대한신장학회

논문분류	춘계학술대회 초록집
제목	Effects of Citrate Versus Acetate Dialysate on Cell Damage, Uremic Toxin, and Inflammation in Patients with Maintenance Hemodialysis
저자	Su Woong Jung1, Da Rae Kim3, Jin Sug Kim1, Tae Won Lee1, Chun Gyoo Ihm1, Ju-Young Moon2, Yang Gyun Kim2, Sang-Ho Lee2, Kyung Hwan Jeong1
출판정보	2018; 2018(1):
키워드	citrate \| acetate \| dialysate \| cell-free mitochondrial DNA \| indoxyl sulfate
초록	Objectives: Dialysis procedure and protein-bound uremic toxin are contributing factors to chronic inflammation in hemodialysis (HD) patients. We aimed to establish whether citrate instead of acetate as an acidifying agent improves dialysis-related cellular damage and removal of protein-bound uremic toxin with inflammation. Methods: In a prospective, randomized, cross-over study, a total of 66 (M:F=37:29, 58.62 ± 12.25 yrs) maintenance HD patients were randomly assigned to receive 13 weeks of citrate dialysate followed by 13 weeks of acetate dialysate, or vice versa. Cell-free mitochondrial DNA (mtDNA) as a marker for cellular damage, indoxyl sulfate (IS) as a key protein-bound uremic toxin, and inflammatory parameters including high-sensitivity C-reactive protein (hsCPR), pentraxin 3 (PTX3), and interleukin-6 (IL-6) were measured at 0, 13, 26 weeks of study period. In addition, we also investigated the effects on anemia, electrolytes, and coagulation. Results: During HD and after 13 weeks, cell-free mtDNA level was significantly increased with acetate dialysate, whereas it remained nearly unchanged with citrate dialysate. Moreover, citrate dialysate resulted in an improvement of predialytic hsCRP compared with acetate (mean change for citrate vs acetate dialysate: -3.33 ± 11.77 vs 0.76 ± 8.45 mg/L, respectively; P=0.03). The citrate dialysate inhibited an increase of IL-6 during HD, however, it showed no effect on an intradiaytic rise of PTX3. IS was significantly decreased after citrate dialysis, but not after acetate dialysate. Ferritin was decreased with citrate dialysate and increased with acetate one. In addition, citrate dialysate allowed the reduction of heparin dose without a difference in aPTT with acetate one. Conclusions: This study provides reduced cellular damage and improvement of hsCRP when citrate was substituted for acetate as acidifying agent. Given marginally increased clearance of IS with citrate dialysis, new strategies to improve its clearance are necessary for more biocompatible dialysis. Figure 1. Effect of citrate and acetate dialysis on cell-free mtDNA and indoxyl sulfate
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