Previous studies have presented prognostic factors for patients with acute kidney injury (AKI) who require continuous renal replacement therapy (CRRT), including elderly age, systemic inflammation, oliguria, fluid imbalance, comorbidities, and need for mechanical ventilation [
The pathogenesis of AKI in critical illness is multi-factorial and complex. Therefore, therapeutic interventions for patients with AKI remain heterogeneous. In particular, it can be said that it is representative issues to determine an appropriate fluid administration dose and fluid removal amount, and the timing of renal replacement therapy.
Fluid overload is strongly associated with adverse clinical outcomes and may contribute to development and persistence of AKI in critically ill patients [
Many studies have consistently highlighted the clinical significance of fluid overload in critically ill patients. Jhee et al [
First, as the researchers noted, it is important to define fluid overload using a decisive rather than arbitrary method. Various methods such as clinical examination, serial weights, cumulative fluid balance (CFB), chest X-ray, lung ultrasound, echocardiography, and bioimpedance analysis can be used to evaluate volume status, but they all have limitations. Therefore, because there is no rapid, objective, non-invasive, and relatively affordable method to quantitatively assess volume status, it is difficult to set a treatment policy for critically ill patients with AKI requiring CRRT. Unlike the study by Jhee et al [
Second, the efforts to avoid positive fluid balance in initial treatment of critically ill patients as proposed by Jhee et al [
Third, given that not all patients underwent standardized early fluid resuscitation from treatment initiation, setting the reference point for fluid overload using cumulative fluid data assessed at 72 hours before CRRT initiation is limited, even though the aforementioned CFB is widely accepted as a method to document fluid balance. We cannot rule out the possibility that positive fluid balance might have been the result of early fluid resuscitation due to hemodynamic instability of the critically ill patients in the study. In addition, even though propensity score matching and adjustment for confounding factors were performed, it is unclear whether hemodynamic stability was properly controlled between the two groups because the authors did not provide data on use of inotropic agents or vasoactive agents. Therefore, the association between fluid overload and mortality may largely be secondary.
Fourth, an additional measurement method for determining the appropriate amount of fluid should have been used. This was mentioned as one of the limitations of the study. The definition of CFB is the sum of each day’s fluid balance over a period of time. Therefore, it cannot be assumed that a positive fluid balance is accompanied by fluid overload. Furthermore, CFB is often inaccurate, and insensible fluid losses are not reflected. Bioimpedance analysis may be a good replacement, even though it has not been verified in critically ill patients with AKI [
In conclusion, the study by Jhee et al [
All authors have no conflicts of interest to declare.
Jae Seok Kim provided intellectual content of critical importance to the work. Byoung-Geun Han participated in the conception and wrote the manuscript. All authors read and approved the final manuscript.