Review of “Hemodialysis leads to plasma depletion of lectin complement pathway initiator molecule ficolin-2” by Nielsen et al

Study Overview

This study by Nielsen et al. investigates the impact of hemodialysis (HD) on the complement system, specifically focusing on the lectin pathway initiator molecules ficolins. The main strengths of the study include its large sample size of 304 HD patients and the comprehensive assessment of various complement components and functional capacities.

Key Findings

A major finding is the remarkable depletion of ficolin-2 after a single HD session, both at the antigenic and functional level. This depletion is likely due to adsorption of ficolin-2 onto the dialysis membranes, triggering lectin pathway activation. Interestingly, higher post-dialysis ficolin-2 levels were associated with increased mortality risk, despite its depletion.

The authors also observed slight decreases in ficolin-1 and classical pathway capacity, suggesting their potential roles in HD-induced complement activation. Additionally, the alternative pathway capacity and C3c levels increased, indicative of overall complement activation.


However, the study has some limitations. The non-included patients differed in certain characteristics, raising potential selection bias concerns. The observational design precludes causal inferences about the relationship between ficolin-2 and mortality. Furthermore, the study did not investigate specific infection or cardiovascular outcomes, which could have provided insights into potential mechanisms linking ficolin-2 depletion and adverse outcomes.


In summary, this study provides valuable insights into the intricate interplay between HD and the complement system, particularly highlighting the significant depletion of ficolin-2 and its paradoxical association with mortality risk. Further research is warranted to elucidate the underlying mechanisms and clinical implications of these findings.

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