Renal Osteodystrophy of the Cervical Spine: Neurosurgical Implications

To the Editor: I read with interest the report by Nair et al ⁽¹⁾. Skeletal complications of chronic renal failure have interested the nephrologists and neurosurgeons at the University of Alabama for some time. Recent work by our group and others has revealed that the destructive, destabilizing spondylarthropathy that long-term dialysis patients develop in the cervical and, rarely, in the thoracolumbar spinal segments is not renal osteodystrophy, but is termed dialysis-associated spondylarthropathy (DAS). It is a distinct entity from renal osteodystrophy caused by secondary hyperparathyroidism. DAS is the result of the diffuse deposition and bony disc and ligamentous infiltration by beta-microglobulin (B2M). This 11,800 molecular weight protein is filtered by the intact, functional glomerulus of the kidney. It cannot be eliminated by contemporary dialysis filters because of its large size. Consequently, patients with chronic renal failure may have serum levels of B2M as much as 50 to 60 times normal.

B2M is deposited throughout the body and is thought to cause a variety of musculoskeletal disorders common to patients with chronic renal failure (carpal tunnel syndrome, tenosynovitis, cardiomyopathy). In the spine, it forms a matrix that is distinct from amyloid. Tissue removed from 12 consecutive surgical patients has stained positive for B2M, negative for amyloid (Congo red stain) and has been sterile on culture medium. At what point bony replacement leads to spinal instability in some of these patients is unknown. DAS results in vertebral body and end plate erosion and disc space collapse, with resultant spinal instability, often with cord compression. This destructive spondylarthropathy may affect adjacent disc spaces or may produce skip lesions (Fig. 4).

Figure 4.

Lateral c-spine radiograph of a 57-year-old man with chronic renal failure (chronic glomerulonephritis) treated with dialysis (only) for 108 months. He presented with severe neck pain and a progressive cervical myeloradiculopathy. This patient underwent vertebrectomies with cord decompression C3 through C6, followed by C2 through C7 allograft strut fusion and halo immobilization. The tissue removed at surgery stained positive for B2M, negative for amyloid.

In comparison, renal osteodystrophy, characterized by subchondral and subperiosteal bone resorption in conjunction with osteomalacia, osteoporosis, and osteosclerosis usually results in alternating osteolysis with osteosclerosis parallel to the vertebral end plates. This appearance has been defined as the “rugger jersey spine.”

Magnetic resonance imaging reveals DAS to be of low-signal intensity on both T1- and T2-weighted images. DAS has never been reported in conjunction with a high erythrocyte sedimentation rate and/or C-reactive protein levels. These latter data should help distinguish DAS from discitis/osteomyelitis. Infection in the spine is not uncommon among chronic dialysis patients as Nair et al. have discussed, but it is usually associated with elevations in erythrocyte sedimentation rate and C-reactive protein levels and is typically of high-signal intensity on T2-weighted magnetic resonance images (because of the increase in water associated with the infectious process). Paravertebral or epidural masses identified on magnetic resonance images are common with infection but have not been reported with DAS.

Patients with DAS occasionally will require neural decompression and/or spinal stabilization. We have been relying on allograft bone as the strut fusion substrate after corpectomy (often multilevel), followed by halo immobilization, with good results (B2M deposition occurs throughout the skeletal system in these patients). We have employed internal fixation hardware with some of these patients, but its use in soft bone is unproven. These are typically very sick patients, but as Nair et al. have demonstrated, they can be effectively and successfully managed with diligence and a multidisciplinary approach.