Associations between cystatin C-based eGFR, ambulatory blood pressure parameters, and in-clinic versus ambulatory blood pressure agreement in older community-living adults

Abstract

OBJECTIVES To determine the relationship between chronic kidney disease (measured by cystatin C-based eGFR) and abnormal ambulatory blood pressure (including nocturnal dipping) in healthy older adults. Further, to assess agreement between clinic and ambulatory blood pressure monitoring. METHODS Serum cystatin C levels were measured to calculate eGFR. Participants underwent clinic and 24-hour ambulatory blood pressure measurement. Multiple linear regression, was performed to examine the association between reduced cystatin C-based eGFR (CKDcys) and blood pressure parameters. Bland-Altman analysis was performed to evaluate agreement between clinic and ambulatory measurements. RESULTS Average age was 72. There were 60 individuals with CKDcys (eGFR < 60 ml/min/1.73m2). Compared to those without CKDcys, individuals with CKDcys were older, more likely to have hypertension and less likely to have normal dipping patterns. After multivariate analysis, the presence of CKDcys was significantly associated with lower mean ambulatory diastolic blood pressure (DBP) (−2 mm Hg, p = 0.048), but not with nocturnal dipping or other blood pressure parameters. Clinic systolic blood pressure (SBP) significantly overestimated mean wake time ambulatory SBP; mean difference was 11 mmHg for those without CKDcys (95% limits of agreement −14 to 35 mmHg) and 14 mmHg for those with CKDcys (95% limits of agreement −13 to 41 mmHg); there was no statistically significant effect modification by CKD status. CONCLUSION In older, seemingly healthy adults, mild CKD was associated with lower ambulatory DBP. The presence of CKD did not affect interpretation of clinic vs. ambulatory blood pressure monitoring, although accuracy of clinic SBP was poor.

Predictive role of endothelin in left ventricular remodeling of chronic kidney disease

“…ET-1 can also promote platelet-derived growth factor (PDGF), TGF release, and indirectly promote myocardial cell proliferation, which leads to cardiac hypertrophy. Another study [ 15 ] found that endothelin receptor antagonists (ETR) can prevent myocardial fibrosis and myocardial cell wall thickening of small arterial blood vessels in uremic rats, confirming that ET-1 is closely related to left ventricular remodeling.…”