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Renal osteodystrophy


Renal osteodystrophy refers to the complex changes in bone that occur in patients with chronic kidney disease (CKD).  These changes accompany the multiple alterations in mineral metabolism in CKD, including changes in calcium, phosphorous, parathyroid hormone (PTH), vitamin D, and fibroblast growth factor 23 (FGF-23).

Clinical Manifestations

Patients with renal osteodystrophy are at increased risk of fracture, and they may experience bone pain. Children may have impaired linear bone growth.

Renal osteodystrophy is intimately associated with other manifestations of altered mineral metabolism in patients with CKD, known collectively as CKD-mineral and bone disorder (CKD-MBD).  Patients with CKD-MBD have a high prevalence of vascular calcification, leading to multiple cardiovascular issues including atheroscelorosis, coronary artery calcification, hypertension, left ventricular hypertrophy, and congestive heart failure.  Extraskeletal calcification can also affect the heart valves and the cardiac conduction system.  Calcification of skin arterioles may lead to a condition of ischemia and necrosis of the skin known as calciphylaxis.


Approximately 8% of the adult population in the US has a glomular filtration rate (GFR) less than 60 mL/min and is at risk of developing renal osteodystrophy and other manifestations of CKD-MBD.

Pathology and pathophysiology

As GFR is reduced below 60 mL/min, renal phosphorous excretion is impaired, resulting in an increase in serum phosphorous. PTH and FGF-23 are stimulated to try to promote phosphorous excretion and maintain relatively normal phosphorous levels. As GFR declines below 30 mL/min, frank hyperphosphatemia develops.

At the same time, conversion of 25-hydroxy vitamin D to 1,25-dihydroxy vitamin D is impaired due to reduced 1-alpha reductase activity in the kidney.  Intestinal calcium absorption is impaired and calcium levels fall, further stimulating PTH secretion.

In the skeletal system, elevated PTH typically causes increased bone turnover, though patients with CKD-MBD may have some degree of skeletal resistance to PTH.  Patients with vitamin D deficiency and/or low calcium may have reduced mineralization. Some patients — particularly patients with aluminum exposure or patients whose PTH has been overly suppressed (see Treatment) — may have a state of low bone turnover called adynamic bone disease.

Differential diagnosis

Primary hyperparathyroidism typically presents with hypercalcemia, hyperparathyroidism, and normal-to-low phosphate in patients with normal or minimally-reduced renal function.

Tertiary hyperparathyroidism typically presents as hypercalcemia, hyperparathyroidism, and normal-to-elevated phosphate in patients with longstanding CKD-MBD.

Osteoporosis and vitamin D deficiency are common disorders in the general population, the majority of which will have normal or minimally reduced renal function.


Renal osteodystrophy occurs in patients with CKD-MBD as a result of the multiple changes in mineral metabolism.

Radiographic and laboratory findings

Serum phosphorous levels are typically normal to elevated, depending on the stage of CKD, adherence to dietary phosphorous restriction, and use of phosphate binders. Calcium levels are typically normal to slightly low.

Measurement of 25-hydroxy vitamin D provides the best assessment of vitamin D status.  Vitamin D insufficiency and deficiency are endemic in the US population, including patients with CKD-MBD. FGF-23 and 1,25-dihydroxy vitamin D are not routinely measured.

PTH levels (measured as intact PTH [iPTH]) will be elevated. iPTH levels between 2 and 9 times the upper limit of normal are considered to be appropriate for patients with CKD-MBD.

In the absence of suspected fracture, plain X-rays are not usually helpful in patients with renal osteodystrophy. DEXA bone densitometry may reveal low bone density.

Bone biopsy is the definitive test in distinguishing high-turnover bone disease from low-turnover bone disease in patients with renal osteodystrophy, and it can also assess mineralization.  Measurement of bone turnover on a bone biopsy is assessed by labeling the bone with tetracycline at two separate times approximately 2 weeks apart. The distance between the two areas of tetracycline deposition can be used to calculate bone growth. (Figure 1)

Risk factors and prevention

Efforts to mitigate the progression of CKD in an individual patient are presumed to reduce the sequela of renal osteodystrophy.  Dietary restriction of phosphorous and supplementation of vitamin D are also presumed to be helpful.

Treatment options

Phosphate binders decrease serum phosphate levels by binding dietary phosphate.  These agents include calcium carbonate, calcium acetate, sevelamer, and lanthanum carbonate.  Aluminum-based binders are no longer recommended for chronic use.  Calcium-based binders should be avoided in patients with arterial calcification, low PTH, or elevated serum calcium.

Vitamin D supplements (ergocalciferol or cholecalciferol) should be given to maintain 25-hydroxy vitamin D levels at greater than 20-30 ng/mL.

Current guidelines recommend maintaining intact iPTH levels within 2-9 times the upper limit of normal for the assay.  Patients with iPTH levels above that range, and patients who have a marked rise of iPTH within that range, should be treated with vitamin D analogues (such as calcitriol, paracalcitol, or doxercalciferol) to suppress PTH secretion by the parathyroid glands.  These agents can cause hypercalcemia and hyperphosphatemia.

Cinacalcet, a calcimimetic agent, also acts directly on the parathyroid gland to decrease PTH secretion. Cinacalcet may cause hypocalcemia and hyperphosphatemia, and is more expensive than a vitamin D analog.  Patients who are refractory to medical therapies may require parathyroidectomy.

Whether or not patients with CKD-MBD and a fragility fracture (or T < -2.5 on DEXA) should be managed with an anti-osteoporotic agent is highly controversial.


Vitamin D analogues appear to confer survival benefits in retrospective analyses of patients with CKD and elevated PTH. Retrospective analyses of cinacalcet trials suggest a reduction in fractures and improved quality of life, but randomized controlled clinical trials are needed.

Holistic medicine

Patients with CKD are advised extensively on diet, which may include recommendations to modify intake of protein (the major source of dietary phosphorous).  Vitamin D supplementation is often recommended.


Despite its utility in clarifying the bone status of patients with renal osteodystrophy, bone biopsy with tetracycline labeling are only rarely performed in clinical practice.

Key terms

Renal osteodystrophy, chronic kidney disease, mineral and bone disorder, adynamic bone disease

Skills and competencies

Understand changes in mineral metabolism in CKD that result in renal osteodystrophy.


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