Abstract
INTRODUCTION: Guidelines recommend oral hydration (OH) to prevent contrast-associated acute kidney injury (CA-AKI) after coronary angiography or intervention, but quantitative protocols are lacking, and practice varies. Shorter hospital stays limit opportunities for post-procedure creatinine monitoring, and real-world OH patterns and their early renal effects remain poorly described. This study aimed to characterize periprocedural weight-adjusted OH trajectories and to assess whether trajectory membership was associated with a change in serum creatinine within 24 h. METHODS: This single-center prospective cohort study enrolled 192 inpatients undergoing coronary angiography or intervention between November 2024 and May 2025. We recorded weight-adjusted oral intake in four windows: pre-12 h, post-0-6 h, 6-12 h, and 12-24 h. We computed partial-overlap dynamic time warping distances and clustered trajectories using partitioning around medoids. Group comparisons used nonparametric tests. The primary outcome was percent change in serum creatinine, and dose-response was assessed with generalized additive models (GAMs) adjusted for baseline creatinine, estimated glomerular filtration rate, comorbidities, procedural indication, contrast volume, and intravenous hydration. RESULTS: After excluding 18 patients for missing periprocedural oral intake or post-procedure creatinine, 174 patients were analyzed (median age 65.0 years, IQR 57.2 to 72.0; 71.8% male). Median weight-adjusted cumulative oral intake was 10.9, 18.6, 23.9, and 33.3 mL/kg for the pre-12 h, post-0-6 h, 0-12 h, and 0-24 h windows. Time-series clustering produced two stable groups (low-OH n = 85, high-OH n = 89; average silhouette = 0.393; bootstrap adjusted Rand index = 0.845). The largest between-group difference occurred in the 0-6 h window (median 4.12 vs. 2.00 mL/kg/h, p < 0.001). No patient met CA-AKI criteria. In adjusted GAMs, the 0-6 h OH rate was not a significant smooth term (edf = 3.79, p = 0.795), and cluster membership was not associated with creatinine change. However, the high-OH cluster had substantially greater 6-h urine output and a larger positive fluid balance (p < 0.001), while serum potassium was similar between clusters. CONCLUSION: Periprocedural OH was generally ample and formed two reproducible patterns. Concentrating oral intake in the first 6 h increased early urine output and positive fluid balance but did not show a significant dose-response association with early serum creatinine change. This null result should be interpreted cautiously because the cohort was generally low-risk, follow-up was short, and the study had limited power. Future studies should validate whether early concentrated OH protects renal function using earlier sensitive biomarkers and by targeting high-risk patients.