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Renal Osteodystrophy

Osteodystrophies Renal

Renal osteodystrophy occurs in the setting of chronic kidney disease, and is associated with imbalance of calcium, phosphorus, parathyroid hormone, calcitriol metabolism, and the process of bone mineralization, since the kidneys are not capable of maintaining proper levels of electrolytes. It is most commonly seen in patients with renal replacement therapy and kidney failure, and the diagnosis is established through evaluation of hormones and electrolytes. Therapy is aimed at correcting electrolytes along with supportive measures.


This condition follows a chronic course. Symptoms related to the condition itself may not be apparent for years. Usually, skeletal symptoms such as bone and joint pain, limited mobility, as well as bone deformities and pathological fractures should indicate that there is an underlying issue with bone mineralization and factors responsible for maintenance of the skeletal system. These symptoms may appear more rapidly in children who are suffering from kidney failure, because bone growth and development is more pronounced, and any malformations and alterations can be more easily observed.

In addition to osteomalacia, and other bone-related symptoms, patients who are on hemodialysis may experience symptoms such as anemia, dialysis-related dementia, characterized by memory loss, hallucinations, and possibly seizures, which should immediately point to aluminum toxicity. Aluminum-based phosphate binders are a part of hemodialysis, and patients may be exposed to toxic concentrations.

Wheelchair Bound
  • The patient for whom the surgery failed remains wheelchair-bound. The Ilizarov method was found to be safe and effective for correction of malalignment due to ROD.[ncbi.nlm.nih.gov]
Cranial Neuropathy
  • This is the first case report of cranial neuropathy associated with ULO.[ncbi.nlm.nih.gov]


The diagnosis of renal osteodystrophy comprises a full electrolyte workup, focusing on the levels of calcium and phosphorus, as well as PTH and vitamin D. Usually, serum calcium levels are low, phosphorus levels are high, values of PTH may be elevated, or sometimes decreased, and vitamin D levels are always low. Serum alkaline phosphatase level should also be evaluated, since it may be elevated in hyperparathyroidism [6].

In addition to serum values of hormones and electrolytes, kidney function should be thoroughly evaluated by obtaining serum creatinine, blood urea nitrogen (BUN), urinalysis, Glomerular filtration rate (GFR) and looking for proteinuria.

Bone biopsy is indicated in order to establish a definite diagnosis of renal osteodystrophy as a separate cause of kidney failure, but its indications are still unclear.

Rugger-Jersey Spine
  • The "rugger jersey" spine occurring in the usual osteosclerosis of renal osteodystrophy has been consistently absent in this variant. Osteonecrosis should be excluded in making the diagnosis of "bone end sclerosis."[ncbi.nlm.nih.gov]
  • Disease processes which cause the osteosclerosis with or without the rugger jersey spine include Paget's disease, osteopetrosis, lymphoma, osteoblastic metastases, fluorosis and myelofibrosis.[smjonline.org]
  • jersey spine) Rugger-jersey spine in Renal osteodystrophy o Also in pelvis, ribs, long bones, facial bones, base of skull (children) o Prognosis § May increase/regress after renal transplantation · Soft-tissue calcifications o Metastatic secondary to[learningradiology.com]
  • […] endosteal, subchondral, subligamentous areas, cortical bone, or trabeculae 5 subperiosteal resorption : characteristic subperiosteal resorption may be seen on radial aspects of middle phalanges of index and long fingers bone sclerosis diffuse bony sclerosis rugger-jersey[radiopaedia.org]
  • RADIOGRAPHIC EVALUATION: Osteopenia, subcortical resorption, lucent metaphyseal bands, widening of metaphysis and "rugger jersey spine".[gait.aidi.udel.edu]
Parathyroid Hormone Increased
  • In CKD the excessive production of parathyroid hormone increases the bone resorption rate and leads to histologic bone signs of secondary hyperparathyroidism. [11] However, in other situations, the initial increase in parathyroid hormone and bone remodeling[en.wikipedia.org]


Since chronic kidney disease is associated with significant morbidity and mortality, and current therapeutic principles only imply maintenance and replacement therapy, the goal of treatment in renal osteodystrophy is to try to establish a somewhat acceptable electrolyte balance, and reduce the severity of bone disease, while attempting to reduce further damage to the kidneys. Strategies to correct electrolytes, as well as hormone levels include:

  • Phosphorus restriction and correction - Since hyperphosphatemia is always observed in this condition, dietary restriction of phosphorus is recommended, according to the grade and severity of chronic kidney disease (for example, recommended daily intake of phosphorus should be 800-1000 mg for adults with stage five CKD, or end-stage renal disease) [7]. Additionally, many patients with CKD, and virtually all hemodialysis patients require administration of oral phosphate binders, such as Ca acetate and Ca carbonate, in doses of 6-15 g/day. They should be taken with meals, because they can bind phosphorus more effectively [8]. Ca acetate is preferred over Ca carbonate in patients who are taking histamine 2 receptor antagonists, or proton pump inhibitors [9], as they are able to dissolve in both acid and alkaline environments, while Ca carbonate dissolves only in acidic pH. Non Ca salts such as sevelamer, are also used. Aluminum-based binders were used, but due to their potential toxicity, their efficacy is being reviewed. They are currently recommended for patients with marked elevation of serum phosphorus (> 7.0 mg/dl or 2.26 mmol/L), for a short duration. They should be then replaced by other phosphate binders.
  • Restriction of Ca intake - it has been observed that use of calcium salts in patients may lead to an increased risk of hypercalcemia, as well as development of metastatic calcifications, which can pose significant cardiovascular morbidity and mortality. For these reasons, guidelines suggest that the total intake of calcium (including dietary intake) should not exceed 2000 mg/day.
  • Magnesium supplementation - Magnesium levels should be monitored in patients with excessive levels of calcium which occurs in those who are taking calcium salts to reduce levels of phosphorus. Magnesium supplementation has been implicated in the treatment of hemodialysis patients in association with calcium disturbances [10].
  • Cause-targeted treatment - Apart from electrolyte correction, the exacts cause of electrolyte disturbances, as well as abnormal levels of PTH, should be investigated and treated accordingly.


Renal osteodystrophy is a chronic condition which occurs in patients with renal failure, and since patients have chronic, irreversible, and progressive deterioration of kidney function, the prognosis is generally poor. It may vary, however, depending on the underlying cause of bone disease and associated electrolyte disturbance, but patients need life-long corrective therapy, usually through hemodialysis [5], along with management of other associated conditions.


Renal osteodystrophy comprises bone disease that occurs along with chronic kidney disease. Bone mineralization, as well as homeostasis of calcium and phosphorus is disturbed, which can present either as highly active (such as in osteitis fibrosa, where increased secretion of parathyroid hormone (PTH) leads to fragile and brittle bones) [2], or suppressed bone mineralization (as in the case of hypoparathyroidism, osteomalacia, as a result of hypocalcemia and vitamin D deficiency, but also aluminum intoxication which can occur in patients on hemodialysis). Malignant diseases should always be suspected when PTH levels are not within physiological limits, especially when hypoparathyroidism is observed. Iron levels, and siderosis have also been implicated in the pathogenesis of this disorder [3].

Apart from diseases which directly affect the metabolic axis of bone development, any disease which can cause chronic kidney disease can predispose individuals to renal osteodystrophy, including systemic diseases such as systemic lupus erythematosus (SLE), amyloidosis, hemolytic-uremic syndrome, and many others.

Children may also develop renal osteodystrophy, since severe renal impairment may be observed amongst them too especially in cases of Alport syndrome, polycystic kidney disease, and medullary cystic disease.


This condition is primarily observed amongst patients with end-stage renal disease, who are usually on hemodialysis [4], implying that middle aged adults, as well as the elderly, are the most common population in which this disorder can be diagnosed. However, renal failure can be observed in patients of all ages and gender, depending on the cause. Certain epidemiological studies have indicated that almost two thirds of patients are Caucasian, while almost one third of patients are African-Americans, implying a racial predilection of this disorder. It has been hypothesized that this disorder should be more common amongst females during menopause, keeping in mind that osteoporosis is much more pronounced in females, which is supposedly a risk factor. However, the disease is equally distributed amongst genders.

Sex distribution
Age distribution


The pathogenesis of renal osteodystrophy involves several mechanisms. It starts with the decreased ability of the kidneys to synthesize active forms of vitamin D, calcitriol. This leads to hypocalcemia, while decreased excretion of phosphate by the kidneys, due to progressive deterioration of renal function with kidney failure and renal disease, results in hyperphosphatemia. All of these change have profound effects on the bone mineralization process, which is tightly regulated by PTH. In renal osteodystrophy, hyperparathyroidism usually occurs, as a compensatory mechanism for low calcium and high phosphorus, by mobilizing calcium stores from the bones. As the kidneys cannot maintain the electrolyte balance, hyperparathyroidism can pose a threat to the skeletal system resulting in osteomalacia. This phenomenon can be observed in osteitis fibrosa.

On the other hand, renal osteodystrophy may also occur in the setting of hypoparathyroidism, when decreased rate of bone mineralization occurs. This can also induce osteomalacia, and osteopenia, and the kidneys are not able to compensate for the electrolyte imbalance.


Prevention of renal osteodystrophy implies regular measurements of serum electrolytes, particularly calcium, phosphorus and magnesium, as well as levels of parathyroid hormone. Through regular check-ups, necessary treatment may be initiated early on, to at least try to slow the progression of kidney disease, which ultimately increases the need for hemodialysis. Dietary, as well as pharmacologic management of serum electrolytes are vital in prolonging the life of the patient, and ensuring some degree of comfort and quality of life, while preventing the early occurrence of complications which occur in renal failure.


Chronic kidney disease (CKD), and end-stage kidney disease - renal failure, can be accompanied with numerous disorders, one of them being renal osteodystrophy [1]. It is usually associated with abnormal bone mineralization process, due to hyper (or hypo)parathyroidism, calcitriol deficiency, and hyperphosphatemia, since the kidneys are unable to form calcitriol from vitamin D, and the electrolyte shifts caused by different bone diseases cannot be corrected. It is most commonly seen in patients on renal replacement therapy, and the elderly. The diagnosis is achieved through evaluation of serum electrolytes, mainly calcium, phosphorus, vitamin D levels, as well as parathyroid, and other hormone levels, to identify the cause, and initiate proper treatment, which consists of electrolyte correction and supportive therapy. The cause can rarely be addressed, since renal failure treatment can only be supportive. However bone diseases should be investigated and treated accordingly.

Patient Information

Renal osteodystrophy is a disease of the bones which occurs in patients with chronic kidney disease, and it usually follows a chronic course. This disorder occurs because the kidneys are unable to compensate for the changes in electrolyte levels, principally the levels of calcium and phosphorus, due to diseases that target the skeletal system, such as abnormal production of parathyroid hormone. Due to impaired kidney function, synthesis of vitamin D cannot be fully performed. Vitamin D is an important mediator of calcium metabolism and bone growth. As mentioned, this disease is most commonly seen in patients with chronic diseases of the kidney, including those who need hemodialysis. It is equally distributed among genders, while Caucasian population comprises about two thirds of all cases. Children may also develop renal osteodystrophy if they have some hereditary conditions which predispose them to develop this disease.

Symptoms of renal osteodystrophy are usually seen in the later stages, and include bone and joint pain, as well as fractures without apparent cause, and bone deformities, which may be observed more commonly in children, because bone growth is more pronounced during this period. The diagnosis can be achieved through detailed laboratory investigations including serum electrolytes, renal function tests, and levels of parathyroid hormone. The prognosis usually depends on the cause. Unfortunately, chronic kidney disease is a progressive, and eventually fatal disease, but certain steps to prolong the quality and duration of life of the patient may be taken. These include dietary restriction of phosphorus and calcium, as high phosphorus is observed in these patients, and in more severe cases, intake of so called "phosphate binders" which prevent absorption of phosphorus from food. Other measures include correction of magnesium, since magnesium levels are almost always disturbed when calcium levels are abnormal. Management of primary disease is vital in managing renal osteodystrophy.



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  2. Terai K, Nara H, Takakura K et-al. Vascular calcification and secondary hyperparathyroidism of severe chronic kidney disease and its relation to serum phosphate and calcium levels. Br. J. Pharmacol. 2009;156(8): 1267-78.
  3. Velásquez Forero F, Altamirano E, Ramos PT. High frequency of iron bone deposits in a Mexican population with renal osteodystrophy. Nephrol Dial Transplant. 1998;13(3):46-50.
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  5. Gonzalez EA, Martin KJ. Renal osteodystrophy. Rev Endocr Metab Disord. 2001;2(2):187-93.
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  7. Locatelli F, Cannata-Andia JB, Drueke TB, et al. Management of disturbances of calcium and phosphate metabolism in chronic renal insufficiency, with emphasis on the control of hyperphosphataemia. Nephrol Dial Transplant. 2002;17(5):723-31.
  8. Emmett M. A comparison of clinically useful phosphorus binders for patients with chronic kidney failure. Kidney Int Suppl. 2004;(90):S25-32.
  9. Ritz E. Managing mineral balance in end-stage renal disease. Nephrol Dial Transplant. 2004;19(1):i1-i3. 
  10. O'Donovan R, Baldwin D, Hammer M, et al. Substitution of aluminium salts by magnesium salts in control of dialysis hyper¬phosphataemia. Lancet. 1986;1(8486):880-2.

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Last updated: 2018-06-22 02:41