Is there a practical role for bone biopsy in chronic kidney disease?
Chronic Kidney Disease–Mineral and Bone Disorder (CKD‐MBD) encompasses the mineral, bone, hormonal and calcific cardiovascular abnormalities that develop in patients with CKD.1 These are influenced by age, nutrition, menopausal status, corticosteroids, vitamin D status, levels of FGF23 and other factors including changes over time in dialysis regimens and the choice of phosphate binders.2 Fracture risk in patients with CKD‐MBD is much higher than in the general population and increases across the CKD spectrum. Both bone volume and bone quality, incorporating changes in turnover, mineralization, cortical porosity and trabecular bone architecture, deteriorate through CKD stages 3 to 5. Bone mineral density (BMD) by standard dual‐energy X‐ray absorptiometry does not capture many of these factors, and consequently, BMD thresholds for quantitating fracture risk are higher in CKD patients.3 Measurement of serum parathyroid hormone (PTH) and biochemical bone turnover markers are helpful but also lack sensitivity and specificity for diagnosing the bone pathology that is present. Until newer diagnostic modalities such as use of the trabecular bone score, high‐resolution peripheral quantitative CT and quantitative CT with finite element analysis have been adequately trialled in the CKD cohort, bone biopsy remains the gold standard for assessing the evolving skeletal changes of renal osteodystrophy (ROD) and the only currently available tool that accurately delineates effects of therapies.
Alterations to bone morphology in CKD‐MBD comprise a heterogeneous group of metabolic bone disorders that develop as CKD progresses and affect the volume of cortical and trabecular bone (osteoporosis/osteosclerosis), bone turnover (high in hyperparathyroidism, and low in adynamic bone disease) and mineralisation rates (prolonged in osteomalacia). To achieve standardization in the reporting of bone biopsies, and so that the limited number of biopsy studies might be compared, the histomorphometric indices that have been adopted are turnover (T), mineralisation (M) and bone volume (V); the TMV classification. Often, only measurements of trabecular bone are reported; however, prominent cortical changes of increased porosity and reduced cortical thickness occur in patients with CKD (Fig. 1). These under‐reported changes are critical, because the cortex contributes significantly to bone structure and integrity in patients with CKD as it does in the normal population.