Successful renal transplantation in the right iliac fossa 2 years after serious deep venous thrombosis in a patient with systemic lupus erythematosus

Deep venous thrombosis (DVT) possibly occurs in the perioperative period, and induces serious complications such as a pulmonary embolism. On the other hand, allograft renal vein thrombosis leads to a high incidence of graft loss. We experienced a case in which a serious DVT occurred prior to renal transplantation; however, a successful renal transplantation in the right iliac fossa was performed after 2 years of anticoagulant therapy. It is suggested that the external iliac vein even after suffering from DVT can be anastomosed to an allograft vein successfully, when enough blood fl ow or a lower venous pressure is confirmed. However, one should be aware of the risk factors and the adequate management of thrombosis in renal transplantation because of the serious complications of DVT and the poor prognosis of allograft vein thrombosis.     

Recurrent lupus nephritis in a rejected renal allograft

SUMMARY: The case of a 48-year-old female patient who underwent renal transplantation because of an end-stage renal disease after membranous glomerulonephritis (WHO class V) in systemic lupus erythematosus (SLE) is presented. the patient lost one cadaveric allograft immediately after transplantation because of renal vein thrombosis, presumably caused by anti-Cardiolipin antibodies. A second cadaveric allograft showed a stable function for several years before slowly deteriorating. an abrupt increase of serum creatinine led to the suspicion of a final episode of acute rejection. A biopsy was performed, which showed an overlap of rejection and recurrent iupus nephritis in an advanced chronically damaged allograft. the lupus nephritis recurred as the same WHO class V as in the native kidney, but without significant predictive clinical or serological signs of SLE activity. the case presented and a review of the literature indicate that the frequency of recurrent lupus nephritis might be underestimated, and earlier surveillance biopsies in transplanted SLE patients should be considered.     

Successful Use of the Inferior Mesenteric Vein for Renal Transplantation

For renal transplantation, the standard venous drainage of the allograft is via the iliac vein. In unusual circumstances, such as thrombosis or agenesis of the iliac veins and the inferior vena cava, portal venous drainage may be a suitable option. We report a case in which the inferior mesenteric vein was used for venous drainage of a cadaveric renal allograft.     

Spontaneous rupture of renal allografts: the importance of renal vein thrombosis in the cyclosporin era

Spontaneous renal allograft rupture occurring within 14 days of transplantation occurred in 15 patients from 791 consecutive transplants. In each of eight patients treated with azathioprine and prednisolone there was pathological evidence of rejection and only two patients had thrombosis of the renal vein. Of the seven cases occurring in patients treated with triple therapy regimen (low dose cyclosporin, prednisolone and azathioprine), histological evidence of rejection was present in only three cases, but renal vein thrombosis was found in all seven. Spontaneous rupture of a transplanted kidney, a relatively uncommon complication, is more likely to be due to renal vein thrombosis than to rejection in the cyclosporin era.     

移植肾动脉血栓形成的原因与对策

目的：探讨移植肾动脉血栓形成的原因和预防措施.方法：报告5例移植肾动脉血栓形成患者的临床资料.结果：1例动脉血栓发生于术中,4例分别发生于术后第2、5、10、12天.4例诊断明确后行移植肾切除术,另1例取出了肾动脉和肾静脉内的血栓,恢复了移植肾血供,但终因移植肾未恢复功能而切除.结论：移植肾动脉血栓形成多发生于术后早期,其主要原因与外科吻合技术相关,另外还与动脉粥样硬化、动脉分支多,以及冷缺血时间过长等有关.该并发症预后差,应以预防为主,早期诊断和及时手术治疗是关键.     

Noninvasive radiological diagnosis of renal vein thrombosis in renal transplantation.

Thrombosis of the allograft renal vein is a rare complication of renal transplantation. Of 557 consecutive renal transplants performed between January 1, 1985 and November 30, 1989, 3 cases occurred for an over-all incidence of 0.4%. In 2 cases the diagnosis was made preoperatively with renal scintigraphy and duplex Doppler sonography. No graft was salvaged, despite timely diagnosis in 2 patients. We conclude that the diagnosis of renal vein thrombosis in the renal allograft recipient should be suspected clinically and by the radiographic findings of absent perfusion on renal scintigraphy, and the detection of an arterial signal, albeit abnormal, on duplex Doppler sonography. When diagnosed, nephrectomy appears to be the only treatment.     

Allograft renal vascular thrombosis--lack of increase with cyclosporine immunosuppression

Several recent reports have demonstrated an increased incidence of allograft renal vascular thrombosis in patients receiving cyclosporine alone or as part of multiple drug regimens when compared with patients receiving azathioprine (AZA) and prednisone (P). To determine whether CsA therapy is indeed a risk factor for renal artery or vein thrombosis, we examined the incidence of these complications in 224 adult renal allograft recipients who were prospectively randomized and stratified by risk to treatment with either CsA-P (n = 117) or AZA-P-antilymphocyte globulin (n = 107) between September 1980 and October 1983, and in 452 adult and 87 pediatric patients on triple (AZA-P-CsA) or quadruple (AZA-P-CsA-ALG) therapy protocols between July 1984 and November 1987. In the randomized trial, one of 107 AZA-P-ALG patients (0.9%) and two of 117 CsA-P patients (1.7%) developed renal vein thrombosis (P = 0.94), and there were no cases of arterial thrombosis. Though CsA levels were elevated in one of the two CsA-treated patients at the time of their events, and both these patients demonstrated other predisposing factors for thrombosis. In the triple/quadruple therapy era, there were no cases of renal vein thrombosis, and the only case of renal artery thrombosis occurred in a pediatric recipient who was not receiving CsA at the time. These data, when taken together with a critical review of the conflicting literature, strongly suggest that factors other than immunosuppression with CsA, including surgical technique, allograft rejection, use of multiple artery and/or pediatric donor kidneys, and postoperative hypotension, are important in the pathogenesis of allograft renal vascular thrombosis. It seems possible, however, that high initial dosing of CsA might trigger this complication in the early posttransplant period when other predisposing factors are present.     

Management of Thrombophilia in Renal Transplant Patients

Renal allograft recipients with thrombophilia (a hypercoagulable state) are at higher risk for early allograft loss. Following an episode of allograft renal vein thrombosis in a patient subsequently diagnosed with protein C deficiency, we adopted universal screening for hypercoagulable risk factors. Patients with a history of a thromboembolic event underwent laboratory screening for thrombophilia. Eight patients with a defined hypercoagulable disorder or a strong clinical history of thrombosis even in the absence of hematologic abnormalities were treated with anticoagulation following renal transplantation. We reviewed the outcomes of these eight patients and all renal transplant recipients at our center who developed thrombotic complications after renal transplantation. Since the introduction of universal screening for hypercoagulable risk factors, 235 consecutive transplants were performed without allograft thrombosis. Eight patients with evidence of thrombophilia, recognized before renal transplantation, received perioperative heparin and postoperative oral anticoagulation. Two of these eight patients developed perinephric hematomas requiring evacuation, blood transfusion, and temporary withholding of anticoagulation. Of interest, two of the remaining 227 patients, not identified with thrombophilia before surgery, developed thrombotic complications after renal transplantation. A hypercoagulable disorder was subsequently documented in each. Identifying patients with thrombophilia before transplantation and defining their management presents many challenges. The risk of allograft thrombosis must be weighed against the risk of perioperative bleeding and the need for long-term anticoagulation. Recommendations for managing thrombophilia in renal transplant recipients are suggested based on our experience and review of the literature.     

Renal vein reconstruction with interposition allografts in cadaveric renal transplantation

Abstract. The short or injured renal vein in cadaveric transplantation is a surgical challenge. Over a 2-year period, we have performed ex vivo renal vein lengthening with an interposition vascular allograft in 17 recipients of cadaveric kidneys. Indications for renal vein extension allografts were a short right renal vein ( N = 12), procurement injury to the vein ( N = 4), and double renal vein ( N = 1). In six cases (35.3%), ex vivo renal artery reconstruction was performed in combination with the venous repair. Our preferred approach is to employ allograft material in ex vivo reconstruction under cold storage conditions. Bench surgery ranged from 10 to 30 min, and the mean in situ anastomosis time was 20 min. The mean length of renal vein prior to reconstruction was 12 mm, and the mean length of venous interposition allograft after revascularization was 27 mm. There were no episodes of vascular thrombosis or primary nonfunction. Three patients (17.6%) required postoperative hemodialysis for acute tubular necrosis, which was subsequently resolved. The mean serum creatinine at 1 month post-transplant was 1.7 mg/dl. These preliminary results suggest that ex vivo renal vein reconstruction with an interposition allograft is a safe and effective modality which should be added to the transplant surgeon's armamentarium in select cases.     

Renal allograft rupture with iliofemoral thrombophlebitis.

Spontaneous rupture of a renal allograft in the early posttransplant period is associated with tachycardia, hypotension, oliguria, swelling, pain, a falling hematocrit level, and tenderness at the transplant site. Occasionally, the ruptured allograft can be saved by control of the hemorrhage. Deep vein thrombophlebitis, a common occurrence after prolonged surgery and cortocosteroid therapy, is less common in renal allograft transplantation, but may be associated with renal vein thrombosis. The simultaneous occurrence of deep vein thrombophlebitis, renal vein thrombosis, and allograft rupture contraindicates anticoagulent therapy. We present a patient in whom ipsilateral deep vein thrombophlebitis developed eight days after a cadaveric renal allograft, followed in two days by hypotension, a falling hematocrit level, oliguria, and a painfall mass at the allograft site. Surgical exploration revealed a ruptured allograft with iliofemoral and renal vein thrombosis and profuse hemorrhage. A transplant nephrectomy was performed.     

Back-table renal allograft angioscopy and thrombolysis

Poor back-table perfusion of a renal allograft may occur as a result of intravascular thrombosis of the renal artery branches. We herein report such a case where back-table angioscopy was performed to confirm the diagnosis, followed by successful thrombolysis using urokinase under hypothermic conditions.     

Renal allograft loss due to proximal extension of ileofemoral deep venous thrombosis

Renal allograft recipients with thrombophilic (hypercoagulable) states are at higher risk for early allograft loss. Presumably, the combination of endothelial injury at surgery and thrombophilia predisposes to arterial or venous thrombosis. Of 270 consecutive renal transplants at our center one allograft failed secondary to renovascular thrombosis. At exploration the iliac and renal veins were thrombosed. Thrombectomy and re-implantation were attempted, but unsuccessful. Also noted at surgery was extensive clot in the femoral vein that could not be removed by embolectomy catheters. Post-operatively, a Doppler ultrasound confirmed the presence of extensive deep venous thrombosis (DVT) in the femoral and popliteal veins. The adherent nature of this clot, the extent of clot found less than 12 h after renal transplantation and the absence of leg edema suggested that the DVT existed prior to surgery. This case demonstrates that a pre-existing, asymptomatic DVT can precipitate allograft thrombosis and highlights the importance of diagnosing thrombophilia in patients undergoing renal transplantation. Current practices in our unit have evolved to include screening for thrombophilia in all patients with a suggestive history. As thrombophilic states are increasingly appreciated in the end-stage renal disease population, effective management of these patients while on hemodialysis and at the time of renal transplantation presents an ongoing challenge.     

Venous thrombectomy in patients presenting with iliofemoral vein thrombosis after renal transplantation

In this study 14 patients presented with 15 episodes of iliofemoral vein thrombosis after renal transplantation. Seven patients (group 1) had viable renal grafts and were treated with conventional anticoagulation. Eight patients (group 2) had non-viable renal grafts and were subjected to graft nephrectomy and simultaneous venous thrombectomy without anticoagulation. The patients in group 2 had rapid resolution of the signs and symptoms of the iliofemoral vein thrombosis, and noninvasive vascular investigation at follow-up revealed competent and patent deep veins in all patients. In contrast, only 50% of the patients in group 1 had normal venous studies at follow-up. We recommend that renal transplant recipients who develop iliofemoral vein thrombosis and nonviable allograft postoperatively should be subjected to venous thrombectomy at the time of graft nephrectomy.     

Salvage of renal allograft function and lower extremity venous patency with thrombolytic therapy: Case report and review of the literature

Five months after a cadaveric renal transplant a 69-year-old man was admitted with caval, iliac, and renal allograft vein thrombosis that occurred in the setting of a previously placed caval filter. The patient's urine output and renal function deteriorated rapidly. Thrombolytic therapy with urokinase was begun, and lysis of the thrombus occurred in 72 hours. The patient's renal function returned to baseline, and the transplant was salvaged. Moreover lower extremity venous patency and valvular function were maintained. We report the case and review the literature on thrombolytic therapy for renal allograft vein and lower extremity deep venous thrombosis. (J VASC SURG 1995;21:691-6.)     

Increased coagulation factor levels leading to allograft renal vein thrombosis

A patient with end-stage kidney disease is described, who lost his renal allograft in the early post-transplant period due to allograft renal vein thrombosis. Prior to transplantation, he had been treated by hemodialysis and lost several vascular accesses because of thrombosis. A search for potential thrombophilic factors disclosed a unique combination of increased clotting factor levels, i.e. FVIII, FIX, FXI and homocysteine. More common hereditary and acquired hypercoagulability factors have been excluded in this patient. While clotting factor deficiencies are well known causes of hemophilia, their levels should also be measured in the workup of transplant candidates with a history of multiple vascular access thrombosis.     

Gene expression of plasminogen activator inhibitor 1 in transplant kidneys complicated by renal vein thrombosis: a combined study by in-situ hybridization and immunohistochemistry

In an attempt to understand the pathogenesis of renal vein thrombosisoccurring early after renal transplantation, gene expressionof plasminogen activator inhibitor-1 (PAI-1) was investigatedby an in-situ hybridization technique. The cases examined weresix transplant kidneys complicated by renal vein thrombosis,four ‘normal’ kidneys and five time-matched transplantkidneys not complicated by renal vein thrombosis but showingacute tubular necrosis, infection, or normal histology. Thecell types expressing PAI-1 mRNA were also studied by combinedin-situ hybridization and immunohistochemical double stainingtechniques. Our results showed that PAI-1 mRNA was expressedin transplant kidneys complicated by renal vein thrombosis butthere was no detectable expression in ‘normal’ kidneys,nor in time-matched transplant kidneys not complicated by thrombosis.Double staining showed that PAI-1 mRNA was predominantly expressedby capillary endothelial cells, particularly around large- ormedium-sized renal arteries and small nerves. Smooth-musclecells in the wall of major or medium-sized renal arteries alsoshowed positive expression of PAI-1 in three of six thrombosedtransplants. However, endothelium in the major renal vein showedrelatively little signal. The pattern was different from thatin rejection. The possible relevance of these findings is discussed.     

Recurrent renal vein thrombosis and renal failure associated with antithrombin-III deficiency

This paper describes a healthy 13-year-old girl presenting with acute flank pain and anuria due to renal vein thrombosis. A similar spontaneous and unexplained thrombosis resulted in the loss of the contralateral kidney 1 year earlier. Urgent surgical thrombectomy and anticoagulation resulted in moderate recovery of renal function. Predisposition to venous thrombosis in this child was secondary to a marked familial deficiency of circulating antithrombin-III. An early diagnosis of this condition is essential for the formulation of preventive measures and may lead to specific therapeutic intervention at the onset of acute thrombotic complications.     

Detection of renal allograft rejection with (125I) fibrinogen

The ability to differentiate renal allograft rejection from other causes of impaired renal function using [¹²⁵]fibrinogen was evaluated using a rabbit renal transplantation model. By measuring radioactivity over the kidney and comparing it to that over the heart, rejection could clearly be differentiated from renal artery or vein thrombosis, hydronephrosis or ischemic damage.     

Membranous glomerulopathy following kidney transplantation. Association with renal vein thrombosis in two of nine cases

The association of renal vein thrombosis and membranous glomerulopathy in native kidneys has been well documented. However, this association has only occasionally been described following renal transplantation. A review of 693 renal transplant recipients revealed 77 (11%) in whom persistent, heavy proteinuria (greater than 2 g/24 hr) developed. Renal histology was available in all 77 patients. A diagnosis of membranous glomerulopathy was made in 7 patients. Two further cases were added on the basis of biopsy findings--1 patient had a protein excretion of 1.7 g/24 hr, the other had microscopic hematuria and red cell casts in the urine. Renal venography was performed in 4 cases. The decision to perform venography was based on clinical criteria (thrombophlebitis or marked edema of the leg on the side of the allograft), and/or histological criteria (associated interstitial edema and venous congestion). Renal vein thrombosis was present in 2 patients. Three of the 9 patients had membranous glomerulopathy as the cause of their end-stage renal disease; 2 of these patients had received kidneys from living-related donors. Four of the patients were classified as having de novo membranous glomerulopathy on the basis of having a different cause for their end-stage renal disease. Two patients were classified as having unspecified membranous glomerulopathy; both of these patients had had chronic glomerulonephritis, but there was lack of characterization of the original glomerular disease. Seven of the 9 patients continued to have stable allograft function 1-12 months after the diagnosis of membranous glomerulopathy was made in the renal allograft. The remaining 2 patients both had associated renal vein thrombosis; 1 had progressive deterioration of renal function and returned to dialysis 24 months after the diagnosis of membranous glomerulopathy had been made, while the other died of unrelated causes 27 months after the diagnosis had been made.     

Renal allograft rupture is associated with rejection or acute tubular necrosis, but not with renal vein thrombosis.

BACKGROUND: Whereas rejection was reported to be the most common cause of renal allograft rupture (RAR) in the pre-cyclosporin era, renal vein thrombosis (RVT) is purported to be the main cause of RAR in patients taking cyclosporin. The extremely low incidence of RVT in our series (0.11%) prompted us to analyse our collective with regard to RAR. METHOD: Between 1974 and 1999, 1811 renal transplants were performed. Patients with RAR, defined as a tear of the renal capsule and parenchyma, were identified and possible underlying factors studied. RESULTS: RAR was diagnosed in nine male and five female recipients (0.8%) with a median age of 36 years. Immunosuppression consisted of azathioprine and prednisolone in seven patients and of cyclosporin-based therapy in the seven others. At exploration five grafts were removed immediately: three because of irreversible rejection, one because of deep wound infection, and one with a twisted renal vein. Six of the nine salvaged kidneys have been functioning after a mean observation time of 45 months. In the pre-cyclosporin era RAR was associated with acute rejection in five out of seven cases as compared with only three of the seven on cyclosporin treatment. Core biopsies might have been the cause in three cases. CONCLUSION: RAR is a rare complication after renal transplantation. Acute rejection still represents the most frequent cause of RAR in the cyclosporin era.