Transplant renal vein thrombosis usually occurs early after surgery with a reported prevalence of 0.1% to 4.2%. It is a devastating event that ultimately leads to graft loss in almost all cases. There are many pre­disposing factors related to donor, recipient, surgery, and immunosuppression, with mechanical factors being considered the most common causes of transplant renal vein thrombosis. The clinical mani­festations of acute renal vein thrombosis are nonspecific and are not dissimilar to the features of urine leak, urinary obstruction, or severe acute rejection. The diagnosis of transplant renal vein thrombosis depends on a high index of clinical sus­picion and duplex ultrasonographic scans. Although venography remains the criterion standard, this procedure is invasive and nephrotoxic, due to use of ionizing contrast agents and also due to exposure to ionizing radiation. There are 2 therapies that have been described in the literature for salvaging a renal allograft with transplant renal vein thrombosis: thrombolytic therapy and surgical thrombectomy. The usual end result is renal allograft nephrectomy because the diagnosis is almost always too late.

Key words : Allograft, Kidney, Vascular complications

Introduction

Renal transplant offers the best option for treatment of patients with endstage renal disease.¹ Despite advances in kidney transplant, postoperative vascular complications are major challenges, occurring in 1% to 10% of transplanted patients.^2-6 The most common vascular complications include transplant renal artery stenosis, renal graft arterial or venous thrombosis, and arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterialcalyceal fistulas.^5-7

Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant, with a reported prevalence of 0.1% to 4.2 % of all transplants.^2,8-11 Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases.^5,12-14 The prevalence of TRVT is higher in deceased-donor than in livingdonor transplant. This may be because livingdonor transplant procedures are usually done under more favorable conditions and are not usually subjected to ischemic injury.^2,10

Causes of transplant renal vein thrombosis
The pathogenesis of this devastating complication is often multifactorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.

When considering donor risk factors, use of a donor’s right kidney is associated with the development of renal graft thrombosis,^8,9,14,15 due to the short vein and long artery of the right kidney. The short renal vein can be easily compressed postoperatively by the kidney swelling due to ischemic damage, acute tubular necrosis, or urinary obstruction. The right kidney is more difficult to position, especially if multiple renal arteries are present and the long artery can be easily kinked.^8,9

Multiple graft vessels have been also implicated in renal graft thrombosis in some studies,¹⁵ although refuted in others.^13,14 In addition, prolonged ischemia time¹² and vascular injuries have been found to be donor risk factors for renal graft thrombosis.¹³ The prolonged ischemia time could potentiate thrombogenicity of the endothelium, or a resulting acute tubular necrosis with graft edema could lead to decreased perfusion and thrombosis.¹²

Older age of donors is associated with an increased risk of graft thrombosis.^16-19 This is probably because donor hypotension together with ischemiareperfusion injury may cause the activation of a procoagulant surface from cytokines and the recipient’s immune response with atherosclerotic vessels.²⁰

Recipient-related risk factors include extremes of age,^12,15,16,21 which may call for more complex surgical procedures, especially with atherosclerotic vessels predisposing to a higher incidence of thrombosis, and variations in vessel sizes between the donor and recipient, especially with pediatric transplant procedures. Other recipientrelated risk factors include pretransplant dialysis modality,^22,23 in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis, due to elevated plasma procoagulant factors, hypercoagulable states, including antiphospholipid antibody syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene.^{8,12,22,24,25} Perioperative hemodynamic status,^11,26 in which hypotension and dehydration could predispose to acute kidney injury, hypoperfusion, and thrombosis, and primary renal disease such as membranous nephropathy^11,22,26-28 have also been identified as risk factors for venous graft thrombosis.

A variety of technical issues have also been implicated as risk factors of TRVT, including kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation.^{8,11,12,23,24,26}

The following mechanical causes are considered the most common causes of TRVT: a kink in the renal vein, compression by hematomas or lymphoceles, anastomotic stenosis, and extension of an underlying deep venous thrombosis.^10,23,28-31 In our experience, compression of the renal vein by the renal artery is another risk factor, especially in contralateral transplant procedures (right kidney into the left iliac fossa and left kidney into the right iliac fossa).

Regarding immunosuppression, TRVT can also be triggered by administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and antithymocyte/antilymphocyte globulin.^21,32-34

Cyclosporine can increase the risk of graft thrombosis, based on different effects of the drug on hemostatic factors, namely, enhancement of thromboxane A2 release, thromboplastin generation, platelet aggregation, factor VIII activity, and decreased thrombomodulin activity, hence downregulation of the protein C anticoagulant pathway.^35,36 Calcineurin inhibitors may also induce hypofibrinolysis by increasing the expression of plasminogen activator inhibitor.³²

Clinical manifestations of transplant renal vein thrombosis
The typical clinical presentation is usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock.^8,9,13,15,25

Chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.²⁴

Clinical diagnosis may be easy in cases of acute renal vein thrombosis, although not specific, with diagnosis perhaps confused with the occurrence of a urologic complication or acute rejection, the 2 most frequent complications during the early post­operative period. Transplant renal vein thrombosis may be complicated by pulmonary embolism, especially when it is associated with and related to the extension of deep vein thrombosis of lower limb veins.^8,24

Diagnosis of transplant renal vein thrombosis
The diagnosis of TRVT is usually based on a highly suspicious clinical presentation, triggering assess­ment using duplex ultrasonography. The clinical diagnosis can be difficult in cases of chronic vein thrombosis, as it is initially asymptomatic.²⁴

Conventional grayscale ultrasonography with color and spectral Doppler is used immediately posttransplant for early detection of complications and evaluation of the renal allograft; it also allows calculation of resistive index and pulsatile index, which may predict early and longterm outcomes of noncomplicated renal transplants (Figure 1).^7,36,37-41 It is noninvasive and is an easily available tool that avoids use of ionizing radiation and iodinated contrast media. It is generally considered safe in the hands of a trained and skilled operator.³¹

Conventional grayscale ultrasonography has limited application, especially with increasing renal volume and a dark/edematous cortex in the early phase, transitioning to a smaller kidney with echo­genic cortex as the disease progresses. Because the vascular anastomoses are deep in the recipient’s pelvis, thrombus in the renal vein is rarely seen on conventional ultrasonographic imaging.⁴⁰

Duplex ultrasonography characteristically reveals reversed arterial diastolic flow (ie, the arterial waveform positive during systole and negative during diastole), a spikelike systolic component, and nonvisualization of the renal vein (Figure 2). Reversed or absent diastolic flow is a sign of extremely high vascular resistance in small intrarenal or large extrarenal vessels.^{7,37,39,42-45} This high vascular resistance indicates graft dysfunction and correlates with increased risk of graft loss.³⁹

The reversed diastolic waveform was described (in the main or segmental renal arteries), when retrograde blood flow occurred at any time point during the diastole, regardless of whether antegrade flow has happened. There are 3 typical shapes of reversed diastolic waveforms: type 1 or “transient” waveform (Figure 3A), in which the reversed diastolic waveform returns to baseline before end diastole; type 2 or “plateau” waveform (Figure 3B), in which a flat reversed flow remains relatively constant throughout diastole; and type 3 or “inverted M” waveform (Figure 3C), in which reversed flow throughout diastole has middiastolic deceleration.³⁹

A finding of isolated reversed or absent diastolic arterial flow is sensitive and not pathognomonic and nonspecific to TRVT and may also be seen in an array of causes (Figure 4), such as severe acute rejection, severe acute tubular necrosis, hematoma, and vascular kink.^39,40,44 Acute rejection and acute tubular necrosis are the most common causes of reversed diastolic flow, whereas TRVT remains an uncommon cause of reversed diastolic flow.^37,39,46

Previous studies have described a plateaulike or inverted M waveform associated with TRVT, whereas reversal of flow that is limited to the early diastole has been seen with severe rejection or acute tubular necrosis of the graft.⁴⁷ However, this observation was not confirmed by Lockhart and associates,³⁹ who showed that all 3 waveform types could be present in TRVT patients, and reversed diastolic waveform types were not specific for any cause. The entire diastole flow waveforms (plateau-like and inverted M shapes) represent higher vascular resistance and are associated with a higher rate of graft loss than transient waveform morphologies.^37,39,48,49

The diagnostic capability of ultrasonography is influenced by the patient’s body habitus, the avail­ability of suitable acoustic windows, and the operator’s skill.⁴⁴ Although angiography remains the criterion standard for the diagnosis of renal vascular pathology, it is invasive and associated with significant nephrotoxicity. Other investigations, such as nuclear medicine scintigraphy or magnetic resonance angiography, offer excellent alternatives to the criterion standard with no nephrotoxicity and a greater sensitivity than ultrasonography.^41,50-52

Magnetic resonance imaging is now considered a reliable tool for evaluation of renal allografts andthe diagnoses of most complications. Magnetic resonance angiography is increasingly used to screen for vascular abnormalities in renal allografts (Figure 5).^41,51,53 Due to fear of nephrogenic systemic fibrosis after gadoliniumbased contrast agents in patients with decreased glomerular filtration rate, imaging modalities have been developed to view the vessels without intravenous contrast.^41,44

Limitations of magnetic resonance imaging include the inability to image patients with pace­makers, greater cost, lack of portability, and prolonged examination time, which is not suited to these critically ill patients.⁴⁴

Management of transplant renal vein thrombosis
Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy. The surgical management of vascular complications must include surgical exploration of the allograft.⁵⁴

Successful emergency surgical thrombectomy has been reported in the early posttransplant period. Operative interventions can facilitate better evalu­ation of the cause of thrombosis and can allow for the correction of technical complications and without too many technical difficulties caused by fibrosis.^11,55,56

Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period.^57-60 Surgical thrombectomy has risks associated with anesthesia and postoperative infection in an immunosuppressed state,⁵⁴ but thrombolytic treatment can cause lifethreatening hemorrhage, especially in the perioperative period, and may lead to clot migration when lytic therapy is initiated.^55,61 However, this is not the case in every patient; there are reports of successful thrombolytic therapy in the early posttransplant period.⁵⁴

Combined percutaneous mechanical thrombec­tomy and localized catheterdirected thrombolysis have been tried safely and effectively in TRVT, notably after the second week after transplant with subacute or chronic TRVT and also in acute TRVT when prolonged thrombolysis has failed or is contraindicated.^{55,57,59,62,63}

The success rate for these interventions is variable among different studies, which are either case or cohort studies. Unfortunately, there are no large randomized controlled studies of sufficient power to assess the relative efficacy of different management approaches. Moreover, the longterm outcomes after salvage procedures need to be determined.

Preventive strategies
Because graft thrombosis is difficult to treat and graft loss is the usual outcome, development of preventive strategies is of paramount importance. First, technical issues seem to play a major role; therefore, meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable importance in avoidance of TRVT. Sufficient training in the techniques of vascular anastomosis and graft recovery is critical, to avoid multiple attempts during the operation and the subsequent iatrogenic vascular trauma. A long renal vein is considered a risk factor of thrombosis in our experience; we routinely shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis. We prefer ipsilateral transplant (right to right and left to left) whenever possible and also in cases of short renal vessels (eg, livingdonor transplant procedures) to avoid compression of the renal vein by the renal artery.

Attention to intravascular volume status in patients undergoing renal transplant is recommended. Transesophageal Doppler has been used to monitor the fluid balance during the procedure because it has been more accurate than measurement of central venous pressure.^64-67 Meticulous clinical assessment and duplex ultrasonography monitoring during the early posttransplant period followed by timely intervention may result in successful salvage of a renal allograft.^54,56

Some transplant centers have used strict protocols for postoperative monitoring of the renal allograft to allow prompt, early diagnosis of any complications. Such protocols include an hourly measurement of urine output, daily duplex ultrasonography scanning, and daily measurements of serum creatinine and electrolyte levels.⁵⁴ This proactive surveillance approach posttransplant may lead to an early diag­nosis, thus allowing salvage of the renal allograft.

Lowdose aspirin and low-molecular-weight heparin may also have benefits in preventing renal vein thrombosis in high-risk patients, especially in recipients with hypercoagulable profiles or those who received kidneys with more than 1 renal artery.⁶⁸

Conclusions

Patients who are at high risk for TRVT should be identified and followed postoperatively to allow prompt diagnosis and prophylactic measures. A meticulous postoperative protocol is critical to graft and patient survival. A coordinated multidisciplinary team approach is crucial in improving successful outcomes regarding such complex and urgent situations. The prevention of TRVT by careful attention to predisposing factors, including technical details of surgery procedures, is always more effective than treatment of this dreadful com­plication, since it may be too late to salvage a renal allograft once TRVT has been established.

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