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Introduction: This study aimed to investigate changes in complement system‐related molecules in patients undergoing hemodialysis. Methods: Patients >18 years of age on maintenance hemodialysis were included. Using enzyme‐linked immunosorbent assays (ELISA) methods complement related molecules ficolin‐1, ficolin‐2, ficolin‐3 mannose‐binding lectin, long pentraxin 3, complement activation products C3c, and complement activation potentials were measured before and after a single hemodialysis treatment. All patients were dialyzed with synthetic high flux filters >1.6 m2, respectively, Polyamix and Polysulfone, and the Kt/V was maintained >1.3. Findings Three hundred and four patients were included. There was a modest decrease in plasma level of ficolin‐1 (p < 0.001). Ficolin‐2 was virtually depleted with median 3.9 (interquartile range [IQR]: 2.6–6.1, range 0.3–13.5) μg/ml before dialysis to median 0.0 (IQR: 0.0–0.5, range 0.0–5.5) μg/ml after dialysis (p < 0.001). No significant difference before and after hemodialysis was seen for mannose‐binding lectin and long pentraxin 3 (p > 0.05). In a random subgroup of 160 patients ficolin‐2‐binding, ficolin‐3‐mediated lectin pathway capacity and classical pathway capacity were significantly decreased due to hemodialysis. The complement capacity of the alternative pathway was increased after hemodialysis (p = 0.0101), while mannose‐binding lectin‐mediated lectin pathway capacity was unaltered (p = 0.79). There was an increase in the complement activation product C3c (p < 0.0001), while the concentration of total C4 and C3 did not change (p > 0.158). Multivariate Cox proportional hazard analyses showed an increased risk for all‐cause mortality with increasing ficolin‐2 (p = 0.002) after hemodialysis. Discussion Plasma ficolin‐2 was virtually depleted from the circulation after hemodialysis. However, elevated plasma ficolin‐2 levels after hemodialysis was independently associated with increased mortality. [ABSTRACT FROM AUTHOR]