Correspondence: Carotid intima-media thickness, fibroblast growth factor 23, and mineral bone disorder in children with chronic kidney disease

Main text

We appreciate the opportunity to respond to Dr. Christian Saleh’s letter and to clarify aspects of our study findings. We sincerely value the thoughtful comments and the chance to further reflect on our study’s limitations. Our research aimed to identify factors influencing high carotid intima-media thickness (cIMT), elevated fibroblast growth factor 23 (FGF23), and poor mineral and bone disorder (MBD) control in children with chronic kidney disease (CKD) within our resource-constrained setting [1]. We anticipate that our findings will serve as a baseline for future studies involving a larger patient cohort and will help refine the limitations identified in the current study.

We recognize the importance of reproducibility, operator dependency, and methodological rigor in cIMT measurements. To minimize variability, we employed a single, blinded examiner with extensive training, ensuring adherence to a standardized protocol. Measurements were conducted individually at different time points rather than in batch readings, which are recommended for optimal consistency. To assess reliability, 10 of the 42 cIMT measurements were reassessed by a senior cardiologist. Agreement between the blinded examiner and the senior cardiologist was evaluated using the kappa (κ) statistic, yielding a κ value of 0.782, indicating moderate reliability [2].

We appreciate Dr. Saleh’s suggestion that incorporating multiple measurements from different angles or artery views, along with a more extensive protocol, could further improve reliability [3]. Additionally, we acknowledge the role of cardiac synchronization in accounting for systolic and diastolic variability [4]. However, due to logistical and clinical constraints—particularly the limited cooperation of pediatric patients and restricted access to advanced facilities—this was not feasible [5,6,7]. Nonetheless, our standardized measurement protocol may have helped mitigate this limitation to some extent. We agree that future studies should integrate cardiac gating to enhance precision, and we acknowledge this as a limitation of our study.

Regarding methodological comparisons, we acknowledge that different techniques were employed by [8,9,10] specifically cardiac synchronization and edge-tracking devices, which limits direct comparisons with our manually performed measurements. We appreciate this important perspective and recognize these methodological discrepancies and their potential impacts on the interpretation of our results.

In summary, despite these acknowledged limitations, we hope our study provides meaningful insights into predictors of elevated cIMT in pediatric CKD. We are grateful for this constructive dialogue and the opportunity to refine our discussion, and we will consider these aspects in future research.