title: Complement activation in the tubulointerstitium: AKI, CKD, and in between.
abstract: Complement activation is actively regulated to prevent injudicious activation, such as on peritubular endothelia and basolateral aspects of tubules. Miao et al. studied mice in which the key complement regulator, Crry, was deleted from tubular cells. This lacked functional consequence in unmanipulated animals. Yet, following ischemia-reperfusion, there was greater injury due to alternative pathway activation of C5. When the balance between complement activation and regulation is tipped towards the former, pathologic complement activation can ensue.
authors.affiliation: Division of Nephrology, Department of Medicine, University at Buffalo School of Medicine and Biomedical Sciences, Buffalo, New York, USA.
authors.forename: Jyoti E
authors.initials: JE
authors.lastname: Brar
authors.affiliation: Division of Nephrology, Department of Medicine, University at Buffalo School of Medicine and Biomedical Sciences, Buffalo, New York, USA.
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Quigg
mesh_terms: D000818:Animals; D020022:Genetic Predisposition to Disease; D011951:Receptors, Complement / Q000235:genetics* / Q000378:metabolism*; D015427:Reperfusion Injury / Q000235:genetics* / Q000473:pathology*
chemical_list: D011951:Receptors, Complement