#706 Outcomes and risk factors of widened difference in estimated glomerular filtration rate by creatinine or cystatin C: adjust model development with >300,000 UK Biobank participants

Abstract Background and Aims Recent studies emphasize the clinical importance of discrepancies between cystatin C-based CKD-EPI eGFR (eGFRcys) and creatinine-based CKD-EPI eGFR (eGFRcr). This study examines the implications of eGFR differences (eGFRdiff) on clinical outcomes and aims to develop an adjustment model using eGFRcr and associated clinical variables. Method Using data from 343,854 UK Biobank participants, we stratified into three groups based on eGFRdiff: lower (eGFRcys–eGFRcr <−15), middle (−15 ≤ eGFRcys–eGFRcr and eGFRcys–eGFRc ≤15), and upper (eGFRcys–eGFRcr >15). We analyzed the risks of death, myocardial infarction (MI), and ischemic stroke in groups with eGFRdiff <−15 and eGFRdiff >15 using Cox models. Logistic regression identified variables associated with eGFRdiff. We developed and validated a regression model using eGFRcr and associated variables. Results Individuals with eGFRdiff <−15 had increased risks of death (HR: 1.37 [1.30–1.44]), MI (HR: 1.23 [1.15–1.33]), and ischemic stroke (HR: 1.19 [1.08–1.31]). Variables associated with eGFRdiff <−15 included high waist/hip circumference, high body weight, low fat-free mass, high total food/fat/carbohydrate intake, low protein intake, diabetes, and larger kidney volumes. A simplified regression model was developed using eGFRcr, sex, age, height, weight, and BMI. In the validation set, the adjusted R2 correlation between eGFRcys and eGFRcr improved from 0.32 to 0.47 with the simple model. The adjusted model improved clinical outcome prediction [net reclassification effect 0.554, 0.530, 0.508 for death, MI, and ischemic stroke]. Conclusion eGFRdiff <−15 is associated with increased clinical risks. An adjusted model approximating eGFRcr to eGFRcys demonstrated improved clinical outcome associations.