Avascular
bone necrosis is a relatively rare but significant complication in renal transplant recipients because it causes progressive
pain and invalidity. It can be the consequence of the action of numerous causative factors, but it is mostly connected to
corticosteroid treatment.The underlying pathophysiologic mechanism is a diminished blood flow to the bone leading to
necrosis and bone destruction. During the past 25-years period, 570
renal transplantations and five combined kidney and
pancreas transplantations were performed in our centre. A part of the patients was lost to follow-up due to the separation of Croatia from the former Republic of Yugoslavia. After
transplantation, we revealed aseptic
necrosis of the femoral head in five female patients. All patients had a history of treatment with pulse doses of
corticosteroids. At
transplantation the average age of the patients was 52.2 yrs (range 46 to 62 yrs), and dialytic treatment before
transplantation lasted in average 9.2 yrs (range 2.5 to 21.2 yrs). The period between
renal transplantation and the development of clinical signs of avascular
bone necrosis lasted in average 1.2 yrs (range 0.3 to 2.3 yrs). We will demonstrate our 62-year old female patient with terminal
renal failure caused by post-streptococcal
glomerulonephritis, who was treated with
peritoneal dialysis 2.5 years before
renal transplantation. Twenty months before
renal transplantation the patient received pulse doses of
corticosteroids, together with
immunoglobulins and
plasmapheresis, for the treatment of an acute
polyradiculoneuritis Guillaine Barré. After
transplantation a standard immunosuppressive protocol was applied which included
tacrolimus,
mycophenolate mofetil,
corticosteroids and induction with
basiliximab. Four months after
transplantation the patient started to feel
pain in the right hip after longer standing, in addition to the earlier long-lasting problems caused by bilateral
coxarthrosis. The pelvic radiograph showed subchondral radiolucencies in the lateral part of the head circumference spreading into the proximal part of the neck of the right femur, which indicated the presence of aseptic
necrosis, but these changes could have also been caused by
coxarthrosis. Unexpectedly, magnetic resonance imaging (MRI) did not reveal changes characteristic for avascular
bone necrosis. Due to the progressively worsening of
pain and the radiographic finding, the patient was submitted to
decompression surgery of the femoral head. The
surgical procedure was performed under diascopic guidance (C-arm) which allowed the correct positioning of a Kuerschner wire. A cannulated drill (diameter 4.0 mm) was placed over the wire and we performed two drillings of the spongiosis of the femoral head through to the subchondral area. Postoperatively, the patient was soon verticalized and advised to walk with crooks during a period of six weeks. This time is necessary to allow the mineralisation and strengthening of the bone which is now better vascularised. The patient recovered well and had no more
pain. In renal transplant recipients it is most important to raise suspicion and verify the presence of avascular
bone necrosis early, because timely bone
decompression surgery can eliminate
pain and cure the patient or it can prevent or delay bone destruction. When clinical signs of avascular
bone necrosis arise and radiographic or standard MRI findings are negative, additional investigations (i.e. SPECT or MRI with contrast) should be performed to confirm or exclude the diagnosis. In latter phases of the disease,
surgical decompression of the femoral head cannot lead to permanent amelioration, and it is inevitable to perform more invasive
surgical procedures like "resurfacing" or
bone grafting in younger patients, or the implantation of total hip endoprotheses.