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Bone disorder Although, the term “renal” points to a disease related to kidneys, renal osteodystrophy is in fact a bone disorder that occurs when kidneys fail to maintain the proper levels of calcium and phosphorus in blood.

According to Health Care Financing Administration report, more than 230,000 Americans are under treatment for end-stage renal disease.

Etiology of renal osteodystrophy

The etiology of renal osteodystrophy is not completely understood but a suggested mechanism of the disease is that the primary retention of phosphates by diseased kidneys result in a condition called hyperphosphatemia - high levels of phosphates. This condition is causing hypocalcaemia - low levels of calcium, resulting in secondary hyperparathyroidism - increased level of parathyroid hormone. This, of course primarily affects the bone tissue.

The fact is that, in healthy adults, bone tissue is continually being remodeled and rebuilt.


Calcium is one of the most important elements in our body and a mineral that builds and strengthens bones. If calcium levels in blood become too low, parathyroid glands localized in the neck just behind the thyroid gland, release a hormone called parathyroid hormone. The primary role of this hormone is to evacuate the calcium from various body structures, primarily bones, and raise blood calcium levels!


Phosphates, which are found in most foods, , also help regulate calcium levels in blood and bones. Since humans may ingest too much of these substances- the primary role of healthy kidneys is to remove excess phosphates from blood.

When there is something wrong with the kidneys and they stop working normally, phosphate levels in blood can become too high. As the levels of phosphates are getting higher- levels of calcium in blood are getting lower!

This information gets to the parathyroid glands, which are producing more parathyroid hormone then usual, resulting in the loss of calcium from the bones. Parathyroid hormone also raises calcium levels by osteoclast activation (specific bone cells made for the bone dissolution), stimulation of intestinal calcium absorption and various other renal effects.

Calcitriol –vitamin D

There is one more possible cause of this condition: affected kidneys fail to produce a hormone called Calcitriol, a form of vitamin D which is similar to parathyroid hormone and which helps calcium absorbtion from food into the blood and bones. This may cause osteosclerosis, soft tissue calcification, and bone resorption and osteoporosis- disorder of the bones that results in hypo-mineralization following the cessation of bone growth.

Based on which part of the bone is loosing calcium, bone resorption can be:

  • subchondral- may be seen in distal clavicles, sacroiliac joints, and pubic joints
  • trabecular- in most cases scull is affected with this type of resorption
  • endosteal,
  • intracortical,
  • subperiosteal- hands and feet are affected
  • subligamentous and subtendinous - typically occur in the clavicle underlying the coraco-clavicular ligaments

Possible signs

The bone changes caused by renal osteodystrophy can begin many years before symptoms appear in adults with kidney disease. And that is exactly what makes this condition potentially undetectable and very dangerous! This condition does not have to cause any visible symptoms, but in most cases, patients complain of bones and joints pain. In late stages of the disease, bone deformation and fractures may also occur. There have also been cases of bent bones, rickets and delayed growth! Typical sites or target bones are the concave surface of the femoral bone, scapula, pubic parts and ribs.

Renal osteodystrophy may also cause several nonspecific signs and symptoms such as unexplained bone pain, general weakness and different mild skeletal deformities.

Risk factors

  1. age - Older patients are much more vulnerable to osteoporosis, even without kidney disease

Age of the patient   


Younger than 20 years   

1.8% of patients

Between 20-44 years 

26% of patients

Between 45-64 years

38.7% of patients

Between 65-74 years

20.6% of patients

Older than 74 years   

12.9% of patients

  1. Menopause- hormone imbalances during the perimenopause period can cause some fluctuations in blood calcium levels, although man and woman are almost equally distributed among patients
  2. Race – it is proven that Caucasian people are diagnosed with this condition much more often than other races. Here is some statistical data about distribution of this condition among races in the U. S.

Race of the patients                                                                                       Percentage
Caucasian                                                                                                             61.1%
African-American                                                                                                  32.3%
Asian/Pacific Islanders                                                                                          3.5%
Native Americans                                                                                                    1.6%
Other/unknown                                                                                                        1.6%

Consequences and complications

If the disease is left untreated, there are several complications of renal osteodystrophy  some of which can only be detected in late stages of the disease.
Most common complications are

  •     Thin bones                                                                         
  •     Slow bone growth
  •     Bone deformities
  •     Renal rickets
  •     Short stature
  •     Osteoporosis

The condition is most serious when it comes to young children because their bones are still growing. This is causing much more serious deformities than in older people or adults!
Children’s legs can bend inward or outward and most of them are expected to be of short stature as adults.

Diagnosis of renal osteodystrophy

    1.  X-ray - radiographic examination in patients with symptoms of renal osteodystrophy may reveal osteopenia, looser zones, amyloid depositions and complete fractures of the bones. Problem is that, although X-ray examination can demonstrate many specific findings of renal osteodystrophy, sometimes, patients may have only osteopenia!
    2. CT-scan – CT is probably the best method for diagnosing the pathological fractures of the bones as well as the deposits of amyloid structures in the joints
    3. MRI- scan – Unlike previously mentioned diagnostic tools, MRI helps evaluate several soft  tissue damages and ligament ruptures localization
    4. Nuclear medicine findings – This condition can easily be mixed up with metastases of cancer because it also produces diffuse and focal skeletal uptake of radiopharmaceuticals
    5. Blood analisys - To diagnose renal osteodystrophy, doctor may take a sample of blood to measure levels of calcium, phosphorus, PTH, and calcitriol.
    6. Bone biopsy – This method involves removing a small sample of bone from the hip under local anesthesia and examining the sample under microscope

Renal Osteodystrophy Treatment

The key of any successful osteodystrophy treatment is to control PTH levels. This should prevent calcium from being withdrawn from the bones.

  •   Problems with parathyroid glands - When the primary cause is uncontrolled parathyroid glands, which are producing PTH, they should be controlled with a change in diet, dialysis treatment, or medication. If this method fails and levels of PTH cannot be controlled, the parathyroid glands may need to be removed surgically and the procedure is called parathyroidectomy!
  •  Problems with kidneys - If kidneys fail to produce adequate amounts of hormone calcitriol- then it should be replaced with substitute therapy. This means that patient should take synthetic calcitriol as a pill or in an injectable form. Calcium supplements could also be very helpful as well as the several medications called phosphate binders that should be used with meals such as calcium carbonate, calcium acetate, sevelamer hydrochloride, or lanthanum carbonate. Several studies have proven that frequent hemodialysis, at least five times a week, could be beneficial to patients. Renal transplantation is the last thing that could help a patient if all other treatment methods fail.

Basic treatment strategies

Therapy Goals  


1. Keep phosphate below 5.5 mg/dL

Dietary phosphate restriction
Calcium acetate with meals to "bind" phosphate
Newer phosphate binders such as sevelamer are helpful
Longer hours on dialysis
Aluminum hydroxide as last resort

2. Keep serum calcium in normal range Calcium carbonate
Calcitriol if necessary
Adjust dialysate calcium 3. Control PTH Calcium supplements
Vitamin-D metabolites that are less likely to produce hypercalcemia (paricalcitol)
Partial parathyroidectomy may become necessary 4. Avoid vascular calcifications By keeping the level of calcium in blood within normal range 5. Treatment of low bone density

Experts are still discussing whether the treatment of low bone density is necessary at all because:

  • There is no evidence that bisphosphonates help prevent fractures
  • Bisphosphonates increase PTH and lower bone formation
  • Raloxifene may be useful in postmenopausal women
  • No studies of calcitonin
  • Estrogen may probably be beneficial in younger women, but there is the increased
  • risk of coagulation problems
  • Estrogen dose should be half that used in normal women 
Dietary changes – The main objective of the dietary changes is to reduce phosphate intake. It is one of the most important steps in preventing this bone disease. Many types of food are rich in phosphates (milk, cheese, dried beans, peas, nuts, peanut butter). Although almost all types of food contain phosphates,, the aforementioned types should be avoided as much as possible.
Exercise – Several researches have proven that regular exercise can increase bone strength and reduce the level of osteoporosis.