LDLR and familial hyperaldosteronism: Researches of LDL receptor function have revealed additional mechanisms for the pathogenesis of FH (defects in apoli-poprotein [apo] B impairing binding with the LDL receptor and gain-of-function mutations in proprotein convertase subtulisin/kexin type 9 [PCSK9] that enhance LDL receptor degradation) [8].