The growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis is disrupted in chronic kidney disease (CKD), yet its upstream regulator, growth hormone–releasing hormone (GHRH), has never been measured in kidney failure. GHRH receptors are expressed in the kidney, and preclinical studies suggest GHRH agonists exert reno- and vasoprotective effects independent of GH. Whether GHRH changes after kidney transplantation (KTx) or relates to gut-derived uremic toxins is unknown.
