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      Skeletal Disproportion in Children with Chronic Renal Disease

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          Objectives: To assess stature and skeletal disproportion in children with chronic renal disease. Methods: Cross-sectional study of height (HT), sitting height (SH), subischial leg length (SILL), sitting height/height ratio (SH:HT) and disproportion score (SH SDS minus SILL SDS) in 56 children (M:35) with median age 11.4 years (range 4.5,18.7) with chronic renal disease. Results: There were 19 children with chronic renal insufficiency, 6 receiving peritoneal dialysis and 31 after renal transplant. The median HTSDS for the whole group was –1.21 (–2.8, 0.35). The median SH:HT ratio in non-transplanted children and renal transplant were 0.51 (0.49, 0.53) and 0.50 (0.48, 0.53), respectively (p = 0.02). The median disproportion score of the whole group was –3.2 (–4.8, –1.8). There was a significant correlation between disproportion score and SH:HT (r = 0.5, p = 0.005). SH:HT ratio was negatively related to duration of illness (r = 0.4, p = 0.005). Conclusion: Children with chronic renal disease have significant body disproportion and this may be due to a disproportionately greater effect of disease and treatment on spinal growth.

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          Effect of growth hormone treatment on the adult height of children with chronic renal failure. German Study Group for Growth Hormone Treatment in Chronic Renal Failure.

          Growth hormone treatment stimulates growth in short children with chronic renal failure. However, the extent to which this therapy increases final adult height is not known. We followed 38 initially prepubertal children with chronic renal failure treated with growth hormone for a mean of 5.3 years until they reached their final adult height. The mean (+/-SD) age at the start of treatment was 10.4+/-2.2 years, the mean bone age was 7.1+/-2.3 years, and the mean height was 3.1+/-1.2 SD below normal. Fifty matched children with chronic renal failure who were not treated with growth hormone served as controls. The children treated with growth hormone had sustained catch-up growth, whereas the control children had progressive growth failure. The mean final height of the growth hormone-treated children was 165 cm for boys and 156 cm for girls. The mean final adult height of the growth hormone-treated children was 1.6+/-1.2 SD below normal, which was 1.4 SD above their standardized height at base line (P< 0.001). In contrast, the final height of the untreated children (2.1+/-1.2 SD below normal) was 0.6 SD below their standardized height at base line (P<0.001). Although prepubertal bone maturation was accelerated in growth hormone-treated children, treatment was not associated with a shortening of the pubertal growth spurt. The total height gain was positively associated with the initial target-height deficit and the duration of growth hormone therapy and was negatively associated with the percentage of the observation period spent receiving dialysis treatment. Long-term growth hormone treatment of children with chronic renal failure induces persistent catch-up growth, and the majority of patients achieve normal adult height.
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            Placebo-controlled, double-blind, cross-over trial of growth hormone treatment in prepubertal children with chronic renal failure

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              Mechanism of transplantation-associated bone loss.

               Randy Sprague (2000)
              Successful renal transplantation is associated with abnormalities of function of the musculoskeletal system. Some of these problems result from incomplete resolution of abnormalities of mineral metabolism associated with end-stage renal disease, such as persistent hyperparathyroidism, hypercalcemia and decreased vitamin D. However, it is now appreciated that skeletal abnormalities, especially osteopenia with subsequent fractures, develop following transplantation. Most of the new disorders of bone and mineral metabolism are secondary to the immunosuppression required to prevent rejection. Glucocorticoids can not only induce osteonecrosis, but also increase the risk for fractures by decreasing cancellous bone mass and synthesis of bone matrix, and dampen the linear growth response in pediatric recipients. Other immunosuppressive agents, especially the calcineurin-phosphate inhibitors, independently exert a negative effect on bone. Future investigation is required to develop a better understanding of the pathophysiologic mechanisms involved in post-transplant bone disease in order to develop rational approaches for prevention and treatment.

                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                19 November 2003
                : 60
                : 5
                : 221-226
                aBone and Endocrine Research Group, and bThe Renal Unit, Royal Hospital for Sick Children, Yorkhill, Glasgow, UK
                74035 Horm Res 2003;60:221–226
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 2, References: 23, Pages: 6
                Original Paper


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