Renal osteodystrophy

• A term used to describe collectively all of the skeletal changes associated with chronic renal disease
• These changes include;
  • Increased osteoclastic bone resorption mimicking osteitis fibrosa cystica
  • Delayed matris mineralization (osteomalacia)
  • Osterosclerrosis
  • Growth retardation
  • Osteoporosis

 

• Bone disorders in patients with end stage renal failure are divided into 2 main types;
  • High turnover osteodystrophy is characterised by increased bone resorption and formation with the former predominating
  • Low turnover or aplastic disease is manifested by little osteoclastic and osteoblastic activity and less commonly osteomalacia
• Patients generally have a mixed pattern of disease

 

Pathogenesis

 

• Chronic renal failure results in phosphate retention and hyperphosphataemia
• Hyperphosphataemia induced secondary hyperparathyroidism because phosphate regulates PTH secretion
• Hypocalcaemia develops as the levels of 1,25-dihydroxyvitamin D₃ fall because of decreased conversion of 25-[OH]₂D₃ to the more active metabolite 1,25-[OH]D₃ and reduced intestinal absorption of calcium from the intestine
• Increased PTH activity. 1,25-(OH)₂D₃ would normally suppress PTH secretion
• The resultant secondary hyperparathyroidism produces increased osteoclast activity
• Metabolic acidosis associated with renal failure stimulates bone resorption and the release of calcium hydroxyapatite from the bone matrix
• Aluminium (and iron) deposition at the site of mineralization interferes with the deposition of calcium hydroxyapatite and hence promotes osteomalacia. The sources of aluminium are often iatrogenic and include dialysis solutions and oral aluminium containing phosphate binders
• Patients that undergo long term haemodialysis form b-microglobulin containing amyloid masses in the bone and periarticular tissue. This is an additional complication