1
Honorary Renal Transplant Surgeon, Royal Children’s Hospital, Melbourne, Australia
2
Tribhuvan University Teaching Hospital, Kathmandu, Nepal
Corresponding author details:
David M. A. Francis
Honorary Renal Transplant Surgeon
Royal Children’s Hospital
Melbourne,Australia
Copyright:
© 2018 Francis DMA. This is
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international License, which permits unrestricted
use, distribution and reproduction in any
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Renal Allograft Rupture (RAR) is an unusual and serious complication of renal
transplantation. Early reports gave incidences of 2.5–9.6% [1-4], while papers published
since 2000 reported incidences of 0.35–2.7% [5-8]. Introduction of Cyclosporine as
background immunosuppressant and use of anti-lymphocyte agents for prophylaxis and
treatment of acute rejection have reduced the occurrence of RAR [3,9] presumably due to
reduction in the incidence and severity of rejection.
RAR occurs because of trauma or any cause of swelling of the transplanted kidney. Trauma to the transplant may result from direct blunt injury [2]; insertion of a nephrostomy tube [10]; and operative [11], open [12,13] or percutaneous [9,14,15] renal biopsy. The author treated a patient whose longstanding kidney transplant ruptured following hyperextension and stretching of the abdomen while bungee jumping.
‘Spontaneous’ RAR is due to swelling of the allograft because of acute cellular rejection [4,5], antibody-mediated rejection [16], acute tubular necrosis [5,8,9], allograft ischaemia and focal necrosis [2,15], abscess formation [14], obstructed efferent lymphatic vessels [4,14,17], ureteric obstruction causing hydronephrosis [4,15,18] and renal vein thrombosis with or without ileo-femoral vein thrombosis [2,3,5]. Intrarenal pressure has been shown to almost double in kidneys with acute rejection [19].
Factors that may contribute to RAR include the method of kidney preservation [2,20,21],
capsulotomy at the time of transplantation [11,15], a prothrombotic effect associated
with cyclosporine [4] and postoperative anticoagulation [2,22] for haemodialysis, plasma
exchange and prevention of thrombosis.
Most cases of spontaneous RAR occur within the first two to three weeks after
transplantation [3,9]. Patients experience sudden onset of severe pain over the transplanted
kidney, simultaneous tenderness and swelling of the graft, signs of hypovolaemia and
blood loss, increased drain output and oliguria if the graft is functioning [9]. Investigations
to visualise the transplanted kidney are unnecessary as they may delay urgent operative
intervention. Renal angiography, ultrasound, renal isotope scanning and computerised
tomography [7,10,11] can confirm the clinical diagnosis by demonstrating increased
transplant size, disruption of cortical integrity, parenchymal rupture and perinephric
haematoma.
Patients require urgent exploration of the transplant together with active resuscitation.
The aim of the intervention is to control bleeding and repair the kidney, evacuate the
perinephric haematoma and treat the underlying cause of the rupture. Ruptures of the
renal parenchyma are usually multiple and frequently along the convex border of the
kidney [9,11,16].Every attempt should be made to salvage the transplant [7,8,9,22].Several
different methods of repair have been reported. Haemostatic material (Oxycel [9], fibrin
sealant [23], fascia and muscle [21], tissue glue [24], collagen foam [17]) is placed into the
split which is then over sewn [9]. The renal parenchyma is fragile but can be sutured by
passing sutures through Oxycel or teflon pads [9], placed on the renal surface where the
suture needle enters and exits the parenchyma. External compression can be provided by
wrapping the allograft instrips of fascia [23], peritoneum [22], polyglycolide (dexon) mesh
[17], polyglactin 910 (vicryl) absorbable mesh [24] or strips of lyophilized human Dura
[13], if the parenchyma is deemed unsuitable for suture. Kidneys should be biopsied at the
time of repair so that the underlying cause of the rupture can be identified [9]. Transplant
nephrectomy is performed only if haemorrhage cannot be otherwise controlled.
Most reports indicate that satisfactory medium and long-term graft survival can be
obtained in the absence of renal vein thrombosis [3,5,8,9,13,16,17]. Haemorrhage must be controlled, re-rupture and infection prevented, acute rejection (if
present) [25] successfully treated and chronic allograft nephropathy
avoided.
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