In summary, the findings of impaired IGF-1 synthesis, together with modest elevation of GH-levels due to decreased renal clearance, and increased IGF plasma binding capacity, provides evidence of a multilevel, homeostatic failure in the GH-IGF-1 system in CKD, which has paved the way for studies proving the stimulatory growth effects of GH in short children with CKD [163]. The gene discussed is GH1; the disease is chronic kidney disease.