Citrate Formulation Determines Filter Lifespan during Continuous Veno-Venous Hemofiltration: A Prospective Cohort Study

Abstract

Introduction: We conducted an 8-month prospective single-center observational study in patients with acute kidney injury treated with continuous veno-venous hemofiltration (CVVH) to compare the impact of two citrate formulations on filter lifespan (FLS). Methods: Patients received CVVH at a delivered dose of 25 ml/kg/h. Multivariable linear regression was performed to assess the influence of different variables on circuit lifespan. Results: We included 59 patients, 28 received the 10/2 formulation and 31 received the 18/0 formulation. Median (interquartile range) FLS was significantly prolonged with the 18/0 solution compared with the 10/2 solution (4.10 (2.45-5.75) vs. 2.68 (0.47-4.99) days, p = 0.001). No confounding variables (difference in ionized calcium target, citrate flow or dose, platelet count, hematocrit, vascular access location) affecting filter capacity or lifespan between the 2 formulations were identified. Conclusions: Under similar conditions of CVVH and calcium targets, a Prismocitrate 18/0 formulation significantly improved FLS as compared with Prismocitrate 10/2.

Chloride content of solutions used for regional citrate anticoagulation might be responsible for blunting correction of metabolic acidosis during continuous veno-venous hemofiltration

“…Veno-venous access was obtained via a 13 F double-lumen polyurethane catheter (Joline, Swiss Confederation) inserted in the right internal jugular or a femoral vein. CVVH was delivered according to a dedicated protocol inspired by Tolwani et al [17] and presented in detail previously [6]. This included standardized order sets and initial settings for all patients.…”

“…Calcium chloride initially ran at 6 mL/h through a separate central venous line. Calcium infusion was titrated to maintain plasma ionized calcium levels between 1,0 and 1,2 mmol/L [6]. PC10/2 was delivered before the filter and started at a rate of 2200 mL/h.…”

“…Conversely, in patients with decreased capacity to metabolize citrate (eg hepatic failure), accumulation can lead to high anion-gap metabolic acidosis [3–5]. Acid-base status is also affected by the amount of administered chloride and bicarbonate buffer, and occasionally by respiratory (over)compensation [6, 7]. Finally, when administered as a trisodium salt, excess citrate may induce hypernatremia [8].…”

Regional Citrate Anticoagulation for Continuous Renal Replacement Therapy: All Citrates Are Not Created Equal!

“…Post-filter iCa in this study, however, was much lower in the C14 than in the C11 group (0.40 vs. 0.52 mmol/l, p < 0.0001). Jacobs et al [11] strictly kept post-filter iCa levels between 0.2 and 0.3 mmol/l in all patients receiving RCA with either C18 or C10/2 and reported better filter survival with the higher-concentrated liquid (median 98.4 vs. 64.3 h; C18 vs. C10/2, p = 0.001).…”

“…However, no definite answer can be provided because post-filter ionized calcium (iCa) concentrations were not reported. Indeed, keeping post-filter iCa within tight limits has been shown to ensure more optimal anticoagulation, better regulation of buffer supply, and an improved FLS [11] . Egi et al [10] found a prolonged mean FLS when a more concentrated citrate solution was used (17.1 vs. 12.2 h; C14 vs. C11).…”