COVID-19 as a potential trigger of complement-mediated atypical HUS
Carine El Sissy, Antonin Saldman, Gilbert Zanetta, Paula Vieira Martins, Coralie Poulain, Raphaël Cauchois, Gilles Kaplanski, Jean-Pierre Venetz, Mickaël Bobot, Hélène Dobosziewicz, Laurent Daniel, Marie Koubi, Salima Sadallah, Samuel Rotman, Christiane Mousson, Manuel Pascual, Véronique Frémeaux‐Bacchi, Fádi Fakhouri
Abstract
Endothelial cell (EC) injury has emerged as a hallmark of infection resulting from severe respiratory coronavirus 2. mplement dysregulation is also a well-established pathogenic mechanism of a rare form of renal thrombotic microangiopathy (TMA), the atypical hemolytic uremic syndrome (aHUS), triggered by complement-induced EC damage. date, renal TMA has been very rarely documented in the COVID-19 setting. We report on 5 patients with COVID-19associated renal TMA, among whom 4 tested patients carried complement genetic susceptibility factors for aHUS.