Less is known about the role of hepatokines (adropin, fetuin-A, selenoprotein P, alpha-1-microglobulin) produced by hepatocytes as a result of oxidative stress and microvascular inflammation in progressive dysfunction of other organs in HF, including adverse cardiac remodeling, renal damage, adipose tissue inflammation and skeletal muscle myopathy [20]. This evidence concerns the gene AHSG and hydrops fetalis.