Abstract: TH-PO448

Differential Effects of Arterial Stiffness versus Fluid Overload on High Blood Pressure According to Renal Function in Patients at a Risk of Cardiovascular Disease

Session Information

Category: Chronic Kidney Disease (Non-Dialysis)

  • 303 CKD: Epidemiology, Outcomes - Cardiovascular

Authors

  • Kwon, Jaeyeol, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Korea (the Republic of)
  • Han, Seung Hyeok, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Korea (the Republic of)
  • Wu, Meiyan, College of Medicine, Severance Biomedical Science Institute, Brain Korea 21 PLUS, Yonsei University, Seoul, Korea (the Republic of)
  • Nam, Boyoung, College of Medicine, Severance Biomedical Science Institute, Brain Korea 21 PLUS, Yonsei University, Seoul, Korea (the Republic of)
Background

Pathogenesis of hypertension is multifactorial in patients with chronic kidney disease (CKD). In this study, we explored the relative contribution of arterial stiffness and fluid overload to blood pressure (BP) in these patients. We evaluated 1531 patients of Cardiovascular and Metabolic Disease Etiology Research Center-High Risk (NCT02003781), a prospective observational cohort study of high risk patients with cardiovascular disease.

Methods

BP, arterial stiffness, and volume status expressed as an extracellular water/total body water ratio (ECW/TBW) were measured by 24-h BP monitoring, pulse wave velocity (PWV) and bioelectrical impedance analysis measurement, respectively.

Results

In patients with CKD, multiple linear regression analysis showed that both PWV and ECW/TBW were significantly associated with 24-h systolic BP (SBP). The area under the receiver operating characteristic curves (AUCs) for predicting 24-h SBP ≥130 mmHg significantly increased after PWV was added to conventional factors regardless of CKD status. However, the AUCs did not increase in ECW/TBW-based models. When a cut-off level of 24-h SBP was defined as 140 mmHg, predictability of ECW/TBW for elevated BP significantly improved in patients with CKD, but not in those without CKD. This association was further confirmed by the net reclassification and integrated discriminant improvements, RMSE with adjusted R2, and interaction effects. In summary, as kidney function declines, fluid overload significantly contributes to high BP. The impact of fluid overload on BP is only observed in late stage of hypertension in patients with CKD.

Conclusion

Our findings suggest that a stepwise approach is required in the management of hypertension, depending on CKD stages.