Osteoporosis and adynamic bone in chronic kidney disease

Abstract

Among the chronic kidney disease–mineral bone disease (CKD-MBD) disorders, osteoporosis and adynamic bone are highly prevalent, and they have been consistently associated with low bone mass, bone fractures, vascular calcifications and greater mortality in general and CKD populations. Despite the fact that osteoporosis and adynamic bone have similar clinical outcomes, they have different pathogeneses and clinical management. In osteoporosis, there is a lack of balance between bone formation and bone resorption, and less new bone is formed to replace bone losses. Osteoporosis is defined by the World Health Organization as “a disease characterized by low bone mineral density and micro architectural deterioration leading to low bone strength and increased risk of fractures.” In the general population, there is a good correlation between dual-energy X-ray absorptiometry measurements and bone fractures, but this is not the case with CKD patients. Despite the fact that we have a great number of active antiosteoporotic drugs, the experience in CKD patients is limited. Adynamic bone is suspected based on biochemical parameters, mainly parathyroid hormone (PTH) and bone alkaline phosphatase, but it needs to be proven using a bone biopsy, where a low or zero bone formation rate and a reduction or absence of osteoblasts and osteoclasts should be found. The clinical management of adynamic bone has important limitations and currently does not allow taking many active measures. Treatment is mainly based on the prevention of risk factors known to induce PTH oversuppression, such as aluminium and calcium load and very high doses of vitamin D receptor activators. Due to the limitations in the treatment of both conditions, prevention plays a key role in the management of these disorders.