Purpose of review: Fractures are a common problem in chronic kidney disease (CKD). The 2009 KDIGO (Kidney Disease: Improving Global Outcomes) review of the bone and mineral disorders highlighted areas of uncertainty and stressed the importance of further research. This review includes studies published since that report with a focus on the bone.
Recent findings: Bone biopsies have shown a shift toward more adynamic bone, which may be associated with vascular calcifications. There are important racial differences in skeletal metabolism. Bone density may be helpful in identifying patients who have fractures, but neuromuscular tests perform better than radiographic ones. Even if bone density can predict fractures, it is still not clear what can be done in patients who have advanced stages of CKD. New data show interrelationships of fibroblast growth factor 23 (FGF23) secretion, parathyroid hormone, and wnt-signaling pathways. High FGF23 could have a negative impact on the bone.
Summary: These advances suggest that caution must be used prior to treatment with medications that inhibit bone turnover. Racial differences in response to vitamin D therapy need more careful delineation. Medications which inhibit wnt-signaling offer hope but development of new therapies to treat the bone disease will rely on further understanding of bone and vascular physiology.