EXPERIMENTAL AND CLINICAL TRANSPLANTATION

Objectives: Vascular complications, especially immediate events during kidney transplant, are the major cause of graft loss, and prompt surgical intervention is important for salvage of the graft and recipient. In this study, our aim was to show our experiences with vascular interventions and their effects on graft outcomes in transplant patients with suspected immediate vascular events.

Materials and Methods: Over 24 years (from 1990 to 2014), 2100 renal transplant procedures (1562 living and 538 deceased donors) were performed by one fixed team. We reviewed the recipients to find cases with immediate vascular complications, including artery or vein kinking or torsion, renal artery thrombosis, and renal vein thrombosis. Diagnosis of a vascular event was suspected when urinary output suddenly stopped and was confirmed by color Doppler ultrasonography or immediate exploration. Characteristics of the patients and events, surgical interventions for saving grafts, and graft outcomes were assessed.

Results: Our study included 28 vascular accidents (1.3% of total renal transplants). Arterial kinking or torsion, venous kinking or torsion, renal artery thrombosis, and renal vein thrombosis occurred in 11 (0.52%), 2 (0.09%), 12 (0.57%), and 3 patients (0.14%). Nine of the 11 cases of arterial kinking occurred with use of internal iliac artery. Eleven of 13 grafts with vascular kinking or torsion were saved by immediate surgical intervention, but only 4 grafts in patients with renal artery thrombosis and only 1 graft in patients with renal vein thrombosis were saved by surgical intervention. Delayed graft function occurred in all cases of saved renal artery and renal vein thrombosis but only in 5 cases (4 arterial and 1 venous) of vascular kinking or torsion.

Conclusions: The incidence of immediate vascular complications was 1.3% in our study. Sudden cessation of urine after renal transplant is a warning sign, and immediate diagnosis of vascular events will help salvage the graft with proper intervention.

Key words : Renal artery thrombosis, Renal transplantation, Renal vein thrombosis, Vascular surgical procedures

Renal transplant is the treatment of choice for patients with end-stage renal disease.¹ In previous studies, vascular complications were found in approximately 1% to 5% of patients who underwent renal transplant, accompanied by possible significant morbidity and mortality.² Immediate vascular complications occur within a few hours or days after transplant and include kinking or torsion of the kidney graft’s artery or vein, suture line stenosis, or thrombosis. Arterial or vein thrombosis is the main cause of these events, which usually occur due to technical problems. Other causes include hyperacute rejection or thrombophilia.³ We should keep in mind that the most common vascular complication after renal transplant is renal artery stenosis, but the time of clinical presentation varies from 3 months to 2 years after transplant. It is usually diagnosed because of hypertension that is progressively difficult to manage, with or without impaired renal function.^4,5 To minimize morbidity and mortality, all of these complications must be diagnosed quickly and treated appropriately. Herein, we reviewed our experience in the evaluation and treatment of immediate vascular complications from a cohort of 2100 recipients who received renal transplants between 1990 and 2014.

Materials and Methods

We retrospectively reviewed patients who underwent renal transplant at our center between 1990 and 2014 to find cases with vascular complications, including artery and vein kinking or torsion, renal artery thrombosis (RAT), and renal vein thrombosis (RVT). One fixed team performed all of the operations. Donations were from both living and deceased patients.

For our surgical technique, renal artery anastomosis is either done end to end (to internal iliac artery) or end to side (to external iliac artery); however, the preferred method is end-to-end anastomosis unless the internal iliac artery of the recipient is not appropriate for the anastomosis. For the first group, anastomotic ends of both recipient and graft arteries were spatulated at opposite ends. Medial and lateral corners were approximated first using Prolene 6-0 sutures, and then cephalad and caudad margins were sutured using continuous sutures. For end-to-side anastomosis, an appropriate size arteriotomy was made after clamping artery proximally and distally. Graft artery was spatulated, cephalad and caudal ends were approximated, and medial and lateral walls of anastomosis were sutured continuously with Prolene 6-0. In most cases of renal grafts with deceased donors, an aortic patch from the donor was also harvested and used at the site of the arterial anastomosis. Venous anastomosis was done to external iliac vein by end-to-side technique using a Prolene 5-0 suture in all cases. In addition, similar to the artery anastomosis, in most cases of deceased donors, we take the cuff of the inferior vena cava along with the renal vein during the right-sided nephrectomy.

Postoperatively, patients were kept in a dedicated transplant unit under careful clinical observation and monitoring. Renal function tests and other serum biochemical parameters were monitored on a daily basis; more frequent monitoring depended on the patient’s condition. Two-dimensional ultrasonography and color Doppler ultrasonography were performed whenever there was clinical suspicion or evidence of suboptimal renal function. Diagnosis of a vascular event was suspected when urinary output suddenly stopped and confirmed by color Doppler ultrasonography or immediate exploration whenever needed. Renal angiography was done in stable patients if there was suspicion of any vascular complication on immediate evaluation. Patients with early graft loss secondary to acute rejection and patients with long-term vascular complications, such as arterial stenosis, arteriovenous fistula, and pseudoaneurysm occurring after biopsy of renal allograft, were excluded from the study. Immediate vascular complications were classified as renal artery thrombosis (RAT), renal vein thrombosis (RVT), arterial kinking or torsion, and venous kinking or torsion. We assessed and analyzed patient characteristics, type of surgical interventions for saving grafts, and patient and graft outcomes using SPSS software (SPSS: An IBM Company, version 18.0, IBM Corporation, Armonk, NY, USA).

Over a period of 24 years (March 1990 to December 2014), 2100 renal transplant procedures were performed by one fixed team at our center, with 1562 patients (74.4%) receiving kidney transplant from living donors and 538 patients (25.6%) receiving kidney transplant from deceased donors. The mean age of patients was 44 years (range, 6-65 y).

In the total patient cohort, 28 patients (1.3%) showed immediate vascular accidents. Mean age of these patients was 49 years (range, 20-63 y), with 15 women and 13 men.

Arterial kinking or torsion occurred in 11 patients, and venous kinking or torsion occurred in 2 patients. Renal artery thrombosis occurred in 12 patients, and RVT occurred in 3 patients. We found that 9 of 11 cases with arterial kinking or torsion occurred in transplants that used the internal iliac artery. In addition, 9 of 12 cases of RAT occurred in patients with end-to-end anastomosis (Table 1). Of 12 cases of RAT, atheromatous arteries were seen in 5 patients (41.6%) (either in donors or recipients), with 4 of the donors having multiple arteries (33.3%). For RVT, 2 donors had multiple vessels (66.6%). All occurrences of thrombotic events with multiple vessels were seen in deceased donors. We found that 11 of 13 grafts with vascular kinking or torsion were saved with immediate surgical intervention; however, only 4 grafts of the RAT group (33.3%) and 1 graft of the RVT group (33.3%) were saved by surgical intervention. In patients in which the transplants were saved, thrombosis was incomplete and in other cases it was complete. The mean time between diagnosis of the vascular event and exploration was less than 2 hours.

In thrombotic cases, we reopened the anastomosis and performed small venotomy or arteriotomy, washed and perfused the graft with heparinized Ringer solution, and finally restored the revascularization. Delayed graft function occurred in all cases of saved RAT and RVT but in only 5 cases of vascular kinking or torsion (4 arterial and 1 venous).

Surgical complications in renal transplant can be divided into vascular complications, urologic complications (including ureteric complications and lymphocele formation), and general surgical problems such as bleeding and wound infections.³ Of these, vascular complications are probably the most critical, which can lead to sudden loss of renal allograft. The rate of vascular complications has been reported differently in previous studies. In Srivastava and associates, it was 1.29%, 2.55% in Aktas and associates, 2.8% in Osman and associates, 4.2% in Dimitroulis and associates, 5.4% in Basic and associates, and 8.8% in Salehipour and associates.3,6-10 A high incidence was also reported in a study from Safa and associates. In 55 recipients, they reported 20 vascular complications (37%); however, they do not state reasons for the high vascular complication rate.¹¹ In our study, the incidence of immediate vascular accidents was 1.3%. Because we excluded other delayed complications, such as arterial stenosis, arteriovenous fistula, and pseudoaneurysm, our results could be comparable to previous studies.

Different types of vascular complications may occur after renal transplant. The most important immediate types are RAT and RVT, which can occur as a result of arterial kinking, arterial torsion, venous kinking, and venous torsion.^6-10 The cause of these complications remains somewhat unclear. Renal artery stenosis, arteriovenous fistula, and pseudoaneurysm can also occur, although patients who had these were excluded from our current study. The causes of the various vascular complications in renal transplant are multifactorial. Technical errors or recipient-related factors such as hypercoagulopathies and decreased cardiac output may be important contributions to cause.³ Some studies have shown that vascular complications occur in grafts from deceased donors more frequently than in those from living donors.¹⁰ In addition, Osman and associates stated that grafts with multiple renal arteries have more stenotic or thrombotic complications.⁷

Renal artery thrombosis in the transplanted kidney is a major cause of graft loss in the early posttransplant period. It is an uncommon complication, with a reported incidence ranging from 0.5% to 4%.^12,13 In our study, 42.8% of all vascular events were due to RAT (0.57% of total patients in our study cohort). Sudden reduction or cessation of urine output and elevation of serum creatinine levels are usually the only clinical presentation of transplant RAT, and a high degree of suspicion is required in the early postoperative period for timely diagnosis.¹⁴ In our study, the most important symptom used to diagnose RAT was sudden reduction of urine output, even shown during the recovery period. Therefore, in these situations, with immediate reopening of the site of surgery, we were able to find the anatomic problem, such as kinking or twisting, before the occurrence of thrombosis. Whenever there is sudden decrease in urine output early after transplant, immediate color Doppler ultrasonography is useful to diagnose RAT before attributing it to other more common causes, such as acute rejection or acute tubular necrosis.³ Radionuclide imaging may reveal a severe reduction or absence of allograft perfusion. Catheter-based angiography and magnetic resonance angiography are the main methods to confirm diagnosis. Although angiography appears to be the criterion standard for diagnosis, it may not be feasible in emergency situations. Progress in interventional radiology has allowed the diagnosis of this complication even without use of contrast media, protecting the already compromised renal graft. When thrombosis leads to complete arterial obstruction, graft loss may occur; however, when thrombosis spares the renal artery trunk and affects only the smaller distal branches, the clinical presentation is milder and the outcome better.¹⁵

The main cause of transplant RAT is technical errors. Twisting or kinking at the site of anastomosis and dissection caused by injury to intima may also cause this complication.³ In our study, RAT occurred more frequently in patients who received their grafts from deceased donors. This may be because of more vascular anomalies seen in these patients, requiring more vascular reconstructions. The longer cold ischemia time is also another important factor. We found that 75% of RAT occurrences were in patients needing use of the internal iliac artery. Therefore, it seems that deceased donations and end-to-end anastomosis may be the key risk factors. Other rare causes include acute rejection episodes, external compression by adjacent hematoma or lymphocele, hypercoagulative state, severe hypotension, toxicity from immunosuppressive agents such as cyclosporine or sirolimus, and administration of OKT3, especially when used in combination with high doses of methylprednisolone.^16,17

Transplant RAT is a surgical emergency. Immediate exploration is the only chance to save the transplanted kidney. Although transplant nephrectomy is inevitable in many cases, surgical thrombectomy with repair of the anastomosis is usually performed. The role of interventional management in graft artery thrombosis is not yet clearly defined, but several successful cases of catheter-directed thrombolysis with or without percutaneous angioplasty and/or stent placement have been reported. Catheter-directed thrombolytic agent administration is not recommended during the first 10 to 14 days after transplant due to a major risk of postoperative bleeding.^8,15 In only 33.3% of our patients, the graft was saved by emergent exploration, but all showed delayed graft function. On the other hand, 90% of grafts with arterial kinking or torsion survived. It seems that nonthrombotic events have better survival.

Renal vein thrombosis is one of the major vascular complications after transplant and one of the most important causes of immediate graft loss. The rate of RVT in transplanted kidneys is reported to be between 0.15 and 6%.3,18 In our study, the incidence of RVT was 10.7% of vascular events (0.14% of total patients). The most important cause of RVT is technical factors, including torsion or kinking of the graft vein, a long vein, and injury to the vascular endothelium during surgical manipulation or back-table procedures.⁸ Technical problems may occur, especially in the setting of right donor nephrectomy because of short and thin-walled renal vein. The cuff of the inferior vena cava and the renal vein had been removed during right-sided nephrectomy, resulting in no technical difficulties during anastomosis, and this appears to be the predominant cause of the low incidence of RVT.3 We have taken these inferior vena cava patches only in deceased donors. In addition, similar to that shown previously regarding incidence of RVT being greater with deceased donations versus living donations, in our study, all of the 3 cases of RVT occurred in deceased donor grafts. Higher doses of cyclosporine, common in the early years of its use, are also associated with higher incidence of venous thrombosis.¹⁹Another important cause is hypercoagulopathies, such as deficiency of antithrombin III, protein C, or protein S.²⁰ Renal vein thrombosis usually presents with sudden onset of oliguria and hematuria associated with intensive pain or discomfort over the graft area. Ipsilateral lower extremity edema, low-grade fever, and in severe cases massive hemorrhage may also be seen. If clinical signs and symptoms are suspicious for RVT, color Doppler ultrasonography is useful for confirmation of diagnosis. The main finding in color Doppler ultrasonography is lack of flow in the renal vein, with other findings being swollen graft, a clot covering the lateral margin of the kidney, and abnormal arterial signal with a plateau-like reversed diastolic flow.²¹ Magnetic resonance venography is more accurate but not so often used as a routine evaluation method. Surgical exploration is almost always required. Although most cases lead to renal graft loss, surgical thrombectomy may be useful in some patients. Some reports have shown successful treatment of RVT using thrombolytic agents.²² Because RVT usually leads to graft loss, prevention may be the best treatment option. Moreover, it is important to point out that in a few cases surgical exploration may only show kinking of the vein; in these patients, the graft may successfully be saved. In our study, although the 2 patients with venous kinking or torsion had graft survival, only 1 of 3 patients with RVT had graft survival. Delayed graft function occurred in all cases of RVT and in 50% of venous kinking cases.

An important positive point of our study is the large population that we evaluated, although a main limitation is the retrospective design. Prospective studies may be helpful to confirm our results.

The incidence of immediate vascular complications in our study was 1.3%. Vascular events were more common in deceased donor grafts and with end-to-end anastomosis using the internal iliac artery. Sudden cessation of urine after renal transplant is a warning sign, and immediate diagnosis of the vascular event will help salvage the graft with proper intervention.

Volume: 15 Issue: 5 October 2017

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