Learning objectives: To review the normal growth pattern in childhood and its alteration in chronic kidney disease. To understand the mechanisms believed to be responsible for growth failure in chronic kidney disease. To understand the new evidence supporting therapy for growth failure in chronic kidney disease. To identify targets for future therapies for treatment of growth retardation in chronic kidney disease. Introduction 1 2 4 5 6 Alteration of normal growth patterns in CKD Linear growth is unique to childhood. Complex biological processes are responsible for maintaining normal growth. 7 5 3 7 1 GH and IGF axis 1 8 9 Fig. 1 IGFBPs 8  8 10 GH resistance GH receptors 11 12 13 Janus kinase/signal transducer and activator of transcription signaling 2 14 14 Fig. 2 22 23 SOCS 14  15 16 IGF and IGFBP 17 18 19 20 21 22 23 21 24 25 26 25 Ghrelin 27 Ghrelin has been shown to increase the release of GH which is amplified by co-administration of GHRH, and acts at the level of the hypothalamus and pituitary. The role of ghrelin in the growth abnormalities in CKD has yet to be defined. Treatment with recombinant human growth hormone 28 29 3 1 1 Fig. 3 Asterisks P daggers P 1  26 30 31 25 31 31 2 3 Targets for future therapy: Treatment with recombinant IGF-1 32 33 34 Combined use of rhGH and rhIGF-1 35 Combined use of rhIGF-1 and rhIGFBP3 32 36 IGFBP displacers 37 Conclusion This review of the literature lends support to the concept that CKD is associated with GH “resistance”. Despite adequate treatment with rhGH and improvement in catch-up growth, children with CKD display a final adult height that is often below the genetic target. The potential for newer therapies with rhIGF-1, combined use of rhGH and rhIGF-1, combined use of rhIGF-1 and rhIGFBP3 or IGFBP displacers to improve both the short and long term outcomes in the treatment of the disturbances in the GH/IGF-1 axis in CKD awaits future investigations.