Timmermans SAMEG, et al. - Given hypertensive emergency can induce thrombotic microangiopathy (TMA) in the kidneys with high rates of end-stage renal disease (ESRD) and vice versa, and the conundrum of hypertension as the trigger of TMA or result of TMA on the framework of defects in complement regulation is difficult, researchers investigated complement-mediated TMA by examining patients with hypertensive emergency and TMA on kidney biopsy for ex vivo C5b9 formation on the endothelium and rare variants in complement genes. They noted that 18 (69%) out of 26 cases at the presentation had massive ex vivo C5b9 formation on resting endothelial cells, including 9 patients with at least one rare genetic variant. Progression to ESRD was revealed in 13 (72%, N = 18) and 3 (38%, N = 8) patients with massive and normal ex vivo complement activation, respectively. Overall, experts concluded that the categorization of patients with hypertensive emergency and TMA into distinct classes may be achieved by evaluating both ex vivo C5b9 formation and screening for rare variants in complement genes, with potential therapeutic and prognostic implications. An algorithm to identify patients carrying the highest risk for defects in complement regulation was proposed by experts.