Purpose of review
Disturbances in calcium–phosphate homeostasis play an important role in children with chronic kidney disease, and not only cause renal osteodystrophy but also result in increased cardiovascular morbidity and mortality. This review outlines the current aspects in the pathogenesis, diagnostic approach and treatment of renal osteodystrophy.
The pathogenesis of renal osteodystrophy is under strong influence of the fibroblast growth factor 23/Klotho system, which is able to enhance phosphate excretion and reduce calcitriol synthesis in the kidney. Fibroblast growth factor 23 increases tissue calcinosis and is cardiotoxic, and is independently associated with mortality. Despite improvement in diagnostic imaging (bone density measurements), determination of biomarkers, mainly parathyroid hormone, still plays a central role. New treatment options resulted in improved bone health and also a reduction in mortality was achieved in adults with calcium-free phosphate binders. Substitution of active and inactive vitamin D is important and also has a beneficial effect on proteinuria.
Knowledge about the biochemical and molecular mechanisms of renal osteodystrophy is increasing dramatically and has an impact not only to bone health but also overall morbidity and mortality. This will ultimately translate into further improved diagnostic approaches and novel treatment options.