APOB and familial hyperaldosteronism: Pathogenic/likely pathogenic mutations considered to be responsible for monogenic FH were identified in 25 out of the 52 of probands (48%): 24 with mutations in LDLR, 4 homozygous FH and 20 heterozygous FH (HeFH) carriers and 2 with a mutation in APOB (one of them also carried a pathogenic mutation in LDLR).