Case Author(s): David Hillier, M.D., Ph.D. and Tom R. Miller, M.D., Ph.D. , 6/15/99 . Rating: #D3, #Q4

Diagnosis: Renal osteodystrophy

Brief history:

51 year-old man with bilateral lower extremity pain.


Anterior and posterior images.

View main image(bs) in a separate image viewer

View second image(bs). Lateral skull scintigraphy.

View third image(xr). Lateral skull plain film

Full history/Diagnosis is available below

Diagnosis: Renal osteodystrophy

Full history:

51 year-old man with Bright’s disease (blindness due to uremia) who had kidney transplant in 1993. His serum creatinine level is 4. The patient complains of bilateral lower extremity pain.


21.8 mCi Tc-99m methylene diphosphonate


1. Bone scintigraphy (images 1 and 2):

- Generalized diffuse increased uptake in all bones, with marked increased uptake in the calvarium.

- No focal increased uptake in the lower extremities to explain the patient's pain.

2. Skull plain films (image 3, same day as bone scintigraphy):

- Diffuse patchy, granular “salt and pepper” appearance of the calvarium.


Renal osteodystrophy is a term describing the constellation of metabolic bone disorders that occur with chronic renal failure. These include the high bone turnover disorders; osteitis fibrosa cystica and mixed disease as well as the low bone turnover disorders; osteomalacia and adynamic bone disease. Osteitis fibrosa cystica is caused by hyperparathyroidism and is the most common manifestation of renal osteodystrophy. Mixed disease contains features of both osteitis fibrosa cystica and osteomalacia. Osteomalacia results from aluminum overload that can occur from dialysis or antacid abuse, although this is uncommon today. Vitamin D deficiency is probably a frequent contributing factor in osteomalacia associated with chronic renal failure. Adynamic bone disorder is characterized by decreased osteoblastic cells and absent osteiod.

Osteopenia is very common in patients with chronic renal failure and may be seen in either the high or low bone turnover forms of renal osteodystrophy. Glucocorticoid use by transplant patients contributes substantially to osteopenia.

Beta-2 microglobulin dialysis-related amyloidosis commonly occurs in patients on long-term dialysis (typically longer than 5 years). Carpal tunnel syndrome is usually the first manifestation. It is also characterized by arthralgias, bone cysts, pathological fractures and visceral involvement. Radiographically, juxta-articular lucent bone cysts may be seen.

In early stages of chronic renal failure, prior to bone disease, bone radiopharmaceutical uptake is normal but there is poor renal clearance and therefore soft tissue background will be increased at the normal imaging times. Secondary hyperparathyroidism occurs when there is sufficient loss of renal parenchyma that production of 1,25-dihydroxyvitamin D3 is reduced. This results in reduced intestinal calcium absorption and hypocalcemia. Decreased tubular excretion of phosphate leads to hyperphosphatemia. These changes result in increased parathyroid hormone (PTH) production. This secondary hyperparathyroidism causes osteitis fibrosa cystica, characterized by increased osteoclastic and osteoblastic activity with increased bone resorption and endosteal fibrosis.

“The clinical features of renal osteodystrophy include bone pain, skeletal deformity, growth retardation, fractures, extraskeletal calcifications, myopathy and pruritis” (Hruska, 1997). Bone painn generally occurs gradually and tends to be generalized. Severe bone pain is unusual and, when it occurs, is more typical of aluminum-overload osteomalacia. Bone deformity due to renal osteodystrophy is common, particularly in young children where the findings resemble rickets. A myopathy characterized by proximal muscle weakness may develop in renal osteodystrophy.

Extraskeletal calcification in end-stage renal disease may take the form of tumoral calcifications (peri-articular), medium-sized arterial calcification and visceral calcification (most commonly heart, lungs, kidneys, skeletal muscle and stomach). The propensity for calcification is related to a calcium/phosphate product greater than 75 (except for visceral calcification which seems to be unrelated), degree of hyperparathyroidism, serum magnesium levels, acidosis and local tissue injury.

Radiographic findings in renal osteodystrophy depend on the type of bone disorder and are not sensitive. In secondary hyperparathyroidism, subperiosteal resorption is the most sensitive finding but is only seen in under 50% of patients with histological evidence of resorption. Brown tumors may be seen in secondary hyperparathyroidism, but are less common than in the primary form.

Bone density measurements are frequently obtained in patients with renal osteodystrophy. The measurements are compromised by the presence of woven bone which contributes to the measured bone mineral density, but not to structural integrity.

Treatment of renal osteodystrophy consists of reducing phosphate levels with phosphate binders (such as calcium carbonate), careful control of dialysate calcium levels, correciton of acidosis and administration of vitamin D analogue supplements (especially calcitriol). In a small number of cases, these measures are unsuccessful due to persistent elevated PTH that occurs after chronic overstimulation of the parathyroid glands (tertiary hyperparathyroidism). In these cases, a partial or total parathyroidectomy may be undertaken. Another option is to perform a total parathyroidectomy with transplantation of some parathryoid tissue to the patient’s forearm (where further resection can more easily be undertaken if necessary).


See under differential diagnosis.

Major teaching point(s):

This case has characteristics of a "super scan" with markedly increased skeletal uptake with minimal renal and soft tissue uptake.

Differential Diagnosis List

The differential diagnosis of diffuse increased uptake in the skeleton with respect to the soft tissues includes diffuse metastases (especially prostate, breast, lung, lymphoma and bladder), metabolic bone disease (renal osteodystrophy, hyperparathyroidism, osteomalacia, rickets, hypervitaminosis D), Paget’s disease, myelofibrosis, mastocytosis, aplastic anemia. Increased uptake in the entire skeleton, including the appendicular skeleton, in metabolic bone disease helps to distinguish this from diffuse metastatic disease where increased uptake generally predominates in the axial skeleton.

The marked increased uptake in the calvarium and mandible, as seen in this case, is characteristic of hyperparathyroidism, renal osteodystrophy and anemia. Hyperparathyroidism and renal osteodystrophy may also cause periarticular increased uptake (faintly seen in this case), brown tumors (which may manifest as foci of either increased or decreased uptake), tie sternum, prominant costochondral junctions (also seen with osteomalacia and rickets - the “rachitic rosary”), prominantnt medial clavicles and soft tissue uptake in the lungs and stomach.

The skull plain film in this case reveals the “"salt and pepper"” appearance characteristic of renal osteodystrophy. In cases of severe anemias, a “hair on end” appearance may be seen in the calvarium.m.

This patient has a history of chronic renal failure with renal transplant 4 years ago. The imaging findings are most characteristic of renal osteodystrophy.

ACR Codes and Keywords:

References and General Discussion of Bone Scintigraphy (Anatomic field:Skeletal System, Category:Metabolic, endocrine, toxic)

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Case number: bs102

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