Extracorporeal circuit temperature gradient and hemodynamic instability during continuous renal replacement therapy: an observational study

Introduction Lowering extracorporeal circuit temperature (T° CRRT ) below core temperature (T° CORE ) during continuous renal replacement therapy (CRRT) may modify hemodynamic instability (HIRRT) risk by affecting cardiac output (CO) and vasomotor tone. This study aimed to identify the mediators involved in the relationship between CRRT-to-core temperature gradient and HIRRT risk. Methods This ancillary analysis of a prospective, single-center center study (NCT03139123) included patients with stage 3 acute kidney injury, receiving CRRT for <24 h and with continuous cardiac index monitoring. T° CRRT , T° CORE and hemodynamics parameters were collected 4 -hly between inclusion and day 7 (or end of follow-up). Temperature gradient (ΔT°) corresponded to T° CRRT minus T° CORE . HIRRT (defined as a mean arterial pressure [MAP] <65 mmHg requiring therapeutic intervention) were reported hourly. An exploratory mediation analysis evaluated the effect of ΔT° on HIRRT risk during follow-up, mediated through CO and MAP. Results 42 patients were enrolled in this ancillary analysis (age 68 [58–76], SOFA 12 [8–15], 79% with sepsis), and were followed over 119 [57–143] hours (N = 1012 observations). Decreasing ΔT° (extracorporeal cooling) was significantly associated with higher heart rate, CO and MAP, lower norepinephrine dose, and was associated with a reduction in HIRRT risk in univariate analysis ( P < 0.01). In mediation analysis, ΔT° ≤0°C decreased the probability of HIRRT by 7% (95% confidence interval: 1% to 14%, total effect ). A significant indirect effect was observed (average causal mediation effect [ACME]), operating through MAP and CO mediators (MAP: 5% [2% to 7%]; CO: 4% [1% to 5%]). Conclusions During CRRT, setting the circuit temperature below body temperature was associated with a reduced HIRRT risk, an effect potentially mediated through improvements in MAP and CO.