STUDY OF BONE CHANGES IN CHLDREN WITH DIFFERENT RENAL DISEASES

Abstract

The kidney plays a central role in the control of mineral homeostasis, it maintains the external balance of calcium, phosphorus, and magnesium, synthesizes 1.25 dihydroxy vitamin 03, and 24.25 dihydroxy vitamin 03 and serves as a target organ for degradation of parathyroid hormone (PTH) and clearance of PTH from the circulation. In addition, the kidney provides the major, if not the only rout for elimination of certain substances such as aluminum and B2 microglobulin , that can adversely affect mineral homeostasis and bone when accumulated in high concentration , therefore it is not surprising that progressive reduction of nephron mass is associated with alterations in mineral metabolism . Renal osteodystrophy represents a spectrum from high to low turnover lesions of bone and specific pattern may change during evolution of chronic renal failure as a consequence of specific therapeutic interventions(Salusky, 1995).

As renal disease advances, the production of active vitamin 0 (1.25 (OH)2 03] is impaired leading to reduced intestinal calcium absorption and reduced renal excretion (Schreire and Gottschalk ,1997).

Abnormalities in the metabolism of calcium, phosphorus, vitamin D and parathyroid hormone (PTH). lead to severe abnormalities in the skeleton and tissues in renal failure. Characteristic changes in calcium metabolism include decreased intestinal calcium absorption secondary to low plasma level, bone demineralization, and soft tissue calcifications. An initial increase in serum phosphate and decrease in serum calcitriol concentrations have been