Medicina (Buenos Aires)
versión On-line ISSN 1669-9106
Many children with chronic renal insufficiency (CRI) show growth retardation. Our objective is to describe the natural history of growth in patients with CRI, its pathogenesis and its optimization. Final height remains below percentile 3 in 77% of male and 71% of female patients. The etiology of growth retardation in these children is multifactorial: age at onset, primary renal disease, fluid and electrolyte abnormalities especially acidosis, renal osteodystrophy, inadequate caloric intake and perturbations of growth factors are all implicated. Post Tx, immunosuppressive corticoid therapy and reduced glomerular filtration rate have a significantly negative effect on final height. Growth retardation in both CRI and renal Tx patients is not the result of abnormal growth hormone secretion or decreased levels of IGF-I, but rather of elevated levels of IGF-I binding proteins inhibiting the bioavailability of the IGFs. Optimization of growth includes reduced corticoid dose, alternate-day instead of daily prednisone therapy, or substituting deflazacort for methylprednisone. Several studies have shown that growth hormone (GH) therapy at a dose of 30 UI/m2/week results in growth improvement and this led the Food and Drug Administration to approve the use of GH prior to Tx. The response to GH is better during conservative therapy, less in allograft recipients and substantially less while undergoing dialysis. In conclusion, in those children with short stature, GH treatment should begin at an early age and during conservative therapy, trying to shorten dialysis in order to attain better height at the time of renal transplantation.
Palabras llave : Chronic renal insufficiency; Renal transplant; Dialysis; Growth retardation and renal insufficiency.