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Recent clinical observations underline the link between bone disease and disturbances of mineral metabolism with increased morbidity and mortality of Chronic Renal Failure (CRF). Indeed, in patients with Chronic Kidney Disease (CKD), bone disease may occur either with normal glomerular filtration rate (renal tubular disorders involving pH, Calcium or Phosphate metabolism) or with reduced glomerular filtration rate (the complex endocrine disorder of secondary hyperparathyroidism of CRF). Recently, to underline the clinical burden of this type of secondary hyperparathyroidism, a new clinical term has been introduced: CKD-MBD (chronic kidney disease-mineral and bone disorder). Besides bone disease, the endocrine derangements of mineral metabolism and the accelerated calcification processes of vessel walls are considered together in this syndrome, to highlight the pathogenetic link with cardiovascular disease and the eventual morbidity and mortality. The gold standard technique to diagnose renal osteodystrophy still remains the invasive bone biopsy. The less invasive biomarkers and radiologic techniques are less reliable to evaluate bone histology but are necessary to study the hormonal condition and the mechanical performance of the skeleton, respectively. As for therapy, it has been mostly focused on the control of secondary hyperparathyroidism, but this does not impact significantly the high fracture rate of renal patients. New drugs employed for osteoporosis and targeting specific functions of bone cells promise to open new therapeutic frontiers for renal osteodystrophy and CKD-MBD.