Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease: An Overview

George R. Bailie, PharmD, PhD, FCCP; Shaul G. Massry, MD

Disclosures

Pharmacotherapy. 2005;25(12):1687-1707. 

In This Article

Bone and Mineral Metabolism in Chronic Kidney Disease

Consequences of Derangements

The features and consequences of derangements in mineral metabolism in CKD are the following[3]:

  • Hypocalcemia, then hypercalcemia

  • Secondary hyperparathyroidism

  • Hyperphosphatemia

  • Defective intestinal absorption of calcium

  • Impaired production of calcitriol

  • Bone disease

  • Soft-tissue calcification

Disturbances in mineral and bone metabolism are common in patients with CKD and are associated with increased morbidity, such as bone pain, increased frequency of fractures, bone deformity, myopathy, muscle pain, and ruptures of tendons, as well as retarded growth in children. Derangements in bone metabolism lead to soft-tissue calcification, the long-term effects of which have become an area of growing concern for patients with CKD.[4] Calcification of the lung leads to impaired pulmonary function, pulmonary fibrosis, pulmonary hypertension, right ventricular hypertrophy, and right-sided chronic heart failure. Vascular calcification leads to ischemic lesions, soft-tissue necrosis, and difficulties for kidney transplantation. Elevations in the calcium-phosphorus product are clearly associated with calcification of coronary arteries and with cardiovascular-related mortality in patients undergoing dialysis.[5] Cardiovascular-related deaths remain the primary cause of mortality in patients with end-stage renal disease.

Hyperphosphatemia, hyper- or hypocalcemia, and increased parathyroid hormone (PTH) plasma concentrations, all commonly observed in CKD, are also associated with increased mortality.[6] Thus, prevention of the disturbances in mineral and bone metabolism and their management early in the course of CKD are vital for improving the patient's quality of life and longevity.

Pathophysiology

The processes causing disordered mineral metabolism and bone disease have their onset in the early stages of CKD and continue throughout the course of progressive loss of kidney function. A review of the etiology of renal bone disease, the pathophysiology of soft-tissue calcification, and the evidence for the association between coronary vessel calcification and mortality is beyond the scope of this article. To that end, the reader is referred elsewhere for thorough reviews;[7,2] however, the basic process is outlined in Figure 1.[3]

Figure 1.

Pathogenesis of abnormalities in mineral metabolism and bone disease in chronic kidney disease (CKD). GFR = glomerular filtration rate; 1,25(OH)2D = 1,25-dihydroxyvitamin D; 1,25(OH)2D3 = 1,25-dihydroxyvitamin D3; PTH = parathyroid hormone. (Adapted with permission from reference 3.)

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