The kidney provides the major, if not the only, route for the eliminat
ion of certain substances that adversely can affect mineral homeostasi
s and bone when accumulated in higher concentrations. Renal osteodystr
ophy represents a spectrum from high to low turnover lesions of bone,
and the specific pattern may change during the evaluation of chronic r
enal failure and as a consequence of specific therapeutic intervention
s. This article focuses on the pathogenesis of secondary hyperparathyr
oidism, renal bone diseases, and the clinical manifestations of end-st
age renal bone diseases, and the clinical manifestations of end-stage
renal disease. Biochemical features of the disease are discussed, foll
owed by a review of the methods of treatment for renal osteodystrophy.