases/1,000 person-years. Concordance between fasting blood glucose and HbA levels was low (κ for categorical versions of fasting blood glucose and HbA = 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 HbA level was nonsignificant (P ≥ 0.1). Harrell's C for the models ranged from 0.62 to 0.68.
Limited number of outcome events; predictors limited to measures taken at baseline.
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.
很少有研究探讨慢性肾脏病（CKD）患者中 2 型糖尿病（T2DM）的发病情况。我们的目的是使用几种不同的血糖控制指标来评估 CKD 患者中 T2DM 的发生率和危险因素。
前瞻性队列研究。
共纳入 1713 例肾小球滤过率降低且基线时无糖尿病的患者，这些患者均来自慢性肾脏不全队列研究（CRIC）。
包括肾功能和损伤指标、空腹血糖、糖化血红蛋白（HbA）、稳态模型评估的胰岛素抵抗（HOMA-IR）、人口统计学指标、糖尿病家族史（DM）、吸烟状况、用药情况、收缩压、甘油三酯水平、高密度脂蛋白胆固醇水平、体重指数和身体活动水平。
新发 T2DM（定义为空腹血糖≥126mg/dL 或服用胰岛素或口服降糖药）。
采用κ值评估空腹血糖和 HbA 水平之间的一致性。采用以死亡和终末期肾病为竞争事件的特定原因风险模型来预测新发 T2DM。
总的 T2DM 发生率为 17.81 例/1000 人年。空腹血糖和 HbA 水平之间的一致性较低（空腹血糖和 HbA 分类版本的κ值为 13%）。肾功能和损伤指标与新发 T2DM 之间的关联无统计学意义（P≥0.4）。在多变量模型中，T2DM 与空腹血糖水平显著相关（P=0.002），与 DM 家族史相关（P=0.03）。HOMA-IR 与 T2DM 的调整关联与空腹血糖水平相当；HbA 水平与 T2DM 无显著关联（P≥0.1）。模型的 Harrell's C 值范围为 0.62 至 0.68。
结局事件数量有限；预测因素仅限于基线时的测量值。
CKD 患者的 T2DM 发生率明显高于一般人群，这支持在该人群中更加强化监测。血糖控制指标和 DM 家族史与新发 T2DM 独立相关。
