Year : 2008 | Volume
: 19 | Issue : 1 | Page : 97--101
Complete Recovery of Renal Allograft Function after Sixty Days of Delay following Living Related Transplantation
FA Arogundade1, TA Badmus2, AA Sanusi1, A Faponle3, A Adelusola4, ARK Adesunkanmi2, AA Agbakwuru2, AA Salako2, VA Adetiloye5, OC Famurewa5, FO Fatoye6, E Oyebamiji3, DO Akinola2, A Akinsola1,
1 Renal Unit, Department of Medicine, Obafemi Awolowo University, Ile-Ife, P.M.B 5538 Ile-Ife, Osun State, Nigeria
2 Urology Unit, Department of Surgery, Obafemi Awolowo University, Ile-Ife, P.M.B 5538 Ile-Ife, Osun State, Nigeria
3 Department of Anesthesiology, Obafemi Awolowo University, Ile-Ife, P.M.B 5538 Ile-Ife, Osun State, Nigeria
4 Department of Morbid Anatomy, Obafemi Awolowo University, Ile-Ife, P.M.B 5538 Ile-Ife, Osun State, Nigeria
5 Department of Radiology, Obafemi Awolowo University, Ile-Ife, P.M.B 5538 Ile-Ife, Osun State, Nigeria
6 Department of Mental Health, Obafemi Awolowo University, Ile-Ife, P.M.B 5538 Ile-Ife, Osun State, Nigeria
F A Arogundade
Renal Unit, Department of Medicine, Obafemi Awolowo University, Ile-Ife, P.M.B 5538 Ile-Ife, Osun State
Delayed graft function (DGF), a term employed when a newly transplanted organ does not function efficiently is commonly observed following cadaveric renal transplantation but is very rare after living related transplants. We present a 31-year-old female recipient of a related donor kidney (mother) who had DGF following transplantation due to acute tubular necrosis, probably caused by partial allograft arterial thrombosis, which recovered function after 60 days. Appropriate use of allograft biopsy should be encouraged even in resource-limited settings lest the allograft be assumed to have failed irreversibly.
|How to cite this article:|
Arogundade F A, Badmus T A, Sanusi A A, Faponle A, Adelusola A, Adesunkanmi A, Agbakwuru A A, Salako A A, Adetiloye V A, Famurewa O C, Fatoye F O, Oyebamiji E, Akinola D O, Akinsola A. Complete Recovery of Renal Allograft Function after Sixty Days of Delay following Living Related Transplantation.Saudi J Kidney Dis Transpl 2008;19:97-101
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Arogundade F A, Badmus T A, Sanusi A A, Faponle A, Adelusola A, Adesunkanmi A, Agbakwuru A A, Salako A A, Adetiloye V A, Famurewa O C, Fatoye F O, Oyebamiji E, Akinola D O, Akinsola A. Complete Recovery of Renal Allograft Function after Sixty Days of Delay following Living Related Transplantation. Saudi J Kidney Dis Transpl [serial online] 2008 [cited 2019 Aug 25 ];19:97-101
Available from: http://www.sjkdt.org/text.asp?2008/19/1/97/37444
Delayed graft function (DGF), a term employed when a newly transplanted organ does not function efficiently is commonly observed following cadaveric renal transplantation but is very rare after living related transplants. , It is usually heralded by reduction in urine output and serial elevation in serum urea and creatinine levels and has serious prognostic and long-term implications; hence its early detection and appropriate management is crucial. 
The common causes of DGF include postischemic acute tubular necrosis (ATN), hyper acute or accelerated rejection, mechanical problems of urinary tract, vascular problems and remotely, calcineurin inhibitor toxicity. ,
We present a case of DGF following living related renal transplantation, which recovered function after 60 days.
Miss O.E., a 31-year-old graduate teacher was admitted 56 months ago with a diagnosis of end-stage renal disease (ESRD) secondary to chronic glomerulonephritis. She was evaluated in detail and underwent a living related donor (mother) renal transplantation 51 months ago.
Her initial investigation results revealed bilaterally shrunken kidneys, cardiomegaly and anemia. She was negative to HBsAg, Hepatitis C Virus antibodies and anti HIV I and II antibodies. She was however CMVIgG positive and IgM negative. She was prepared for renal transplantation with regular thrice-weekly hemodialysis, subcutaneous erythropoietin, antihypertensive and antiulcer regime. Her tissue typing done by polymerase chain reaction revealed 1-1-0 mismatches at the A, B and DR loci respectively (i.e. 4/6 matching) with her 51year old mother, who was also seropositive to CMV-IgG but negative to all other serological markers.
The patient received numerous blood transfusions from her other siblings as well as the donor two months before transplantation; the last transfusion was given two weeks prior to surgery. She underwent a living related transplantation four months after admission; with a warm and cold ischemia times of 7 and 48 minutes respectively and a rewarm time (2 nd warm ischemic time) of 88 minutes. There was an initial delay in graft function during which period she was oliguric; the urinary output progressively reduced until she became anuric 12 days posttransplantation.
The patient underwent an ultrasound of the allograft, which revealed normal sized renal allograft with good cortico-medullary differentiation and sinus echoes. Doppler scanning showed a moderate flow but resistance index could not be determined as the caliper was faulty. Renal allograft biopsy carried out on the seventh posttransplant day revealed partially infarcted kidney and severe acute tubular necrosis with thrombosis in some vessels, which could be seen, in vascular rejection and infarction [Figure 1]a and b. The biopsy was repeated on the 17 th and 27 th post transplant days, which showed progressive improvement. The last biopsy revealed some tubular calcification consistent with previous ATN and was otherwise normal [Figure 2]a and b.
She was on triple immunosuppressive therapy included prednisolone, azathioprine and cyclosporin A (3 mg/kg/day), which were commenced 48 hours post-transplantation. Based on the clinical suspicion of vascular rejection with severe acute tubular necrosis and our inability to procure OKT3 or antilymphocyte globulin, she received a course of high dose methylprednisolone with no response. Hence, azathioprine and cyclosporin A were stopped and she was started on mycophenolate mofetil (MMF) and tacrolimus instead as rescue therapy.
Despite the histologic improvement observed in the third biopsy, she remained oliguric. Consequently, she was maintained on thrice weekly hemodialysis, subcutaneous erythropoietin, and antihypertensive drugs along with the immunosuppressive therapy.
She showed signs of renal recovery on the 52 nd day post-transplant when her urinary output progressively improved from 350 mls on the said day to 1200 mls/day one week later. [Figure 3],[Figure 4] show the variations in her serum creatinine and urine volume over time. Thereafter, the need for dialysis reduced until it was discontinued 60 days post-transplantation. The immunosuppressive therapy was scaled down to maintenance doses of 5 mg daily of prednisolone, 50 mg daily of cyclosporin A and 500 mg daily of MMF. Since then, the patient has done very well with excellent quality of life and good allograft function. Her daily urine output averaged 2.5 litres and her serum chemistry during her last clinic visit 51 months post-transplant revealed urea of 39 mg/dl, potassium 4 mmol/L, bicarbonate 25 mmol/L, chloride 118 mmol/L, and creatinine 1.7 mg/dl. Her complete blood count revealed hematocrit of 30%, WBC count of 3800/mm 3 and platelet count of 250,000/mm 3 .
Delayed graft function complicates 8-50% of cadaveric donor transplantations, particularly when kidneys from non-heart beating donors are used; however, it is rare after living donor transplantation.  In fact, DGF portends serious, usually life threatening, complications in living donor transplantation.
Our index patient had a vascular insult, which could have been secondary to partial allograft arterial thrombosis or vascular rejection both of which usually result in graft loss in majority of affected recipients. Even though the resistance index could not be determined, the allograft arterial flow was reported as moderate. The allograft biopsy revealed a partially infarcted organ with extensive tubular necrosis. The nonavailability and consequent non-use of antilymphocyte globulin or monoclonal antibodies known to be effective in vascular rejection, strengthens our diagnosis of partial allograft thrombosis. Vascular insults (arterial or venous), which could be in the form of thrombosis or atheroemboli, are potentially dangerous with very high rate of graft loss. Allograft thrombosis may arise de novo (primary thrombosis) or complicate a rejection process when it is termed secondary thrombosis.
Early allograft loss as high as 45% have been reported following primary thrombosis in cadaveric donor transplantation.  Some of the recognized predisposing factors include increased donor age, prolonged cold ischemia time, a hypersensitized recipient, and transplantation of the right kidney. , Underlying thrombophilic disorders are also known to increase the risk of early graft thrombosis. This has been reported in a male adolescent with combined heterozygous factor V Leiden and prothrombin gene mutation.  Inherited antithrombin deficiency is also known to predispose to allograft thrombosis. , Other recognized risk factors include the presence of antibodies directed against phospholipids or plasma proteins as seen in patients with lupus nephritis and antiphospholipid syndrome.  Our index patient had no features of lupus or inherited thrombophilic disorders.
On the contrary, our patient had received multiple transfusions, had fairly prolonged rewarm time and an allograft from her mother and all these could have predisposed her to allograft thrombosis. The prolongation of the second warm ischemic or rewarm time was caused by technical difficulties encountered during vascular anastomosis. Her eventual recovery of allograft function 60 days after transplant surgery was remarkable, especially so because the only clue to continued medical treatment were the allograft histopathological results, which indicated improvement. A major lesson from this report is the fact that clinical recovery may be delayed in such cases and should be anticipated.
In conclusion, this case of allograft thrombosis that eventually recovered two months post-transplantation deserves a mention. Appropriate use of allograft biopsy should be encouraged even in resource-limited settings lest the allograft may be assumed to have failed irreversibly.
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