The pathogenesis of increased PTH levels in HF is multifactorial: reduced cardiac output and subsequent renal impairment as well liver dysfunction leading to reduced vitamin D production; intestinal congestion jeopardizes dietary Ca2+ and vitamin D absorption; the use of furosemide is associated with increased divalent cation excretion and hyperaldosteronism, both associated with secondary hyperparathyroidism [22,59]. The gene discussed is PTH; the disease is hydrops fetalis.