Introduction
Renal transplantation has become the best treatment of choice for patients with end-stage renal disease (ESRD), which has medical and economic advantages in the low overall mortality and favorable quality of life [
1]. Currently, the standard method for renal transplantation involves the anastomosis of iliac vessels. We describe a special case that the renal vein was twisted by wrong suture causing the second short-term warm ischemia of the allograft after vascular anastomosis. This was solved in 9 min avoiding the second reperfusion and cold preservation.
Case report
A 57-year-old woman with ESRD was admitted for renal transplantation. The primary cause of ESRD was hypertensive nephropathy. The donor kidney was harvested from a donation after cardiac death (DCD) with the warm ischemia for 6 min. The vein of donor kidney was anastomosed end-to-side to the recipient right external iliac vein, and then the surgeon was substituted by another surgeon for this surgery. Subsequently, the artery of allograft was anastomosed end-to-side to the recipient right external iliac artery. Vascular clamps were released after vascular anastomoses, and reperfusion was instantaneous and uniform.
After the allograft was perfused for 2 min, the graft backside became dark red. Severe diffuse hemorrhage was found in the hilum and hemostasis was difficult to achieve the satisfying result. After careful examination, we found the vein of the allograft was fully twisted at the distal end of the vessel (Fig.1 A). The diffuse hemorrhage was the result of the high pressure in the kidney caused by the twisted vein. The position of the allograft was modified to achieve the better blood flow perfusion, but it failed and the twisted portion of the renal vein appeared at the proximal portion instead of the distal end (Fig.1B). Then, the allograft was maintained at the suitable position to keep the vessel partly twisted, and we discussed the solution. Five minutes later, consensus was achieved. The renal artery of the donor was occluded and the renal vein was re-anastomosed end-to-side to the right external iliac vein in original place at the correct angle (Fig. 1C). The whole process as we estimated was finished in 9 min without heparinization. Three minutes after the second reperfusion, the urine flowed out of the allograft. Total time of cold ischemia was 480 min, and standard ureteroneocystostomy was performed. Immunosuppression was maintained with tacrolimus, mycophenolate mofetil and steroids. Aspirin (100 mg/d), Ligusticum wallichii (10 ml/d) and prostaglandin E1 (20 μg/d) were administered for one week to improve the microcirculation and prevent the renal vein thrombosis, which did not affect the hemoglobin level. Prothrombin time (PT) and activated partial thromboplastin time (APTT) test showed normal. The allograft worked well. The blood urea nitrogen (BUN) and serum creatinine (Scr) returned to normal on the 2nd day post-operation (Fig. 2). The postoperative recovery was uneventful, so renal biopsy was not performed. The allograft was monitored by Doppler ultrasound every week. The blood distribution and perfusion status was well and the resistance index was 0.58, 0.64 and 0.66 during post operation three weeks. The patient was discharged 19 days after operation and was followed up for 3 months. The allograft function was as well as the contralateral one from the same donor.
Discussion
According to the previous reports, there are many reasons of the second allograft ischemia during operation. The vasospasm of transplanted kidney is the main reason including external artery spasm, internal artery spasm and inadequate blood supply due to low blood pressure. In these circumstances, enhancing blood pressure, counteracting with renal artery spasm and keeping warm are effective strategies. Other causes included renal artery stenosis, renal artery embolism, renal vein embolism, renal artery and/or vein angulation. Artery and vein embolism can usually be treated with heparin and anti-vasospasm drugs via external iliac artery. Otherwise, renal graft was reperfused
in vitro or
in vivo and underwent revascularization. In addition, hyperacute rejection may also cause allograft ischemia. Grafts were usually discarded because of hyperacute rejection and acute rejection complicated by rupture respectively [
2,
3]. If the renal ischemia during operation is not attributed to hyper-acute rejection, reperfusion should be undertaken, including perfusion
in vitro and
in vivo.
We reviewed the operation and found the surgeon substituted by another surgeon during the surgery was the main cause of the mistake. Under this condition, there are two strategies: one is the second perfusion with perfuse and cold preservation
in vitro or
in vivo, and the other is the procedure as we described. According to previous reports, the renal artery occlusion for<30 min may render the allograft to tolerate the subsequent insult without long-term adverse effects [
4]. The ischemia postconditioning hypothesis stated that multiple brief ischemic episodes applied to an organ would actually protect kidney during a subsequent sustained ischemic insult so that, in effect, ischemia could be exploited to protect that organ from ischemic injury. Postconditioning theoretically allows unrestricted application in clinical settings and, thus, it has attracted much attention to relieve renal IRI [
5]. The reperfusion injury can be mediated by several mechanisms including the generation of reactive oxygen species, cellular derangement, microvessel congestion and compression, polimorphonuclear (PMN)-mediated damage, and hypercoagulation. Previous studies have indicated that postconditioning has protective effects on renal IRI in animal models. The main mechanisms include the reduction of oxygen-free radicals and activated neutrophils, decrease of apoptosis and improvement of microcirculation [
6].
Postconditioning is mainly used in heart surgeries, but not widely applied in the kidney transplantation, because the mechanisms are still poorly understood [
7]. Traditionally, the postconditioning is defined as rapid intermittent interruptions of blood flow in the early phase of reperfusion and involves the mechanical alteration of the hemodynamics. The kidney function following this short-term warm ischemia recovered very well in short-term follow-up. Whether the second warm ischemia within 10 min causes the injury for the donor kidney, it needs more data and long-term follow-up to compare the regular cases. So, more studies are required to confirm our findings. It needs to be studied whether the multiple long time ischemia before IRI causes the effect on the kidney.
Conclusions
According to the experience of the case, we must avoid the second warm ischemia because of the surgeon’s mistake. When the second warm ischemia after vascular anastomosis occurs during the operation due to vessel thrombosis, stenosis or other reasons, the revascularization after the second reperfusion and cold preservation is the preferred strategy. The re-vascularization anastomosis without the second reperfusion and cold preservation in vitro or in vivo is not the usual recommendation. It only can be tried if the second reperfusion and cold preservation can’t be performed.
Higher Education Press and Springer-Verlag Berlin Heidelberg
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