Imaging description

Renal osteodystrophy (ROD) is a general term for a variety of abnormalities of musculoskeletal system secondary to calcium and phosphate metabolic disorder in chronic end-stage renal disease. Hypocalcemia in chronic renal insufficiency leads to secondary hyperparathyroidism, which results in osteoclastic subperiosteal, subligamentous, subchondral, and trabecular bone resorption [1]. It also results in secondary osteomalacia and rickets due to aluminum intoxication, vitamin D deficiency, hypocalcemia, and acidosis. This can lead to complex bony changes. Osteosclerosis in renal osteodystrophy is related either to excessive osteoblastic bone production due to bone resorption or to increased production of mineralized osteoid. Reduced radiodensity in ROD reflects osteomalacia, osteitis fibrosa cystica, and osteoporosis [1].

When sclerotic changes occur in the spine, they do so parallel to the vertebral endplates, creating alternating bands of sclerosis along the endplates and a relative lucency in the middle, giving rise to radiographic findings of the “rugger jersey” spine, classically evaluated in the lateral radiographs [2]. In the spinal column, there is disappearance of transverse trabeculae with preservation of vertical trabeculae, resulting in characteristic vertical striations (Fig. 91.1). The prolonged T1 relaxation time on MRI seen in renal osteodystropy is associated with increased marrow cellularity, thickened trabeculae, and peritrabecular fibrosis [3]. The overall result is decreased T1 signal of the vertebral bodies, which may be mistaken for lymphoma/leukemia involvement or diffuse metastasis. Secondary hyperparathyroidism may also result in soft tissue calcifications (Fig. 91.2)