Abstract

The development of diminished linear growth and bone deformities in pediatric patients with chronic renal insufficiency sugests disturbances in the growth plate (GP) cartilage at the end of long bones. In rodent models of renal failure, the width of the GP has been reported to be increased, decreased, or unchanged compared to rats with intact renal function. Because of the potential role of the various subtypes of renal osteodystrophy on the GP abnormalities in renal failure, we created a model of severe secondary hyperparathyroidism through dietary phosphororous supplementation and we found a similar markedly disorganized GP and diminished expression of the PTH/PTHrP receptor in the GP chondrocytes. In contrast, adynamic renal osteodystrophy induced by dietary calcium supplementation resulted significantly wider GP, particularly of the hypertrophic zone, associated with disturbances in osteoclastic/chondroclastic activity and matrix degradation. These results suggests that renal osteodystrophy may contribute to poor growth in renal failure and the mechanisms differ among the subtypes of renal bone disease. Additionally, disturbances in the growth hormone-insulin-like growth factor (GH-IGF) axis may play a role in impaired linear growth in uremia. At the level of the growth plate, decreased expressions of the IGF-I and GH receptor expression was seen only with combined treatment with GH and IGF-I. Further studies may provide novel insights into the regulation of endochondral bone growth in renal failure, thereby resulting in more effective strategies to prevent and treat growth failure in these patients.

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