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. 2020 Jul 30;8:399. doi: 10.3389/fped.2020.00399

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Copyright © 2020 Haffner.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The etiology of growth failure in CKD is multifactorial and includes intrauterine growth restriction (IUGR), genetic factors, such as parental height and primary kidney disease, prematurity and malnutrition which especially limits growth in children with congenital CKD. Mineral and bone disorder (CKD-MBD), metabolic acidosis, anemia, loss of electrolytes and water, and disturbances of the somatotropic and gonadotropic hormone axes are additional factors. CKD is a state of growth hormone (GH) insensitivity, characterized by a deficiency of functional insulin-like growth factor I (IGF-I), reducing GH receptor expression in target organs like the liver, disturbed GH receptor signaling via the Janus kinase signal transducers, activators of transcription (JAK2-STAT5) due to inflammation-induced SOCS (suppressor of cytokine signaling), and increased IGF-binding capacity due to excess of IGFBPs. Finally, reduced release of hypothalamic gonadotropin-releasing hormone (GnRH), due to uremia-related inhibitory factors such as angiotensin II (AngII) and steroid treatment, may result in decreased circulating levels of bioactive luteinizing hormone (LH), hypogonadism and reduced pubertal growth spurt (13). PTH, parathyroid hormone; FSH, follicle stimulating hormone; IGFBP, insulin-like growth factor binding proteins. Figure and figure legend taken from (13).