Bone Health in Chronic Kidney Disease

Bone loss is the most prevalent condition and is associated with higher morbidity and mortality fractures in chronic kidney disease (CKD). Mechanisms underlying the development of osteoporosis in CKD include dysregulation of receptor activator of the NF-κB (RANK)/RANKL/osteoprotegerin system, excessive Wnt/β-catenin signaling inhibitors, and inflammatory cytokines production. Disturbed bone remodeling comprises high bone turnover disease (osteitis fibrosa cystica by secondary hyperparathyroidism or chronic inflammation) and low bone turnover disease (adynamic bone disease and osteomalacia). Reduced bone mineral density in CKD is due to multifactorial causes, including acid-base disturbances and impaired vitamin D and PTH homeostasis. Low calcitriol level is found to be an independent risk factor for hip fractures. In addition, drug-induced osteoporosis is also an important contributor, like unfractionated heparin, biguanides, glitazones, and glucocorticoids. The alteration of vitamin D metabolism in CKD predisposes bone quantity and quality loss. Supplement of nutritional vitamin D during osteoporosis treatment is beneficial in maintaining BMD in CKD and maintaining bone strength and architectural stability, no matter in high or low bone turnover disease.