Discordance Between Cystatin C-Based eGFR and Creatinine-Based eGFR and Cardiovascular Risk in the FLOW Trial

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Background: Superiority of estimated glomerular filtration rate (eGFR)cystatin C (eGFRcyst) over eGFRcreatinine (eGFRcreat) in cardiovascular risk prediction is established but incompletely understood. It has been hypothesized that low eGFRcyst may be reflecting selective glomerular hypofiltration, characterized by reduced clearance of middle-sized, potentially atherogenic proteins. We analyzed associations of eGFRcyst/eGFRcreat with major adverse cardiovascular events (MACE) and all-cause mortality in participants of the FLOW trial. Methods: GFR was estimated using the CKD-EPI 2009 (eGFRcreat) or 2012 (eGFRcyst) equations. Time to first event was studied using Cox regression. Baseline eGFRcyst/eGFRcreat <0.7 vs ≥0.7 was a fixed factor and adjusted for eGFRcyst and/or eGFRcreat. Results: Of the 3463 participants, 1116 (32%) had eGFRcyst/eGFRcreat <0.7 at baseline (median 0.77) (Figure). Median follow-up was 3.4 years. eGFRcyst/eGFRcreat <0.7 was associated with increased risk of MACE and all-cause mortality (unadjusted hazard ratios [95% confidence interval] of 1.58 [1.31−1.90] and 1.87 [1.57−2.23], respectively). The association was preserved after adjustment for baseline eGFRcyst and/or eGFRcreat, with slight attenuation of effect. Conclusion: In FLOW, eGFRcyst/eGFRcreat <0.7 was associated with substantially increased risk for MACE and all-cause mortality in participants with type 2 diabetes and chronic kidney disease, independent of eGFRcyst. Further research is needed to elucidate potential treatment targets. Funding: Commercial Support - Novo Nordisk A/S

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