Since the first successful organ transplant conducted between twins in 1954, kidney transplant has evolved considerably over the past 50 years. Kidney transplant plays an important role in the treatment of end-stage kidney disease to improve the quality of life and prolong the life of patients. Despite significant advances, postoperative medical and surgical com­plications still represent important causes of morbidity and mortality. Many problems can be avoided through prophylactic correction of abnormalities detected during the preoperative evaluation; however, it is critical that technical mishaps at all stages of the transplant process (donor nephrectomy, benchwork preparation, and implant) be prevented and that careful postoperative monitoring be carried out, including thorough examination by attending physicians. However, despite these advances, surgical complications still present serious problems in kidney transplant recipients.

Key words : Iliac artery dissection, Renal artery thrombosis and stenosis, Urologic complications, Vascular complications

Intraoperative Complications of External Iliac Arterial Dissection

Traumatic external iliac artery dissection (EIAD) after renal transplant is a rare complication, but it should be treated immediately due to its devastating effects on graft and lower limb circulation. External iliac artery dissection is seen more in recipients with diabetes mellitus and comorbid diseases. Vascular atherosclerosis and cardiomyopathy are predisposing factors for EIAD. Besides senility, hypertension, dyslipidemia, smoking, and diabetes, many other risk factors (like anemia, microalbuminemia, and oxidative stress) may play a role in EIAD in patients with end-stage renal disease. External iliac artery dissection after renal transplant appears with hypertension, sudden pain in lower limbs without pulse, oliguria, or anuria. Graft artery and femoral artery blood flow cannot be visualized by Doppler ultrasound. Recipients with EIAD should be treated immediately by percutaneous angioplasty or surgical reconstruction. In the literature, some cases have been treated by percutaneous angioplasty and stenting and/or endarterectomy.¹ The other treatment option is reconstruction with expanded polytetrafluoroethylene (ePTFE) graft. In our center, EIAD complications have occurred in only 2 patients. Both cases were due to vascular clamping, and we treated the patients with expanded polytetra­fluoro­ethylene graft reconstruction technique (Figure 1). The dissected part of the external iliac artery was resected and replaced with a 6- to 8-cm × 8-mm PTFE graft using 6/0 Prolene. The renal artery was then anastomosed to the PTFE graft with 7/0 Prolene continuously. Both patients were doing well at follow-up with normal kidney function (Figure 2, A and B).

Postoperative Vascular Complications

Vascular complications can result from renal graft vessels (renal artery thrombosis, renal vein throm­bosis), the native vessels (iliac artery throm­bosis, pseudoaneurysms, deep venous thrombosis), or both.

Refinement of the operative technique for kidney transplant has greatly reduced surgical complication, morbidity, and mortality rates in recipients. In particular, significant progress has been made regarding methods of vascular anastomosis. The introduction of the Carrel patch vascular technique by Alexis Carrel in 1902 is considered one of the most important steps in transplant surgery.² Some vascular complications associated with renal transplant procedures can be managed with percutaneous techniques. Others call for urgent surgical intervention because of possible graft loss if treatment is not swift and appropriate. The incidence of vascular complications has been reported to be as high as 30% during early stages of transplant development, whereas currently the incidence rate is 0.8 to 6%.³

According to Clarke and associates,⁴ Starzl (1964) mentioned 1 patient who survived removal of pulmonary embolus and complication of the vena cava for 2 months, during which the kidney functioned, but at necropsy the renal vein was occluded by thrombus, which extended to its smallest branches. Another group (Smellie and associates, 1968) attempted to visualize the renal vein by pertrochanteric venography in 3 transplant recipients. In all 3 patients, the renal vein was thought to be patent, although only its terminal portion was demonstrated as such. Other groups reported by Clarke and associates included Walsh, who described arterial complications but did not mention thrombosis of the renal vein in 1969, and Khastagir and associates, who mentioned 2 patients in 1969 in which thrombosis of the renal vessels occurred as part of the rejection process, although the investigators did not specifically describe the renal veins. Finally, Owen in 1969 suggested that, if diagnosed early enough, it was worthwhile to explore thrombosed anastomoses but that it was not often possible to obtain a viable kidney.

In Turkey, the first living donor kidney transplant was performed by Haberal and team on November 3, 1975. Since 1975, Haberal has described different vascular anastomosis techniques. From November 1993 to December 2003, his group performed end-to-side or end-to-end anastomoses using the 4 quadrant running suture technique.⁵ After December 2003, he defined corner-saving renal artery anastomosis.6 In his series, arterial complication rates are 0.35% for thrombosis and 0.7% for stenosis.

Postoperative iliac artery dissection
The dissection of the iliac artery is a rare complication. A few cases have been reported in the literature,^7-9 and one of our patients also presented with this complication. Seven days after transplant, immediate surgery was required. After exploration, the renal artery was separated from the external iliac artery. The kidney was then perfused with histidine-tryptophan-ketoglutarate solution via the renal artery, after a renal vein branch opening. Without opening the main renal vein anastomosis, we replaced the dissected section of the external iliac artery with a PTFE graft, and the graft kidney’s artery was anastomosed to it. At last follow-up, the patient’s kidney was functioning well (Figure 3).

Renal artery thrombosis
Although vascular thrombosis is a rare complication, it has become a major cause of early graft loss, accounting for up to one-third of graft loss within 1 month and up to 45% to 47% within 2 to 3 months. In the pediatric North American Pediatric Renal Transplant Cooperative Study cohort from 1996 to 2001, thrombosis was the most common cause of early graft loss.^2,10

Renal artery thrombosis usually occurs soon after transplant and is a destructive complication, usually resulting in graft loss. Its incidence is reported to range from 0.2% to 7.5%2 or from 0.5% to 3.5%.^11-13 Children have a higher incidence than adults. The most important sign of renal artery thrombosis is instantaneous cessation of urine outflow due to the absence of graft perfusion and the presence of worsening hypertension. In preemptive patients and patients who have preoperative urine output, this sign can be masked. In these patients, postoperative bedside Doppler ultrasonography is recom­mended.¹⁴ The most common causes of renal artery thrombosis are technical complications, including faulty suture techniques producing incomplete intimal reap­proximation with secondary intra­luminal fibrosis.

Since November 1975, our transplant team has performed 2248 kidney transplants. We currently use the four-quadrant running suture technique or the corner-saving renal artery anastomosis for arterial anastomosis. During this period, 8 renal artery thromboses (0.35%) have been seen, with surgical exploration performed in 5 patients, which included thrombectomy, reperfusion, and reanastomoses. The other 3 patients who developed renal artery throm­bosis were treated with percutaneous transluminal angioplasty, thrombolysis, and intraluminal stent placement. One of the 8 patients with renal arterial thrombosis died from a pulmonary embolism at 9 days after transplant. The remaining 7 patients had normal renal function (Figure 4).

Another surgical complication regarding renal artery thrombosis is the possible development of endothelial damage during donor nephrectomy and/or perfusion. The other factors for thrombosis are kinking or twisting of renal artery, postoperative hypotension, hypercoagulable state, atherosclerosis of the donor or recipient vessels, wide disparity in vessel size, increased intrarenal pressure resulting from acute tubular necrosis, hydronephrosis, or cellular rejection. In our center, 7 cases (0.3%) of renal artery kinking were seen, with patients treated via surgical exploration to rearrange the positions of their grafts. All patients had return of normal renal function.

Renal artery thrombosis is a surgical emergency and its diagnosis is made by color Doppler ultraso­nography or surgical exploration. To save the transplanted kidney, immediate exploration with restoration of the blood flow to the kidney is needed. A few cases of graft salvage in transplant renal artery thrombosis with endovascular catheter-directed thrombolysis with or without angioplasty have been reported. More commonly, by the time diagnosis is confirmed, it is already too late, and graft neph­rectomy is the only option left.

Renal artery stenosis
Renal artery stenosis represents the most common vascular complication, with an estimated incidence between 19% and 23% of all transplant recipients.^15-17 In our centers, the rates are 0.5% to 0.75%. Renal artery stenosis is diagnosed first using ultraso­nography and then angiography. Our preferred and initial option for treatment is the interventional radiologic approach. However, in cases where this is not successful, we have resorted to surgical reconstruction.^12-14,17-21

Transplant renal artery stenosis (TRAS) is a relatively frequent, potentially curable cause of refractory hypertension and allograft dysfunction that accounts for approximately 1% to 5% of cases of post­transplant hypertension (renal transplant arterial stenosis). In some series, the incidence of TRAS was reported to be 25%. It usually becomes apparent between 3 months and 3 years after renal transplant, but it can present at any time. Transplant renal artery stenosis can occur at the anastomosis, preanas­tomosis, or postanastomotic renal artery stage. About 50% are located at the anastomosis, and end-to-end anastomoses have a threefold higher risk than end-to-side anastomoses. It frequently presents with worsening or refractory hypertension and/or graft dysfunction in the absence of rejection, ureteric obstruction, or infection. Different locations and timing of disease onset may reflect different causes. Thus, an anastomotic stenosis is most likely related to trauma to the donor or recipient vessels during organ recovery, clamping, or suturing and usually arises early after transplant. Small, subtle intimal flaps or subintimal dissections of the vascular wall precede intimal scarring and hyperplasia that result in narrowing or occlusion of the lumen. The other predictors of TRAS include older donor and recipient age, expanded criteria donors (defined as any deceased donor over the age of 60 y or from a donor over the age of 50 y with 2 of the following: a history of hypertension, a terminal serum creatinine level ≥ 1.5 mg/dL, or death resulting from a cerebral vascular accident), delayed graft function, ischemic heart disease, and induction immunosuppression.

Evaluation of TRAS may be performed with both noninvasive and invasive imaging techniques. Color flow duplex ultrasonography and magnetic reso­nance angiography have now become the primary noninvasive imaging modalities for diagnosis of TRAS, although catheter-based angiography has conventionally been held as the criterion standard in evaluation of arterial stenosis.

Three different treatment options are feasible. If the kidney functions and Doppler ultrasonography finding are normal, the first option for treatment can be medical therapy. In these patients, angiotensin-converting enzyme inhibitors should be used to control blood pressure.

Intervention, either percutaneous or surgical, may be considered if refractory hypertension and/or worsening graft function as measured by increasing creatinine levels are present. Primary treatment with percutaneous transluminal angioplasty with or without stent placement have shown significant improvements in blood pressure and creatinine levels and can be considered as an initial treatment of choice (Figures 5-6-7).

Renal vein thrombosis
Renal vein thrombosis usually occurs within the first 7 days after transplant. The incidence of renal vein thrombosis ranges from 0.1% to 8.2%, and it usually causes graft lost in the early period of transplant.^2,4,10 Risk factors for renal vein thrombosis are surgical technique errors, hypercoagulopathy states such as deficiency of antithrombin III, protein C, or protein S, right kidney transplant with kinking due to short renal vein, transplant in the left iliac fossa with kinking due to position of external iliac vein, dehydration, ipsilateral iliofemoral throm­bo­phlebitis, deep femoral thrombosis, and vascular compression due to hematomas and lymphoceles. Clinical presentations of this condition include sudden oliguria or anuria accompanied by pain, hematuria, and life-threatening hemorrhage due to rupture of the graft. Depending on hemorrhage, patients may develop circulatory shock. For diagnosis, Doppler imaging studies are the best diagnostic tools.^14,17 In our clinic, we routinely apply Doppler ultrasonography examinations on the postoperative third and seventh days for diagnoses of early vascular problems. Furthermore, Doppler ultrasonography must be performed during the immediate postoperative period on clinical suspicion and/or biochemical evidence of renal dysfunction. Evaluations of renal Doppler ultrasonography can confirm the increase in renal volume and absence of venous flow.^13,17,20 An arterial view can show reverse diastolic flow. Perinephric hematomas and lymphocele can also be seen with ultrasonography. External compression of the vessels (hematomas, lymphocele) produce vascular problems. These problems can be solved by percutaneous drainage.

Treatment includes emergency exploration for venous thrombectomy and to restore blood flow. If this treatment is not possible, nephrectomy is performed to save the patient. In our series, we had 4 patients (0.17%) who developed renal vein thrombosis after transplant, with all treated with urgent thrombectomy. Unfortunately, 2 of the treatments were unsuccessful, and the grafts were lost. One patient had a renal vein problem due to external iliac vein thrombosis. Interventional radiologists placed a self-expanding stent to the proximal external iliac vein, and the graft was rescued. At recent follow-up, all patients maintained good graft function (Figure 8). In our center, 9 patients (0.4%) showed renal vein kinking, which was treated with surgical exploration to rearrange the graft positions. At recent follow-up, all patients maintained normal renal function.

Posttransplant Urologic Complications

Urologic complications are the most common surgical complications encountered after renal transplant, causing significant morbidity and mortality.^22-24 Rates of urologic complications after kidney transplant range between 2.5% and 30% of all recipients.^22,23,25-27

Urine leakage
Urologic complications associated with the ureterovesical anastomosis after transplant may cause graft loss and mortality. Incidences of urinary leakage in different transplant centers have ranged from 0% to 8.9%, with incidences of ureteric stricture reported to range from 0.1% to 12.4%. Major urologic complications, for example leakage and stenosis, are often related to the ureteroneocystostomy.^25,28 To avoid urologic complications, clinicians at some transplant centers routinely prefer stenting as this maneuver avoids anastomotic tension, kinking, and ureteral narrowing. In our center, from 1975 to 1983, we performed ureteroneocystostomies using the modified Politano-Leadbetter technique.²⁹ Beginning in 1983, we began using the extravesicular Lich-Gregoir technique in combination with temporary ureteral stenting.²⁹ In September 2003, we began using the corner-saving ureteral reimplantation technique without stenting.^30,31 Because the double J stent increases the risk of postoperative urinary infection and removal of this device requires an invasive procedure, we prefer not to routinely use a double J ureteral catheter. Although there are many disadvantages to this catheter, we do advocate its use in select patient groups such as those with thin graft kidney ureter walls or thin urine bladder walls, especially with transplants involving deceased donations. To evaluate complications early, we use ultrasonographic and scintigraphic findings from days 1, 3, and 7 and creatinine levels on day 7 and at 1 month after transplant. In our series, 1% of patients developed urine leakage after transplant.

Risk factors that contribute to the prevalence of urologic complications need to be determined. So far, many factors have been described in the literature, including several donor and recipient characteristics. Furthermore, problems encountered during graft recovery, prolonged ischemia times, type of uretero­neocystostomy, presence of accessory arteries, and stent placement may influence the incidence of urologic complications.

It has been suggested that urologic complications are caused by an insufficient blood supply to the ureter. Excessive dissection of the site known as “golden triangle” (the site confined by the ureter, kidney and renal artery) should therefore be avoided during graft recovery. Damage of this triangle may lead to necrosis of the distal ureter in 70% of cases.

In most cases, these complications require place­ment of a percutaneous nephrostomy (Figure 9). Sometimes, even a surgical revision is required, leading to additional morbidity and costs.

Ureteral obstruction
Ureteral obstruction occurs in 2% to 10% of renal transplant patients postoperatively, usually presenting within the first few weeks or the first year.^26,28 Prompt diagnosis and remedial treatment are vital to prevent graft loss. Ureteric ischemia is the most common cause, accounting for around 90% of occurrences.^26,28 The other causes are more then 2 arteries, long cold ischemia time, tumor, calculi, lymphocele, hematomas, abscess, kinking, and technical problems. Some occurrences of transplant ureteric stenosis may be associated with ureteric leak or necrosis (Figure 10).

Percutaneous therapy of ureteral strictures consists of balloon dilatation with or without temporary stenting (Figure 11 and Figure 12). Balloon dilatation should be repeated to achieve adequate results, especially in patients with resistant strictures. A cut balloon also may be applied in fibrotic strictures in which a standard balloon dilatation would usually fail. After successful dilatation, most authors suggest temporary stenting of the ureter with a double J stent. Metallic stents have been used to treat ureteral stenoses after failed balloon dilatation, but uroepithelial ingrowth has been a major issue with these devices.^24,26,28

If all of these methods are unsuccessful, surgical treatment should be applied. The options are to perform either a ureteral reimplantation or a ureteroureterostomy using the native ureter (side-to-side or end-to-end) through an abdominal or a kidney incision.

There are 3 different surgical techniques for ureteral stricture management occurring after renal transplant: (1) proximal transections of the anastomosis after anastomosis stricture and making ureteroneocystostomy; (2) excision of the strictured part and end-to-end ureteroureterostomy; and (3) ureteroureterostomy using the native ureter (ipsilateral or contralateral native ureter). At our center, we have performed 4 revisions after urethra strictures. For 2 patients, the old ureteroneo­cystostomy was terminated and a ureteroneo­cystostomy was performed. In 1 patient, we performed native nephrectomy and end-to-side anastomosis between the native urethra and graft’s renal pelvis (Figures 13A and 13B). Figure 14 shows the same patients at postoperative 6-month evaluations. In the other patient, we performed end-to-side anastomosis between the graft’s urethra and native urethra.

Lymphoceles
Another urologic complication in kidney transplant recipients is a lymphocele, which is a fluid collection between the kidney allograft and the bladder. This complication (rate of 0.6%-40%) is caused primarily by extravasation of the lymph from the lymphatic vessels injured during preparation of the iliac vessels of the recipient and unligated lymphatic system from the renal hilum of the donor. Other factors such as acute rejection, urinary obstruction, and graft decap­sulation may contribute to the development of lymphocele. Patients are usually asymptomatic, and spontaneous resolution occurs after a few months.^32-36

The incidence of symptomatic lymphoceles after kidney transplant in our center has been 4.2% (109/2594 total cases). This complication presented with elevated serum creatinine levels in 31 patients (28.4%), pain and abdominopelvic swelling in 53 patients (48.6%), and lower extremity edema in 25 patients (22.9%). Diagnosis of lymphocele was confirmed by ultrasonography. Percutaneous drainage was used for the treatment of lymphocele in 104 patients (95.4%) and for 66 patients (60.5%) who also received povidone iodine injection. In the remaining 5 patients (4.5%), the primary approach was surgical intraperitoneal drainage due to multiloculated collection and inappropriate access for percutaneous drainage. However, in our experience, percutaneous drainage is the most effective approach to treat this complication (Figure 15).

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