Renal Osteodystrophy in Renal Transplant

Julian Paniagua MD, Razia Rehmani MD

Key points

  • Renal osteodystrophy, also known as uremic osteopathy, is the generic term used to describe the spectrum of musculoskeletal and soft tissue findings seen in the setting of chronic renal insufficiency which may require chronic hemodialysis, peritoneal dialysis, renal transplantation and administration of various medications which disturb the delicate biochemical calcium-phosphate metabolism
  • Clinically renal bone disease may manifest as osteomalacia/rickets, secondary hyperparathyroidism, osteoporosis, adynamic bone disease, and aluminum intoxication (secondary to long term dialysis).
  • Secondary hyperparathyroidism results in biochemical disturbances with key findings including bone resorption, osteosclerosis, soft tissue calcifications and brown tumors.
  • Long term hemodialysis and renal transplantation can have several complications such as amyloid deposition, destructive spondyloarthropathy, osteonecrosis and musculoskeletal infections.
  • There are four subtypes of renal osteodystrophy: Osteitis fibrosa cystica, Adynamic bone disease, Osteomalacia, and Mixed uremic dystrophy.
  • Radiological imaging plays an essential role in early diagnosis, treatment and follow up of renal bone disease. The definitive diagnosis of renal osteodystrophy is histologic by bone biopsy. Biochemical bone markers and imaging techniques are increasingly used.
  • The following biomarkers are commonly used: Parathyroid hormone, vitamin D levels, serum calcium and phosphorus, and fibroblast growth factor receptor 23.
  • Treatment focuses on maintaining adequate parathyroid hormone, vitamin D, calcium and phosphorus levels.

Differential Diagnosis

  • Rheumatoid Arthritis
  • Seronegative Spondyloarthropathies
  • Malignancy
  • Infection

Abnormalities in bone morphology in the setting of Chronic Kidney Disease (CKD) is collectively called Renal Osteodystrophy (ROD), which is part of the syndrome of Chronic Kidney Disease-mineral and bone disorder (CKD-MBD). These systemic abnormalities are characterized by abnormal phosphorus, vitamin D, calcium and Parathyroid hormone (PTH) metabolism (1).

The pathophysiology of CKD-MBD involves several feedback loops between vasculature, intestine, bone and kidney. These feedback mechanisms maintain calcium and phosphorus balance. The serum calcium concentration is regulated by multiple factors such as PTH, vitamin D, fibroblast growth factor 23 (FGF23), calcitonin, and estrogen; Figure 1 summarizes calcium and phosphate balance. The pathogenesis of CKD-MBD are mainly attributed to secondary hyperparathyroidism, which is usually a response to the following abnormalities: Phosphate retention, decreased free ionized calcium concentration, decreased 1,25-dihydroxyvitamin D (calcitriol) concentration, and increased FGF23. There is also a decrease in the expression of vitamin D receptors, calcium-sensing receptors, fibroblast growth factor receptors, and klotho in the parathyroid glands. Secondary hyperparathyroidism ultimately causes bone resorption, osteosclerosis, brown tumors, soft tissue and vascular calcifications(2,3).

Figure 1. Summary of Calcium and Phosphate Metabolism

CKD can be caused by numerous etiologies. No organ system is left unaffected from complications of CKD and its treatment. With improved patient survival musculoskeletal complications are increasing recognized.

Key musculoskeletal imaging findings with CKD or ROD are as follows (4):

  • Decreased Vitamin D:
    • Osteomalacia

  • Increased PTH:
    • Brown tumors are caused from excess osteoclast activity and accumulation along with fibrous tissue and demineralized bone.
    • Osteosclerosis, Bone sclerosis may be diffuse. Radiographs in patients with chronic kidney disease may show diffusely increased bone radiodensity. End plates show sclerotic bands, it is known as rugger-jersey spine sign.
    • Bone resorption, Subperiosteal resorption is usually seen in radial aspects of middle phalanges of 2nd and 3rd
    • Periostitis, Demineralization is usually periosteal. Joint margins, endosteal, subchondral, subligamentous areas, cortical bone or trabeculae may also be involved.
    • Osteopenia and fractures. Osteopenia manifested as thinning of cortices and trabeculae.
  • Increased Phosphate and Calcium:
    • Soft tissue deposition.
    • Crystal deposition disease such as gout, chondrocalcinosis, and oxalosis.
  • CRI treatment complications:
    • Steroids- Chronic steroid use results in osteopenia and fractures, avascular necrosis, decreased immunity and predisposition to osteomyelitis and septic arthritis, soft tissue hematoma.
  • Dialysis:
    • Complications include aluminum toxicity.
    • amyloidosis spondyloarthropathy.
  • Chronic acidosis:
    • Can cause tendon rupture.

Treatment of ROD is focused mainly on maintaining adequate vitamin D, calcium and phosphorus levels, thereby avoiding progressive increase of PTH. This can be achieved by reducing dietary phosphorus, using phosphate binders as needed, calcium supplements and/or native vitamin D. If there is no appropriate response, treatment with calcitriol, vitamin D analogs and antiresorptives should be considered. Failure of medical/pharmacological therapy should prompt consideration of parathyroidectomy (5).


  1. Moe S, Drüeke T, Cunningham J, Goodman W, Martin K, Olgaard K, et al. Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2006 Jun;69(11):1945–53.
  2. Secondary Hyperparathyroidism: Pathogenesis, Disease Progression, and Therapeutic Options | American Society of Nephrology [Internet]. [cited 2018 Nov 13]. Available from:
  3. Terai K, Nara H, Takakura K, Mizukami K, Sanagi M, Fukushima S, et al. Vascular calcification and secondary hyperparathyroidism of severe chronic kidney disease and its relation to serum phosphate and calcium levels. Br J Pharmacol. 2009 Apr;156(8):1267–78.
  4. Musculoskeletal manifestations of chronic renal insufficiency. – PubMed – NCBI [Internet]. [cited 2018 Dec 5]. Available from:
  5. Ketteler M, Block GA, Evenepoel P, Fukagawa M, Herzog CA, McCann L, et al. Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder: Synopsis of the Kidney Disease: Improving Global Outcomes 2017 Clinical Practice Guideline Update. Ann Intern Med. 2018 Mar 20;168(6):422–30.


Julian Paniagua, MD
PGY 2 Internal Medicine Resident
St Barnabas Health System
Bronx, NY

Razia Rehmani, MD
Chief of Neuroradiology & Musculoskeletal Imaging
Diagnostic Radiology
St Barnabas Health System
Bronx, New York