What Is Renal Osteodystrophy

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Chronic kidney disease (CKD) is a long-term condition where kidney function deteriorates. It affects approximately 8-10% of the population worldwide.1 Most patients with CKD suffer from a range of bone disorders.

Bone is a multi-layered system that plays a role as a mechanical shield for providing support for our body as well as security. Generally, bone tissue is composed of organic and mineral parts that are interlinked in an organized fashion providing flexibility and ductility. The organic part consists of a protein, called collagen, whilst the mineral part consists of a form of calcium. Bone mineralisation is the process where bone-making cells, osteoblasts, help to produce calcium crystals which then align with the collagen part of the bone. Problems that arise with bone mineralisation give rise to skeletal structural deformities.2

Renal osteodystrophy (osteo = bone and dystrophy = degeneration) is an umbrella term for skeletal abnormalities in patients suffering from CKD or kidney failure.3 It could appear early on in the progression of CKD and may persist even after renal transplantation. The common causes for renal osteodystrophy are mineral and hormonal abnormalities resulting in reduced bone mineralisation.

Types of renal osteodystrophy

Bone is maintained by an event called bone turnover, where defective, “old” bone is broken down (resorption) and restored by “younger”, tougher tissue.4 The range of skeletal abnormalities seen in renal osteodystrophy is classified according to the state of bone turnover. There are two different forms of renal dystrophy:

High bone turnover renal osteodystrophy:

Osteitis fibrosa cystica: With very high levels of bone resorption and formation manifesting as abnormally high parathyroid hormone levels (hyperparathyroidism).

It is characterised by  reduced levels of calcium and vitamin D; increased levels of parathyroid hormone and phosphate.

Low bone turnover renal osteodystrophy:

  • Osteomalacia: Defective mineralisation due to increased breakdown of bones with reduced formation, related to aluminium accumulation. This condition is characterised by soft bones. It is characterised by reduced levels of calcium, vitamin D and phosphate; increased levels of parathyroid hormone and alkaline phosphatase
  • Adynamic bone disease: Defective bone mineralisation due to reduced bone resorption related to over suppression of parathyroid hormone levels. It is characterised by reduced levels of calcium, vitamin D and parathyroid hormone; increased levels of alkaline phosphatase
  • Combinations of these abnormalities are called mixed renal osteodystrophy

Causes of renal osteodystrophy

High bone turnover

Hyperparathyroidism can be classified as primary, secondary, or tertiary. Increased parathyroid hormone levels play an important role in high bone turnover states.5 The most prominent cause of renal osteodystrophy is secondary hyperparathyroidism. The factors involved are:

  • Vitamin D: Reduced serum Vitamin D levels result in decreased intestinal calcium absorption, hypocalcaemia, and hyperparathyroidism which, ultimately, enhances phosphate excretion
  • Phosphate retention: As renal failure enhances, serum phosphate levels increase which, in turn, lowers calcium levels, stimulating parathyroid hormone secretion. Phosphate retention and declining renal function suppress vitamin D synthesis. Further studies suggest that phosphate retention also induces changes in vascular smooth muscle cells6
  • Calcium: Decrease in serum calcium stimulates parathyroid hormone secretion.
  • Calcitriol: Calcitriol can increase serum calcium levels and is required for suppressing parathyroid hormone secretion through the glands. Decreased calcitriol in the body results in secondary hyperparathyroidism due to decreased calcium absorption through the intestine
  • Fibroblast growth factor 23 (FGF-23): FGF-23 inhibition reduces phosphate levels in the body and can lead to secondary hyperparathyroidism

Low bone turnover

Osteomalacia: Occurs due to heavy metal intoxication, mainly aluminium, which inhibits calcium uptake into bone leading to disruption in bone resorption. Other metals are also implicated including iron and cadmium. 

Adynamic bone disease: The pathogenesis predominantly involves parathyroid hormone suppression, leading to low bone turnover and inadequate bone mineralization. Causative factors include:

  • Calcium and vitamin D: Intensive treatment with these in patients of chronic kidney disease leads to chronic suppression of parathyroid hormone
  • Continuous ambulatory peritoneal dialysis (CAPD): Causes large influx of calcium into the body through the dialysate fluid
  • Diabetes mellitus: Increased glucose and decreased insulin levels together suppress parathyroid hormone secretion
  • FGF-23: High levels of FGF23 is present in individuals with renal phosphate-wasting diseases. Increase FGF23 inhibits bone mineralisation7 

Signs and symptoms of renal osteodystrophy

Rise in incidence of fracture in CKD patients suggest risk of renal osteodystrophy. In children with CKD, the occurrence of fractures increases by approximately 2 to 3-fold. Other signs include:

  • Weakness
  • Bone pain
  • Skeletal deformity

Alternatively, symptoms of hypocalcaemia (low calcium) can also be noticed in CKD patients with renal osteodystrophy, including:

  • Abdominal pain
  • Muscle cramps
  • Dyspnea: Inability to breathe fast or deeply enough.
  • Convulsions/seizures

Management and treatment for renal osteodystrophy

Treatments are geared mainly towards prevention as it is difficult to treat patients with advanced stage disease.

  • Dietary restrictions: Controlling phosphate intake helps control the secretion of parathyroid hormone
  • Phosphate binders, such as Sevelamer and Lanthanum, help reduce phosphate absorption.
  • Dialysis to remove phosphate from the blood
  • Vitamin D analogues such as Cholecalciferol (vitamin D3), and less commonly ergocalciferol (vitamin D2) are given to patients who do not undertake dialysis
  • Calcitriol is a hormonally active vitamin D analogue is prescribed to patients with renal failure induced hypocalcaemia
  • Cinacalcet is a calcium receptor sensitiser which works by inhibiting the release of parathyroid hormone
  • Surgical parathyroidectomy, that is, the removal of the parathyroid gland, may be opted for patients with severe secondary or tertiary hyperparathyroidism, who do not respond to drug treatments

Vitamin D analogues may result in hypercalcaemia (high calcium) and hyperphosphatemia (high phosphate). Thus, it is important to monitor and prescribe appropriate doses of these medications. Usually, calcium salts are administered alongside Vitamin D to normalise calcium levels for normal cell activity and to suppress parathyroid hormone.9,10


The gold standard for diagnosis is bone biopsy. Serum levels of other mineral components can be measured including calcium, phosphorus, alkaline phosphatase and parathyroid hormone .10 Alternatively, CT or Dual-energy X-ray absorptiometry (DEXA) to measure bone volume may prove helpful in management of patients with a high risk of fracture.


How can I prevent renal osteodystrophy?

Renal osteodystrophy cannot be prevented, but rather the progression can be slowed down. Diet is an important factor that influences serum mineral levels and, therefore, requires regulation. This includes reducing intake of foods and drinks with high phosphate levels such as, dairy products, bony fish, shellfish, nuts and chocolate. Taking supplements such as vitamin D, is also beneficial to regulate calcium and phosphate levels.

Who is at risk of renal osteodystrophy?

Predominantly, patients with CKD or kidney failure are at risk of renal osteodystrophy.

When should I see a doctor

Patients with CKD should seek advice when they have bone pain, muscle weakness and regular fractures. An individual with CKD may have regular check-ups to measure the blood mineral levels. This will be used as a guide to understand if these patients have developed renal osteodystrophy.


Overall, renal osteodystrophy is the development of abnormal skeletal phenotype due to chronic kidney disease. Abnormalities that arise in mineral levels in the blood is the primary cause for skeletal disorder in individuals with CKD. Unusual mineral levels can be rectified with the aid of treatments. 

Follow your healthcare provider's advice regarding your food, medicines, and dialysis if you have chronic renal disease. Although there is no cure for this illness, there are things you may do to limit its progression and preserve your quality of life.


  1. Milik A, Hrynkiewicz E. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney International Supplements. J Int Soc Nephrol. 2013; 
  2. Dey P. Bone Mineralisation. In: Contemporary Topics about Phosphorus in Biology and Materials. 2020. Available from: https://www.intechopen.com/chapters/71749
  3. Moe SM. Renal Osteodystrophy or Kidney-Induced Osteoporosis? Current Osteoporosis Reports. 2017. Available from:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5506492/
  4. Wiren KM. The Aging Skeleton. C.J. Rosen, J. Glowacki, and J.P. Bilezikian (eds.), Academic Press, San Diego CA, U.S.A., 1999. J Bone Miner Res. 2000; Available from: http://www.academia.dk/BiologiskAntropologi/Osteologi/PDF/Principles_of_Bone_Biology__Second_Edition__2_Vol__Set_.pdf
  5. Narula A, Jairam A, Baliga K, Singh K. Pathogenesis and management of renal osteodystrophy. Indian J Nephrol. 2007; Available from:https://journals.lww.com/ijon/Fulltext/2007/17040/Pathogenesis_and_management_of_renal.2.aspx
  6. Zhang D, Bi X, Liu Y, Huang Y, Xiong J, Xu X, et al. High phosphate-induced calcification of vascular smooth muscle cells is associated with the TLR4/NF-κb signaling pathway. Kidney Blood Press Res. 2017; Available from:https://pubmed.ncbi.nlm.nih.gov/29227975/
  7. Huang X, Jiang Y, Xia W. FGF23 and Phosphate Wasting Disorders. Bone Research. 2013. Available from:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4472102/
  8. Denburg MR, Kumar J, Jemielita T, Brooks ER, Skversky A, Portale AA, et al. Fracture burden and risk factors in childhood CKD: Results from the CKiD cohort study. J Am Soc Nephrol. 2016; Available from:https://pubmed.ncbi.nlm.nih.gov/26139439/
  9. Roberts DM, Singer RF. Management of renal bone disease. Aust Prescr. 2010; Available from:https://www.nps.org.au/australian-prescriber/articles/management-of-renal-bone-disease
  10. Sista SK, Arum SM. Management of adynamic bone disease in chronic kidney disease: A brief review. Journal of Clinical and Translational Endocrinology. 2016. Available from:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5644430/

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This content is purely informational and isn’t medical guidance. It shouldn’t replace professional medical counsel. Always consult your physician regarding treatment risks and benefits. See our editorial standards for more details.

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Melody Deniz

Doctor of Philosophy - PhD, Regenerative Medicine | Osteoarthritis | Gene Therapy, Queen Mary University of London

Melody is a PhD student at Queen Mary University of London where she is researching gene therapy as a novel treatment for osteoarthritis. She has strong scientific and research background having several years of experience in research and development.

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