Complete necrosis of allograft ureter aftercadaveric renal transplantation

Although uncommon, complete necrosis of theureter should be considered in the differentialdiagnosis of early severe graft dysfunction. Thereare a few case reports (1–3) of this happening inteenage and adult patients but no reports, to ourknowledge, of this occurring in young children.We report on two cases of this complication inchildren and discuss the surgical management.

Case 1

In August 1994, a 13.4-kg, 5-yr-old boy withsevere chronic renal failure from megacystismegaureter syndrome with renal dysplasiareceived a pre-emptive 0:1:0 mismatched allo-graft from a 30-yr-old cadaveric donor. The grafthad two arteries on an aortic patch and a singlevein. The graft was placed intra-peritoneally withthe arterial anastamosis being made to a com-mon iliac artery and the venous anastamosis tothe inferior vena cava. The ureter was drainedinto the bladder without the use of a uretericstent. The cold ischaemic time was a little under24 h. Immunosuppression was with cyclosporinbased triple therapy.

The patient was stable post-operatively with anormal blood pressure for age and CVP of 5–10 mmHg. Initial graft function was poor with

little improvement in biochemistry despite aurine output of 27–33 mL/h. Allograft ultra-sound scan showed good perfusion and nohydronephrosis. Isotope renography showedgood perfusion but no excretion. On the basisof this a diagnosis of ATN was made.

On the sixth post-operative day the patientdeveloped a low grade pyrexia, abdominal painand diarrhoea. A clinical diagnosis of rejectionwas made and treatment with 5 days of intra-venous methylprednisolone commenced. By theninth post-operative day there was still noimprovement in renal function and a biopsy ofthe lower pole of the graft was performed. Thisshowed infarction and doppler studies on thetenth day confirmed lower pole infarction. Anexploration of the graft was performed andinfarction of the lower pole of the graft and thewhole ureter was found. The necrotic ureter wasremoved and a direct vesico-pelvic anastamosisperformed by bringing the dome of the urinarybladder up to the transplant renal pelvis. Upperpole biopsy performed intra-operatively showedmild acute cellular rejection.

Post-operatively renal function improved buthis clinical course was complicated by a furtherepisode of biopsy proven acute cellular rejectionand recurrent urinary tract infections. By 39 dayspost-transplant the patient was well with aplasma creatinine of 129 lmol/L and was allowedhome. Unfortunately, 89 days post-engraftment,

Sinha M, Lewis MA, Riad H, Webb NJA. Complete necrosis ofallograft ureter after cadaveric renal transplantation.Pediatr Transplantation 2004: 8: 91–93. � 2004 Blackwell Munksgaard

Abstract: Complete necrosis of a transplant ureter is a rare complicationthat needs to be considered early in cases of severe graft dysfunction ifsuccessful surgical intervention and restoration of graft function is to beachieved. We report on two cases of this complication occurring inchildren and discuss the surgical management. Surgical exploration ofgrafts where there is an early sudden decline in function is imperative asroutine imaging will not exclude this potentially treatable problem.

Manish Sinha, Malcolm A. Lewis,Hany Riad and Nicholas J. A. WebbRoyal Manchester Children's Hospitals, Manchester,UK

Key words: complication – necrosis – surgery –ureter

Dr Malcolm Lewis, Consultant Pediatric Nephrologist,Renal Unit, Royal Manchester Children's Hospitals,Manchester M27 4HA, UKTel.: +44 (0)161 727 2175Fax: +44 (0)7092 172 858E-mail: malcolm.lewis@cmmc.nhs.uk

Accepted for publication 22 July 2003

Abbreviations: ATN, acute tubular necrosis; CVP, centralvenous pressure; ESRF, end stage renal failure.

Pediatr Transplantation 2004: 8: 91–93

Printed in UK. All rights reservedCopyright � 2004 Blackwell Munksgaard

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the patient presented with nausea, vomiting andpyrexia. His plasma creatinine had risen to345 lmol/L. An ultrasound scan showed an echo-genic swollen, non-perfused graft. At explorationthere was thrombosis of the transplant renalartery and histological examination of the graftshowed chronic vascular and cellular rejection.

Case 2

In December 2001, a 15 kg, 5-yr-old male withESRF secondary to nephronophthisis received a1:1:0 mismatched cadaveric allograft from a32-yr-old donor. The graft had a single renalartery and vein anastamosed to the aorta andinferior vena cava during intra-peritoneal place-ment of the kidney. The cold ischaemic time was13 h and 10 min and the warm ischaemic timewas 32 min. The kidney was drained into thebladder. No ureteric stent was used. Immuno-suppression was with triple therapy of tacroli-mus, azathioprine and prednisolone withadditional induction therapy with basiliximabaccording to a randomized controlled trial inprogress at that time.

Initially there was good graft function with aurine output of between 45 and 75 mL/h over thefirst 24 h and a fall in the plasma creatinine from532 to 145 lmol/L. Over the subsequent 12 hthere was a fall in urine output to 8 mL/haccompanied by a rise in plasma creatinine to184 lmol/L. Throughout this time the patienthad been haemodynamically stable with a nor-mal blood pressure for his age and a CVP ofbetween 4 and 9 mmHg. There was significantfluid loss through the patient’s peritoneal dialysiscatheter which had been left in as a wound drainbut the biochemistry of this was suggestive ofserous fluid loss rather than a urinary leak.Despite supportive measures the patient becameanuric by 72 h post-transplantation. An ultra-sound scan showed no hydronephrosis, goodrenal perfusion and free intra-peritoneal fluid.

In view of the unexplained rapid deteriorationin graft function, despite maintained perfusion,an exploration was undertaken. Complete nec-rosis of the transplant ureter and some of thetransplant renal pelvis was found. The necrotictissue was removed, a native left nephrectomyperformed and the native left ureter was anast-amosed to the remaining healthy allograft pelvisover a double J stent. An allograft biopsy wasperformed and a percutaneous haemodialysiscatheter inserted in expectation of a period oftubular necrosis and oliguria.

The biopsy showed no evidence of rejectionand on the sixth post-operative day the patient

began to diurese and renal function improved.The patient was discharged home 14 days afterinitial engraftment with a plasma creatinine of61 lmol/L. At follow up 10 months later thepatient continues to have good graft functionwith a plasma creatinine of 67 lmol/L and nohydronephrosis on ultrasound.

Discussion

Urological complications after renal transplan-tation are an important group of problems thatcan adversely affect outcome. Most complica-tions relate to ureteric leakage or obstruction butcomplete ureteric necrosis has previously beendescribed in adults (3). The most recent reviewlooking at urological complications after livingrelated donation in adults and children quoted anoverall incidence of 8.3% (4). This figure is notdissimilar to incidence rates quoted in olderreview articles (3). Over a 9-yr period fromJanuary 1993 until January 2002 a total of 144renal transplants were performed in children inour institution. In this group there were a total ofseven ureteric complications (4.9%), two ofwhich were the cases of ureteric necrosis des-cribed above (1.4% of transplants, 29% ofureteric complications).

Causes of allograft ureteric necrosis are shownin the Table 1. Vascular insufficiency is probablythe most common cause. The allograft ureterreceives its blood supply solely from the renalartery. Special care needs to be taken whenharvesting a kidney and during preparation ofthe graft for the anastamoses to ensure there isno disruption to the ureteric blood supply. Manyfeel that the routine use of a ureteric stent reducesthe incidence of ureteric problems overall (5), butthese would not prevent ureteric necrosis throughvascular insufficiency.

The more common urological problems ofurinary leakage or ureteric obstruction will bepicked up with either ultrasound, isotope reno-

Table 1. Potential causes of ureteric necrosis

1. Vascular causesArterial ischaemiaMultiple vessels on the graftAberrant blood supply of ureter

Venous ischaemia2. Surgical causes

Damage to ureter during dissection or implantation3. Immunological causes

Ureteral rejection in association with allograft rejectionIsolated ureteral rejection

4. Other causesProlonged preservation timeEffect of preservation fluid

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graphy or analysis of drain fluid once suspectedbecause of graft dysfunction. Ureteric necrosisusually occurs early and, when complete, can leadto renal shutdown and anuria from the graft. Thiswas the case in both of the above cases. Thecombination of reduced or absent urine outputtogether with a rising plasma creatinine in the faceof good perfusion on either doppler ultrasound orisotope renography (but with failure of isotopeexcretion or extravasation), would bring to mindthe diagnoses of ATN or early acute rejection.Performing a percutaneous biopsy showing noevidence of rejection could easily make onecomfortable with the diagnosis of ATN. Thiswould invoke a �wait and see policy� that wouldlead to graft loss should ureteric necrosis bepresent. We therefore feel that, in cases whereATN is not expected, and particularly if there isinitial graft function with an early reverse in thetrend to improvement, severe graft dysfunctionneeds to be investigated with surgical explorationand open biopsy if required, as imaging will notreliably diagnose ureteric necrosis.

With regard to management, both anastamosisof the transplant pelvis directly to the bladder andthe use of a native ureter have been described (6,7). With the high incidence of urological problemsand renal tract dysplasia as a cause of renalfailure in children the latter is probably betterthan the former if ascending infection is to be

avoided. This clearly needs to be borne in mindwhen considering native nephrectomy and neph-ro-ureterectomy in paediatric ESRF patients. Inmany patients infection and vesico-ureteric refluxnecessitates removal of the native ureter(s) beforetransplantation. Wherever possible, however, webelieve the native ureter ought to be preserved foruse, if required, at transplantation.

References

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