Donor and Procedural Factors Associated With Citrate Toxicity During Plateletpheresis

Background Citrate anticoagulation during plateletpheresis can reduce ionized calcium and cause neuromuscular or gastrointestinal symptoms. Identifying donor and procedure-related factors may support earlier recognition and prevention. This study assessed factors associated with clinically identified citrate toxicity among plateletpheresis donors. Methods This analytical observational cross-sectional study included 60 plateletpheresis donors at Dhaka Medical College and Hospital, Bangladesh. Citrate toxicity was defined by any prespecified symptom or sign during the donation encounter. Crude and adjusted prevalence ratios (PRs) were estimated using modified Poisson regression with robust variance. The parsimonious adjusted model included pre-procedure oral calcium exposure, body mass index (BMI), pre-donation platelet count, and anticoagulant citrate dextrose solution A (ACD-A) volume. Calcium administration was non-randomized, and total and ionized calcium were not measured. Results All 60 donors were male; 28 (46.7%) developed citrate toxicity. Compared with donors without toxicity, affected donors had lower mean BMI (24.03 versus 25.56 kg/m²; p=0.020), lower pre-donation platelet count (2.53 versus 3.23×10¹¹/L; p<0.001), and greater mean ACD-A exposure (333.39 versus 259.13 mL; p<0.001). In adjusted analysis, absence of pre-procedure calcium was associated with higher toxicity prevalence (adjusted PR {aPR} 4.42, 95% CI: 2.59-7.56), each 1 kg/m² higher BMI with lower prevalence (aPR: 0.91, 95% CI: 0.85-0.98), and each 50 mL higher ACD-A volume with higher prevalence (aPR: 1.65, 95% CI: 1.24-2.18). Pre-donation platelet count was not independently associated after adjustment (aPR: 0.79 per 0.5×10¹¹/L, 95% CI: 0.56-1.12). Conclusions Clinical citrate toxicity was common and was associated with absence of pre-procedure calcium, lower BMI, and greater ACD-A volume. These findings identify potential monitoring markers but do not establish causality because procedural factors and symptoms were recorded within the same encounter and ionized calcium was not measured. The calcium association should be interpreted as exploratory and hypothesis-generating, rather than as evidence of prophylactic efficacy.