#6829 differential lipidic profile with the use of citrate or acetate dialysates

Abstract Background and Aims Unlike other high-cardiovascular-risk populations, the efficacy obtained from lipid-lowering therapy remains uncertain in dialysis-dependent chronic kidney disease (DD-CKD) patients. This is probably given to the exclusion in clinical trials of patients with very high LDL levels, their population's heterogeneity, accompanying cardiovascular morbidities, and the higher mortality risk explained partly by chronic inflammation. The latter has been associated with the accumulation of uremic toxins, membrane biocompatibility, and acetate-based dialysates, which promote inflammation. Different dialysate weak acidifying agents such as lactic, pyruvic, hydrochloric, or citric acids have surged as less-inflammatory alternatives to acetate. This study aims to evaluate the effects of the metabolism of acetate and citrate in the lipidic profile of DD-CKD patients. Method In a unicentric, cross-over, prospective study, we compared the lipidic profile by assessing the plasma levels of total cholesterol (TC), low-density lipoprotein (LDL), triglycerides (TG), high-density (HDL) and very low-density (VLDL) lipoprotein cholesterol, and lipoprotein (a) [Lp(a)] comparing the use of citrate (CD) vs. acetate (AD) as dialysate buffers, after twelve sessions with each one. Prealbumin was also measured to rule out malnutrition as a potential confounding factor. Prevalent (i.e., dialysis vintage ≥3 months) adult patients on maintenance hemodialysis were included. The dialysis prescription parameters and additional medical treatments remained unchanged during their sessions with both dialysates. Quantitative variables are reported with mean and standard deviation. Normal distribution was assessed with the Shapiro-Wilk test, and the comparisons were made with the Student's paired T-test or Wilcoxon's signed-rank test, accordingly. A two-sided p-value ≤0,05 was considered statistically significant. Results After twelve dialysis sessions with CD, compared to AD, there was a statistically significant decline in TG and HDL and an increase in LDL. There was also a notable but non-significant reduction in VLDL (Table 1). Conclusion There were noteworthy differences in the lipid profile that can only be attributed to the change of dialysis fluid, as we avoided inter-individual (with a cross-over design) and intra-individual (different inflammatory or nutritional profiles would not be expected with this short-term setting) variabilities. Further studies must elucidate if the short-term changes induced in the lipidic profile of DD-CKD patients by the dialysate's weak acid translate into clinical implications.