Dysfunction of FH (whether due to low serum level or due to poor protein function) will lead to failure of inactivation of alternative pathway c3 convertase (C3bBb) on the cell surfaces, including the glomerular endothelial cells leading to severe, unchecked complement activation, and consequently endothelial injury that results in the proliferative lesions of LN, and occasionally may result in secondary thrombotic microangiopathy (14). The gene discussed is FH; the disease is Genetic thrombotic microangiopathy.