A 23-year-old female patient, who had had a fracture of the right ulnar styloid one month ago, reported polyarticular pain on clinical examination and the blood analysis showed severe anaemia with increased acute phase reactants, lymphopenia, creatinin levels of 7.7 mg/dl, and an increased PTH.
Skeletal survey revealed subperiostic bone resorption in phalanges, acromio-clavicular, sacroiliac joints, and pubic symphysis related to hyperparathyroidism, as well as osteosclerosis in iliac bones, suggesting renal osteodystrophy. (Figs. 1, 2).
Other radiological tests were: neck and urological ultrasound scan showed a hypoechoic nodule posterior to the left thyroid lobe corresponding to a parathyroid hyperplasia (Fig. 3) and atrophic kidneys (Fig. 4); spine and pelvis CT scan showed a marked sclerosis in iliac bones and branches, as well as rugger jersey vertebrae (Fig. 5), related to renal osteodystrophy; with small lytic lesions compatible with brown tumours. Very marked subperiosteal bone resorption with increasement of the articular space in sacroiliac joints and pubis symphysis (Fig. 6, 7 and 8)
One month after starting haemodialysis she suffered an accidental fall with severe pain in the right knee. US and MRI findings helped diagnose a complete rupture of the vastus medialis of the quadriceps with retraction of the muscle-tendon joint and articular effusion (Figs. 9 and 10).
Renal osteodystrophy describes a group of musculoskeletal abnormalities caused by chronic renal insufficiency: secondary hyperparathyroidism, osteoporosis, osteomalacia and soft-tissue and vascular calcification. Chronic renal insufficiency (CRI) causes hyperphosphataemia and secondary hyperplasia of the parathyroid and increased PTH levels. Its osseous manifestations are: bone resorption, brown tumours and periosteal reaction.
Other musculoskeletal abnormalities associated with haemodialysis and transplantation are aluminium toxicity that cause osteomalacia, amyloidosis and destructive spondyloarthropathy.
1. The most frequent lesion is bone resorption and involves the radial aspects of the middle and proximal phalanges. Subchondral resorption can be seen in appendicular and axial skeleton: acromioclavicular joint, sternoclavicular joint, sacroiliac joint, symphysis pubis, etc.
2. Brown tumours are vascular fibrous tissue (cystic fibrous osteitis) replacing normal bone marrow.
3. Osteosclerosis is an increase of bone density of the axial skeleton. It involves the vertebral bodies, predominately sclerosis of the superior and inferior end plates and leads to the classic sign “rugby jersey spine”
4. Osteoporosis is frequently present in CRI. It is important to recognise because of its predisposition to insufficiency fractures.
5. Soft-tissue and vascular calcification are caused by hypercalcaemia, local tissue damage and alkalosis.
6. Tendon ruptures have been reported in patients with hyperparathyroidism and mostly in patients who undergo haemodialysis. The most frequent tendon involved is the quadriceps. Tendons are weak and predisposed to tears because of PTH excess that causes tendon calcification, increased ligament and capsular laxity and acidosis with connective tissue elastosis.
7. Other lesions related less frequently are crystal deposition disease, osteomyelitis and septic arthritis, avascular necrosis.
Nowadays all these lesions are not frequently found because IR diagnosis is easy and treatment is established, but knowledge of the range of musculoskeletal radiological appearances associated with CRI and HyperPTH should not be forgotten and help to reach an accurate diagnosis in some patients.
Renal osteodystrophy.
Based on the provided X-ray, ultrasound, and CT images, the following observations are noted:
Given the patient’s chronic renal insufficiency (creatinine 7.7 mg/dL), elevated PTH, and characteristic bone changes (bone resorption, bone sclerosis, possible brown tumors), this is the most likely diagnosis.
While elevated PTH and bone changes can also occur in primary hyperparathyroidism, the severe renal failure and hyperphosphatemia here point towards a renal cause of secondary hyperparathyroidism.
These conditions may likewise result in osteolytic lesions. However, the patient’s blood profile (severe anemia), elevated PTH, and CRF (chronic renal failure) more strongly support the pathophysiology of renal osteodystrophy.
Taking into account the patient’s age, chronic renal insufficiency (markedly elevated creatinine), secondary hyperparathyroidism (raised PTH), bone alterations (bone resorption, possible brown tumors), and multiple fractures indicative of increased bone fragility, the most likely diagnosis is:
“Renal Osteodystrophy with Secondary Hyperparathyroidism.”
Management and rehabilitation should incorporate the following elements:
This report is based on the present imaging and clinical information solely for reference. It does not substitute for an in-person medical consultation or the advice of a professional healthcare provider. For specific diagnosis and treatment plans, please adhere to the assessment and recommendations provided by qualified medical institutions and specialists.
Renal osteodystrophy.
