Patients with TA-TMA experience persistent activation of alternative complement pathway 2 to 6 weeks after GVHD onset. (A) BBPlus is a marker of alternative complement pathway activation. GVHD patients with and without TA-TMA had similar BBPlus levels at GVHD onset (point A on x-axis), but those who did not go on to develop TA-TMA experienced decreases in BBPlus levels over the next 2 to 6 weeks after GVHD onset (point B on x-axis). (B) C4d is a marker of classical complement pathway activation and is elevated in GVHD patients with and without TA-TMA at GVHD onset and decreases in both over time with no statistically significant difference in the change over time. No statistically significant differences were noted for changes in (C) C5b-9 or (D) C5a both markers of terminal complement pathway activation. Differential ongoing activation of the alternative complement pathway appears to be a determinant of developing TA-TMA.