Open AccessAliskiren and the dual complement inhibition concept
Author(s) -
María Vanessa Perez-Gomez,
Alberto Ortíz
Publication year - 2019
Publication title -
clinical kidney journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.033
H-Index - 40
eISSN - 2048-8513
pISSN - 2048-8505
DOI - 10.1093/ckj/sfz142
Subject(s) - aliskiren , eculizumab , glomerulopathy , medicine , complement system , complement (music) , renin–angiotensin system , immunology , antibody , kidney , glomerulonephritis , chemistry , biochemistry , phenotype , complementation , blood pressure , gene
In this issue of Clinical Kidney Journal, Plasse et al. report on the use of high-dose aliskiren as an adjunct therapy in a patient treated with eculizumab for haemolytic uraemic syndrome (HUS). This follows the recent description of the complement factor 3 (C3) activating activity of the enzyme renin and the successful therapeutic use of the direct renin inhibitor aliskiren in three cases of C3 glomerulopathy/dense deposit disease. We discuss the potential clinical and pathophysiological implications of these reports on nephropathies linked to complement, from HUS to C3 glomerulopathy to immunoglobulin A nephropathy as well as the concept of dual complement inhibition for kidney disease.