Diagnostic Radiology/Musculoskeletal Imaging/Metabolic Basic/Renal Osteodystrophy
Renal osteodystrophy is a very broad term used to describe all of the pathologic features of bone related to renal failure. Renal failure and modern therapies (including peritoneal dialysis, hemodialysis, and renal transplant) result in derangments in calcium, phosphate, parathyroid hormone, and bone metabolism.
Chronic renal disease leads to hyperphosphatemia (which binds serum calcium) and decreased production of 1,25-dihydroxycholecalciferol (important in gut uptake of calcium) by the proximal convoluted tubule. Low serum calcium results, which stimulates the production of parathyroid hormone (PTH) by the parathyroid glands. PTH acts to increase bone osteoclast activity, to decrease osteoid formation by the osteoblasts, to increase the kidney's production of 1,25-dihydroxycholecalciferol, to increase active calcium resorption, and to decrease phosphate reabsorption.
In the setting of untreated renal disease, PTH is elevated and resultant high-turnover bone disease occurs. Specifically, hyperparathyroidism leads to bone resorption, commonly from subperiosteal regions and tufts of the phalanges, proximal humerus, tibia and femur, distal clavicle, and calvarium.
The prevalence of hemodialysis and renal transplantation, which helps to normalize PTH, has helped changed the presentation of this disease to a lower-turnover bone disorder. Phosphate binding compounds, including aluminum, inhibit osteoblast activity and contribute to the spectrum of disease.
Renal osteodystrophy can have varied presentation, from vague complaints of bone pain and tenderness to striking skeletal deformity. In adults, the spectrum of disease is dominated by osteomalacia (and resultant bone weakness), and findings of hyperparathyroidism. In children, whose active development is at risk, skeletal deformities (rickets) are more prominent. These include skull flattening in neonates, bowing deformities of the appendicular skeleton in children, and in early adolescence, scoliosis and SCFE. Both adults and children are at increased risk of fracture. Children are additionally at risk of growth retardation.
Imaging findings are many and quite varied. Some of the more prevalent are:
- osteopenia - often seen early.
- thinning of cortices and trabeculae.
- "salt and pepper" skull.
- subperiosteal resorption
- "rugger jersey" spine—sclerosis of the vertebral body end plates.
- primary or secondary hyperparathyroidism
- multiple myeloma
- calcium pyrophosphate deposition disease (CPPD)
- Renal osteodystrophy, University of Washington Department of Radiology
- Wikipedia listing for osteomalacia.
- Wikipedia listing for rickets.
- Medline Plus listing for rickets.
- Haas M. Renal osteodystrophy. Wien Med Wochenschr. 2004;154(5-6):107-18.
- Slatopolsky E, Gonzalez E, Martin K. Pathogenesis and treatment of renal osteodystrophy. Blood Purif. 2003;21(4-5):318-26.
- Martin KJ, Olgaard K, Coburn JW, et al. Diagnosis, assessment, and treatment of bone turnover abnormalities in renal osteodystrophy. Am J Kidney Dis 2004 Mar; 43(3):558-65.
- Kline MJ. Osteomalacia and renal osteodystrophy. 2001 Dec, Emedicine.com.