Renal osteodystrophy is defined as an alteration of bone in patients with chronic kidney disease (CKD). It is one measure of the skeletal component of the systemic disorder of chronic kidney disease-mineral and bone disorder (CKD-MBD). The term "renal osteodystrophy" was coined in 1943, 60 years after an association was identified between bone disease and kidney failure.

The types of renal osteodystrophy have traditionally been defined on the basis of bone turnover and mineralization:<br>

1) mild, slight increase in turnover and normal mineralization;<br>

2) osteitis fibrosa, increased turnover and normal mineralization;<br>

3) osteomalacia, decreased turnover and abnormal mineralization;<br>

4) adynamic, decreased turnover and acellularity; and,<br>

5) mixed, increased turnover with abnormal mineralization.

Signs and symptoms

Renal osteodystrophy may exhibit no symptoms; if it does show symptoms, they can include:

  • Bone pain
  • Joint pain
  • Muscle pain
  • Itching
  • The broader concept of chronic kidney disease-mineral and bone disorder (CKD-MBD) These clinical consequences are acquiring such an importance that scientific working groups (such as the ERA CKD-MBD Working Group) or international initiatives are trying to promote research in the field including basic, translational and clinical research.

Pathogenesis

Renal osteodystrophy has been classically described as the result of hyperparathyroidism secondary to hyperphosphatemia combined with hypocalcemia, both of which are due to decreased excretion of phosphate by the damaged kidney.

Low activated vitamin D<sub>3</sub> levels are a result of the damaged kidneys' inability to convert vitamin D<sub>3</sub> into its active form, calcitriol, and result in further hypocalcemia. High levels of fibroblast growth factor 23 seem to be the most important cause of decreased calcitriol levels in CKD patients.

In CKD, the excessive production of parathyroid hormone increases the bone resorption rate and leads to histologic bone signs of secondary hyperparathyroidism.

Both high and low bone turnover diseases are observed equally in CKD patients treated by dialysis, and all types of renal osteodystrophy are associated with an increased risk of skeletal fractures, reduced quality of life, and poor clinical outcomes.

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File:X-ray of periosteal reaction in renal osteodystrophy.jpg|Projectional radiography ("X-ray") of periosteal reaction.

File:X-ray of ground glass density of the skull by renal osteodystrophy.jpg|Ground glass density of the skull.

  • osteopenia
  • osteomalacia
  • brown tumor should be considered as the top-line diagnosis if a mass-forming lesion is present.

Treatment

Treatment for renal osteodystrophy includes the following:

  • calcium and/or native vitamin D supplementation
  • restriction of dietary phosphate (especially inorganic phosphate contained in additives)
  • phosphate binders such as calcium carbonate, calcium acetate, sevelamer hydrochloride or carbonate, lanthanum carbonate, sucroferric oxyhydroxide, ferric citrate among others
  • active forms of vitamin D (calcitriol, alfacalcidol, paricalcitol, maxacalcitol, doxercalciferol, among others)
  • cinacalcet
  • renal transplantation
  • haemodialysis five times a week is thought to be of benefit
  • parathyroidectomy for symptomatic medication refractive end stage disease

Prognosis

Recovery from renal osteodystrophy has been observed following kidney transplantation. Renal osteodystrophy is a chronic condition with a conventional hemodialysis schedule.

Epidemiology

Renal osteodystrophy is a common disorder associated with chronic kidney disease (CKD), occurring in nearly all affected adults and children. CKD affects an estimated 752 million people globally.