Lytic lesions in chronic renal failure: Brown tumour is a must on the differential

38-year-old man with chronic renal disease on haemodialysis. He presented cutaneous lesions compatible with calciphylaxis and severe musculoskeletal complaints, especially on the left hip. Laboratory results demonstrated elevated parathyroid hormone levels as well as hyperphosphataemia.

The pelvic and leg radiographs requested as a first line examination to assess the hip symptoms demonstrated diffuse reduction of bone mineralisation, compatible with moderate/severe osteopenia. Additionally, a relatively well-defined eccentric bubbly lytic lesion with sclerotic borders was depicted on the medial side of the left femoral diaphysis. On the radiograph there were also severe vascular calcifications related to the known renal dysfunction.
The abdominopelvic and lower limb computed tomography (CT) revealed a heterogeneous pattern of bone mineralisation, with significant loss of the normal bone trabeculation in the femoral shafts and also a “rugger-jersey” pattern in the spine, with an important subendplate sclerosis. In addition, CT confirmed the presence of an expansile soft tissue lesion in the left femoral diaphysis, with well-defined sclerotic borders, causing mild subperiosteal scalloping, but no periosteal reaction associated.
9mTc-sestamibi study depicted an increased uptake on the anatomical site of the right parathyroid gland.

Brown tumours (BT) are one of the rare skeletal manifestations of primary or secondary hyperparathyroidism, occurring in the setting of prolonged disease [1, 2, 4], more often in women.  In fact, BT are not true malignant neoplasms, but rather result from a reparative process, known as osteitis fibrosa cystica, caused by abnormally high osteoclast activity, in which normal bone matrix is substituted for granulation and fibrotic tissue. There is also evidence of haemosiderin deposits within them, leading to its brownish coloration. [2, 4]. Primary hyperparathyroidism is frequently associated with lesions in the parathyroid, like adenomas, hyperplasia or malignant lesions. Secondary hyperparathyroidism is related to systemic resistance to the parathyroid hormone action, normally in the setting of chronic renal disease, vitamin D deficiency [3], with persisting high levels of parathyroid hormone, hypercalcaemia and hyperphosphataemia.
BT can occur in the jaw, skull, mandible, clavicles, pelvis, ribs, spine and extremities (femur).
At imaging, they often present as a well-defined, single or multiple lytic lesion, with non-sclerotic borders, sometimes with cortex thinning, but with no clear aggressive features. Other presentations include an expansible behaviour, bone deformity, multilobular cystic changes, generalised demineralisation and subperiosteal scalloping [1, 2], all as part of the high turnover bone disease. Fractures, compressive syndromes, face deformation and difficulties in eating or breathing can be one of the presentations of this lesions, due to their growing potential [4].  The imaging findings of BT can overlap those of giant-cell tumours, metastases, bone cysts or osteosarcoma [1]. Scintigraphy is helpful for detecting hyperparathyroidism-related bone disease, although conditions like metastatic disease, multiple myeloma, infection, trauma and other metabolic disease can present as “false-positives” [1]. Biopsy is the gold standard approach for the final diagnosis. Occasionally, biopsy can be inconclusive, as BT can histologically resemble other lesions. Having said that, biopsy is not usually performed in the setting of typical imaging features in a patient with known chronic kidney disease. Therefore, a high rate of suspicion, clinical history and laboratory results are all key features for an accurate diagnosis, without the need of an invasive procedure [2].
In this case, the clinical history (haemodialysis) and the additional musculoskeletal manifestations (rugger-jersey spine) were key findings that allowed the radiologist to put BT on the differential diagnosis list. This suspicion led to further examinations, including parathyroid gland ultrasound and scintigraphic assessment, which were both positive.
Partial or complete surgical removal of the parathyroid gland can be considered as treatment when medical approach fails [2]. Upon favourable response, BT can then regress or appear as an area of increased bone sclerosis [2].
In conclusion, the high rate of suspicion of BT tumours can improve patient management.

Written patient consent for this case was waived by the Editorial Board. Patient data may have been modified to ensure patient anonymity.