Assessment and treatment of short stature in pediatric patients with chronic kidney disease: a consensus statement

Abstract

Growth failure is a clinically important issue in children with chronic kidney disease (CKD) and is associated with significant morbidity and mortality. Many factors contribute to impaired growth in these children, including abnormalities in the growth hormone (GH)-insulin-like growth factor-I (IGF-I) axis, malnutrition, acidosis, and renal bone disease. The management of growth failure in children with CKD is complicated by the presence of other disease-related complications requiring medical intervention. Despite evidence of GH efficacy and safety in this population, some practitioners and families have been reluctant to institute GH therapy, citing an unwillingness to comply with daily injections, reimbursement difficulties, or impending renal transplantation. Suboptimal attention to growth failure management may be further compounded by a lack of clinical guidelines for the appropriate assessment and treatment of growth failure in these children. This review of growth failure in children with CKD concludes with an algorithm developed by members of the consensus committee, outlining their recommendations for appropriate steps to improve growth and overall health outcomes in children with CKD.

Improvement in Growth After 1 Year of Growth Hormone Therapy in Well-Nourished Infants with Growth Retardation Secondary to Chronic Renal Failure

“…Length and weight SDS and other nutritional indexes did not change in the group of children who were not treated with GH, indicating that the nutritional management precluded the aggravation of growth failure. In concordance with former studies of older children (17,18), the growth-promoting effect of GH was not associated with exaggerated advancement of bone maturation, worsening of renal function, more difficult metabolic control, or higher incidence of adverse effects. A retrospective study recently showed improvement of height SDS in a group of infants who had CRF and were treated with 0.35 mg/kg per wk GH for 2 years (19).…”

Slipped capital femoral epiphysis and its association with endocrine, metabolic and chronic diseases: A systematic review of the literature

“…Acidosis also changes the pulse amplitude of GH secretion, suppresses serum IGF-1 and decreases the expression of hepatic IGF-1 mRNA, hepatic growth hormone receptor (GHR) mRNA and epiphyseal IGF-1 mRNA [44][45][46].…”

Chronic Kidney Disease: A Life Course Health Development Perspective

“…The in-utero or maternal factors are often major contributors to antenatal renal function and yet may be overlooked during gestation. The impact of ex-utero damage is still not well vetted, but either alone or in combination with in utero insults, may lead to an increased vulnerability to subsequent renal damage as the patient ages and lead to progressive chronic kidney disease sive in the CKD population despite control of modifiable factors such as nutrition, anemia, and hypoparathyroidism (Mahan and Warady 2006). Initial metabolic evidence of growth failure includes phosphate wasting in early CKD (Ben-Dov et al 2007) with progression to decreasing calcitriol levels in stages 2-3 CKD resulting later in low 1,25(OH)2 vitamin D levels and hyperparathyroidism in stages 3-4 (Heidbreder et al 1997), with further hyperphosphatemia and hypocalcemia causing defective mineralization and bony abnormalities as CKD worsens (Wesseling-Perry et al 2012).…”