Regional Citrate Anticoagulation Protocol for Patients with Presumed Absent Citrate Metabolism.

Background: Regional citrate anticoagulation (RCA) is not recommended in patients with shock or severe liver failure. We designed a protocol with personalized precalculated flow settings for patients with absent citrate metabolism that abrogates risk of citrate toxicity, and maintains neutral continuous KRT (CKRT) circuit calcium mass balance and normal systemic ionized calcium levels.
Methods: A single-center prospective cohort study of patients in five adult intensive care units triaged to the CVVHDF-RCA "Shock" protocol.
Results: Of 31 patients included in the study, 30 (97%) had AKI, 16 (52%) had acute liver failure, and five (16%) had cirrhosis at the start of CKRT. The median lactate was 5 mmol/L (interquartile range [IQR], 3.2-10.7), AST 822 U/L (IQR, 122-2950), ALT 352 U/L (IQR, 41-2238), total bilirubin 2.7 mg/dl (IQR, 1.0-5.1), and INR two (IQR, 1.5-2.6). The median first hemofilter life censored for causes other than clotting exceeded 70 hours. The cumulative incidence of hypernatremia (Na >148 mM), metabolic alkalosis (HCO3- >30 mM), and hypophosphatemia ( P <2 mg/dl) were one out of 26 (4%), zero out of 30 (0%), and one out of 30 (3%), respectively, and were not clinically significant. Mild hypocalcemia occurred in the first 4 hours in two out of 31 patients, and corrected by hour 6 with no additional Ca supplementation beyond the per-protocol administered Ca infusion. The maximum systemic total Ca (tCa; mM)/ionized Ca (iCa; mM) ratio never exceeded 2.5.
Conclusions: The Shock protocol can be used without contraindications and is effective in maintaining circuit patency with a high, fixed ACDA infusion rate to blood flow ratio. Keeping single-pass citrate extraction on the dialyzer >0.75 minimizes the risk of citrate toxicity even in patients with absent citrate metabolism. Precalculated, personalized dosing of the initial Ca-infusion rate from a table on the basis of the patient's albumin level and the filter effluent flow rate maintains neutral CKRT circuit calcium mass balance and a normal systemic iCa level.
Competing Interests: M. Heung reports consultancy agreements with Baxter Inc, Potrero Medical Inc., and Wolters Kluwer (Lexicomp); reports receiving research funding from Centers for Disease Control, Patient-Centered Outcomes Research Institute, and Veterans Affairs; reports receiving honoraria from National Kidney Foundation; and is a scientific advisor or member of Associate Editor/Editorial board, Advances in CKD. D. Humes reports consultancy agreements with SeaStar Medical; having an ownership interest in Innovative BioTherapies, Inc. and SeaStar Medical, Inc.; reports receiving research funding from Innovative Biotherapies, Lowell Pharmaceuticals, Renal Research Institute, SeaStar Medical, and Sygin; reports being a scientific advisor or member of Innovative Biotherapies and SeaStar Medical. B. Szamosfalvi reports receiving research funding from Renal Research Institute. B. Wagner reports having an ownership interest in Able-Wagner, Inc. L. Yessayan reports receiving research funding from renal research institute and being a Section Editor for ASAIO Journal, Renal\Extracorporeal Blood Treatment. R. Sohaney reports being funded by a training grant from the National Institutes of Health (5T32DK007378-40). All remaining authors have nothing to disclose.
(Copyright © 2021 by the American Society of Nephrology.)