Renal Vascular Thrombosis Research Articles

Renální vaskulární trombóza u novorozence - 1. část

Renální vaskulární trombóza u novorozence - 1. část

Renální vaskulární trombóza u novorozence - 2. část

Renální vaskulární trombóza u novorozence - 2. část

Rare Clinical Cases of Renal Artery Thrombosis

Objective: Renal vascular thrombosis is a thrombotic blockage of the major renal arteries resulting in acute damage or chronic kidney disease. The study aims to analyze rare clinical cases of renal artery thrombosis with following renal infarction.
 Materials and methods: The article present a retrospective study of examination and treatment results of patients diagnosed with the renal arteries thrombosis in the urological hospital of the Irkutsk Clinical Hospital No. 1 in the period 2012-2020.
 Results and Discussion: During the entire observation period, there were two clinical cases of acute renal artery thrombosis. The 86-year-old woman developed thrombosis because of atrial fibrillation, which was probably the result of inadequate correction (insufficient dose of anticoagulant). Kidney infarction had complications like rapid suppuration because of chronic urinary infection and calculus of the renal pelvis. It resulted in nephrectomy with subsequent recovery. The second case was the 45-year-old man examined according to existing standards, and the diagnosed-on time in the first hours of the disease. However, complete thrombosis of the right renal artery neutralized the effectiveness of conservative therapy with warfarin. In this case, nephrosclerosis and renal failure were natural.
 Conclusion: Renal artery thrombosis is a rare pathology that requires special attention from the clinician due to the high risk of renal function loss. Timely diagnosis and correct treatment tactics are especially important.
 Bangladesh Journal of Medical Science Vol.20(3) 2021 p.550-555

Is intraoperative heparin during renal transplantation useful to reduce graft vascular thrombosis?

The standard treatment for end-stage renal disease is renal transplantation. As vascular anastomoses are performed during the surgery, it may expose to a risk of vascular thrombosis. This raises the question of using intravenous heparin during the procedure. The purpose of this study was to compare the incidence of renal transplant vascular thrombosis in the perioperative period based on whether the patients received or not intraoperative heparin. A single center retrospective study was conducted on a cohort of consecutive patients who underwent renal transplantation between 2011 and 2015. Patients were divided into two groups: patients not receiving heparin vs. receiving heparin at the dose of 0.5mg/kg. A Doppler ultrasound was performed at day one postoperatively to assess the occurrence of vascular thrombosis. Hemorrhagic complications and the need for postoperative transfusion were also assessed. In total, 261 patients were included. Fifty-one patients received heparin (19.5%). Patient's baseline characteristics were comparable between the groups. No significant difference was found regarding the incidence of vascular thrombosis (6% for both groups, P=1). In addition, no difference was found regarding hemorrhagic complications requiring surgical revision (P=1) as well as early postoperative transfusion rate (P=0.57). Our results suggest that intraoperative IV heparin doesn't improve the risk of vascular thrombosis following renal transplantation. However, intraoperative IV heparin was not significantly associated with a higher rate of hemorrhagic complications suggesting that heparin can be safely used if required in some selected patients at higher risk of thrombosis. 3.

Renal allograft loss due to renal vascular thrombosis in the US pediatric renal transplantation.

Renal vascular thrombosis (RVT) is a major cause of early allograft loss in the first year following pediatric kidney transplantation. We examined recent trends in allograft loss due to RVT and identified associated risk factors. We identified 14,640 kidney-only transplants performed between 1995 and 2014 with follow-up until June 30, 2016, in 13,758 pediatric patients aged < 19years from the US Renal Data System. We examined the 1-year incidence of allograft loss due to RVT by year of transplant, and plotted the trend over time. Cox proportional hazards models were used to investigate the relationship between year of transplant as well as recipient, donor, and transplant characteristics with allograft loss due to RVT. The incidence of allograft loss due to RVT consistently declined among pediatric kidney transplant performed between 1995 and 2014. Among transplants performed between 1995 and 2004, 128/7542 (1.7%) allografts were lost due to RVT compared to 53/7098 (0.8%) among transplants performed between 2005 and 2014; average 1-year cumulative incidence was 1.5% (95% CI, 1.3-1.9%) and 0.6% (95% CI, 0.5-0.8%), respectively. Increased risk for allograft loss due to RVT was associated with en bloc kidney transplantation (HR, 3.42; 95% CI 1.38-8.43) and cold ischemia time ≥ 12h (HR, 1.78; 95% CI, 1.15-2.76). Interestingly, these risk factors were more prevalent in the latter decade. The incidence of allograft loss due to RVT significantly and continuously declined among pediatric kidney transplants performed between 1995 and 2014. The causes for this improvement are unclear in the present analysis.

Pharmacokinetics of Enoxaparin After Renal Transplantation in Pediatric Patients.

Enoxaparin is commonly used in the prevention of renal allograft vascular thrombosis but off-label in children, and no consensus exists regarding the optimal dosing and dose adjustment. In this retrospective study, 444 anti-Xa levels were obtained from 30 pediatric renal transplant recipients in order to investigate enoxaparin population pharmacokinetics. The main results were (1) 25% of children achieved the target anti-Xa activity 36hours after initiation of treatment, (2) anti-Xa time courses were best described by a 1-compartment open model with first-order absorption, (3) body weight but not renal function was the sole covariate influencing clearance and volume of distribution, and (4) large between-subject and between-occasion variabilities in anti-Xa activity were observed. However, creatinine-based estimated glomerular filtration rate in the first post-renal transplantation hours may not reliably reflect the actual renal function of the children. Based on the final population model, a Bayesian-based program was developed in order to estimate the individual pharmacokinetic parameters on a single anti-Xa measurement, allowing determination of the next enoxaparin dose that will quickly achieve an appropriate anti-Xa activity (targeting 0.3-0.5IU/mL) and anticoagulation. Finally, these results should help standardize practices that remain to date largely heterogeneous in pediatric intensive care units.

Renal Involvement in Antiphospholipid Syndrome.

Antiphospholipid syndrome is a complex autoimmune disease, characterized by the presence of vascular thrombosis, obstetric, hematologic, cutaneous, and cardiac manifestations. Renal disease in patients with antiphospholipid syndrome was not recognized in the first descriptions of the disease, but later on, the renal manifestations of the syndrome have been investigated widely. Renal manifestations of antiphospholipid syndrome conform a wide spectrum of diverse renal syndromes. Hypertension is one of the most frequent, but less commonly recognized renal alteration. It can be difficult to control as its origin is renovascular. Renal vascular thrombosis can be arterial or venous. Other alterations are renal infarction and vascular thrombosis in arterial territories. Venous thrombosis can be present in primary and secondary antiphospholipid syndrome; it presents with worsening of previous proteinuria or de novo nephrotic syndrome, hypertension and renal failure. Antiphospholipid syndrome nephropathy is a vascular disease that affects glomerular tuft, interstitial vessels, and peritubular vessels; histopathology characterizes the renal lesions as acute or chronic, the classic finding is thrombotic microangiopathy, that leads to fibrosis, tubule thyroidization, focal cortical atrophy, and glomerular sclerosis. Antiphospholipid syndrome nephropathy can also complicate patients with systemic lupus erythematosus, and there is vast information supporting the worse renal prognosis in this group of patients with the classic histopathologic lesions. Treatment consists of anticoagulation, as for other thrombotic manifestations of antiphospholipid syndrome. There is some evidence of glomerulonephritis as an isolated lesion in patients with antiphospholipid syndrome. The most frequently reported glomerulonephritis is membranous; with some reports suggesting that immunosuppressive treatment may be effective. Patients with end stage renal disease commonly are positive for antiphospholipid antibodies, but it is not clear what is the role of aPL in this setting. Patients with vascular access may have complications in the presence of antibodies so that anticoagulation is recommended. Patients ongoing renal transplant with persistent antiphospholipid antibody positivity may have early and late graft failure.

Traumatic Bilateral Renal Artery Thrombosis: A Case of Kidney Salvage with Local Lytic Therapy and Systemic Anticoagulation in the Setting of Poly-trauma

We present a case of acute blunt traumatic bilateral renal artery thrombosis in the setting of multisystem trauma. Catheter-directed thrombolysis with tissue plasminogen activator afforded kidney salvage with return of glomerular filtration rate to normal values at the time of patient discharge. included a small left subdural hematoma, a left hemothorax and lung contusion. Bilateral renal infarctions with traumatic renal vascular thrombosis, and a right renal pelvis tear with minimal contrast extravasation was demonstrated. The remaining abdominal viscera were without acute injury. The right renal infarct was extensive compared to the left and involved the majority of the right kidney (Figure 1). A visceral angiogram confirmed bilateral renal infarctions, greater in the right kidney. The thrombus on the right renal artery was large and extending to several interlobar arteries (Figure 2). A catheter was placed in the right main renal artery for infusion of tissue plasminogen activator (TPA) at 2 mg/hr for four hours after an initial bolus of 8 mg for a total dose of 16 mg. The time from injury to the treatment with TPA was approximately 5 hours. The patient was also placed on systemic heparin drip due to the bilateral nature of the renal artery thrombosis. This decision was made following consultation with a neurosurgeon as the patient also had an acute subdural bleed. A collaborative decision was reached to proceed with

Renal vascular thrombosis in the newborn.

Neonatal renal vascular thrombosis is rare but has devastating sequelae. The renal vein is more commonly affected than the renal artery. Most neonates with renal vein thrombosis present with at least one of the three cardinal signs, namely, abdominal mass, macroscopic hematuria and thrombocytopenia, while unilateral renal artery thrombosis presents with transient hypertension. Contrast angiography is the gold standard for diagnosis but because of exposure to radiation and contrast agents, Doppler ultrasound scan is widely used instead. Baseline laboratory tests for platelet count, prothrombin time, activated partial thromboplastin time and fibrinogen concentration are essential before therapy is initiated. Maternal blood is tested for lupus anticoagulant and anticardiolipin antibody. Evaluation for prothrombotic disorders is warranted when thrombosis is clinically significant, recurrent or spontaneous. Management should involve a multidisciplinary team that includes neonatologists, radiologists, pediatric hematologists and nephrologists. In addition to supportive therapy, recent guidelines recommend at least prophylactic heparin therapy in the majority of cases to prevent thrombus extension. Thrombolytic therapy is reserved for bilateral thrombosis compromising kidney function. Long-term sequelae, such as kidney atrophy, systemic hypertension and chronic kidney disease, are common, and follow-up by pediatric nephrologists is recommended for monitoring of kidney function, early detection and management of hypertension and chronic kidney disease.

Renal Involvement in Antiphospholipid Syndrome

Renal involvement can be a serious problem for patients with antiphospholipid syndrome (APS). However, this complication has been poorly recognized and studied. It can be present in patients who have either primary or systemic lupus erythematosus-associated APS. Clinical and laboratory features of renal involvement in APS include hypertension, hematuria, acute renal failure, and progressive chronic renal insufficiency with mild levels of proteinuria that can progress to nephrotic-range proteinuria. The main lesions are renal artery stenosis, venous renal thrombosis, and glomerular lesions (APS nephropathy) that may be acute (thrombotic microangiopathy) and/or chronic (arteriosclerosis, arterial fibrous intimal hyperplasia, tubular thyroidization, arteriolar occlusions, and focal cortical atrophy). APS can also cause end-stage renal disease and allograft vascular thrombosis. This article reviews the range of renal abnormalities associated with APS, and their diagnosis and treatment options.

Successful living‐related kidney transplantation in a boy with inherited dysfibrinogenemia

In kidney transplantation, it is essential to avoid acute vascular complications, such as hemorrhage and renal vascular thrombosis, which may often lead to allograft loss. Inherited dysfibrinogenemia is a rare coagulation disorder with a wide spectrum of clinical manifestations, such as excessive bleeding and thrombosis. A 12-yr-old boy, previously diagnosed with renal hypodysplasia, was found to have reduced fibrinogen concentrations. Coagulation tests assessing surgical risk during kidney transplantation showed a discrepancy between functional and immunologic fibrinogen concentrations. Gene analysis confirmed inherited dysfibrinogenemia, with a heterozygous mutation in FGA (Aα Arg16His) in the patient and his mother. Based on the molecular and functional properties of the mutation, and a familial phenotype, in which his aunt had experienced a previous bleeding episode, the patient was considered at greater risk of bleeding than of thrombosis. The patient was administered fibrinogen concentrate before surgery, and kidney transplantation was performed with his father as the organ donor. The patient received additional prophylactic infusions of fibrinogen concentrate postoperatively, and his postoperative course was uneventful. Accurate diagnosis of dysfibrinogenemia, including gene analysis, is important for correctly managing patients with this coagulation disorder who are undergoing kidney transplantation.

Systemic Heparinisation in Laparoscopic Live Donor Nephrectomy

Introduction. Systemic heparinisation is advocated during laparoscopic live donor nephrectomy (LDN) as a preventative measure against renal vascular thrombosis during the warm ischaemic interval. This study compares the outcome with and without the administration of systemic heparinisation. Methods. A retrospective analysis was performed on 186 consecutive LDN patients between April 2008 and November 2012. Systemic heparin (2000–3000 IU) was administered intravenously to donors (hep n = 109). From January 2010, heparin was not used systemically in this group of LDN (no hep n = 77). Outcome measures included donor and recipient complications, initial graft function, and 12 month graft survival. Results. The demographics of both heparinised and non-heparinised donors were similar. The warm ischaemic time (WIT) was comparable in both groups (WIT; hep 5 ± 3 versus no hep 5 ± 3 minutes; P = 1.000). There was no difference in complication rates, no episodes of graft thrombosis, and no incidences of primary nonfunction in either group. Delayed graft function occurred in 4/109 and 1/77 (3.6% versus 1.2%; P = 0.405) and there was no significant difference in graft survival (P = 0.650). Conclusion. Omitting systemic heparinisation during laparoscopic donor nephrectomy is a feasible and safe approach that does not compromise donor or recipient outcome.

Cold Intravascular Organ Perfusion for Renal Hypothermia During Laparoscopic Partial Nephrectomy

We report initial data on the safety and functional outcomes of renal hypothermia with arterial cold perfusion during partial nephrectomy. From June 2007 to June 2009, 31 consecutive patients underwent laparoscopic partial nephrectomy with hypothermia using renal arterial perfusion with cold, lactated Ringer's solution during renal ischemia. Doppler echography was done intraoperatively to evaluate renal perfusion. Complication data were reported prospectively. Median followup was 57 weeks (IQR 28, 83). The lowest recorded renal temperature during ischemia was 14C. Median tumor size was 4.0 cm (IQR 2.7, 6.2). Median estimated blood loss was 150 cc (IQR 100, 275). Median ischemia time was 35 minutes (IQR 26, 41). Doppler echography identified intrarenal arterial blood flow postoperatively in all cases. The median change in the estimated glomerular filtration rate from preoperatively to postoperative day 2 was 4 ml per minute (IQR -29, 19). Two months postoperative in 20 patients the median change was 3.5 ml per minute (IQR -6, 16.5). At last followup in 31 patients the overall change in the estimated glomerular filtration rate was -0.5 ml per minute (IQR -6, 6). Six complications developed in a total of 5 patients, of which 5 were grade 2 or less. One grade 3 postoperative hemorrhage from an arteriovenous fistula at the tumor resection site was treated with angiography and selective embolization. Cold intravascular perfusion during laparoscopic partial nephrectomy can achieve renal hypothermia below 15C. It is not associated with an immediate risk of renal vascular injury or thrombosis, as measured by Doppler echography in this series. Early changes in postoperative estimates of renal function appear minimal.

Preventing Graft Thrombosis After Renal Transplantation: A Multicenter Survey of Clinical Practice

Background Renal allograft vascular thrombosis is a complication that often results in graft loss. Since there are no guidelines on immediate postoperative thromboprophylaxis, we performed a telephone survey of clinical practice in all renal transplantation centers in France. Methods Each center considered 4 cases relating to renal transplant candidates on dialysis with an increasing risk of thrombosis: Case 1: patient with no identified risk factors; Case 2: patient with an earlier incidence of deep vein thrombosis; Case 3: patient with ischemic heart disease on antiplatelet therapy; Case 4: patient with atrial fibrillation taking a vitamin K antagonist (VKA) with lupus nephritis syndrome. Results The treatments proposed by the centers (%) were: Case 1: No anticoagulation therapy (57.1%), calcium heparin at prophylactic doses (P-dose) (40%), or unfractionated heparin (UFH); (P-dose; 2.9%). Case 2: No anticoagulation therapy (34.3%), calcium heparin (P-dose; 51.4%), or UFH (P-dose; 5.7%). Case 3: (A) Interruption of aspirin (65.7%), and either no anticoagulation therapy (21.7%) or substitution of aspirin by calcium heparin (P-dose; 56.6%) or by UFH (P-dose; 8.7%). (B) No interruption of aspirin (34.3%), and either no additional prophylaxis (58.3%) or calcium heparin (P-dose; 33.3%). Case 4: Interruption of VKA (100%), and UFH at a curative dose (68.6%), UFH (P-dose; 14.3%), or calcium heparin (P-dose; 11.4%). Conclusions Practices varied widely in the absence of studies of sufficiently high power. There is a need for a preoperative classification of thrombotic and hemorrhagic risk among renal transplant candidates and for consensus guidelines.

Antiphospholipid Syndrome and the Kidneys

To study the relationship between antiphospholipid antibodies and kidney diseases. We reviewed the medical literature from 1968 to 2005 using MEDLINE and the keywords antiphospholipid syndrome, anticardiolipin antibodies, lupus anticoagulant, hypertension, renal artery stenosis, renal vascular thrombosis, thrombotic microangiopathy, and glomerulonephritis. The renal manifestations of the antiphospholipid syndrome may result from thrombosis occurring at any location within the renal vasculature, that is, in the renal artery trunk or branches, intraparenchymal arteries and arterioles, glomerular capillaries, and the renal veins. The spectrum of these manifestations includes renal artery stenosis and/or malignant hypertension, renal infarction, renal vein thrombosis, thrombotic microangiopathy, increased allograft vascular thrombosis, and reduced survival of renal allografts. More recently nonthrombotic conditions like glomerulonephritis have also been reported. The kidney appears to be a major target organ in both primary and secondary APS. Early detection of renal involvement may improve the prognosis of these patients.

Urogenital trauma: imaging upper GU trauma

Objectives: This article will define the current controversies and concepts in the classification, clinical presentation, imaging approaches and management of upper urinary tract trauma. Materials and methods, results: This review will include the experience of the authors in the field of renal trauma over a 32-year period. Current thinking accepts the view that significant renal trauma is generally present when there is gross hematuria, signs of shock, or other clinical signs of severe injury. In most patients, suspected renal injury will be evaluated as a part of the overall assassment of the patient for suspected intraperitoneal injury. The authors will stress some exceptions to the rule. Conclusions: Most trauma experts now advocate conservative management, unless the patient is unstable or a renal vascular thrombosis or avulsion is suspected. Similarly, penetrating trauma to the kidney in and of itself no longer requires mandatory surgery. In the United States, computed tomography (CT), especially spiral CT, is considered the best diagnostic study, if available. Intravenous pyelography (IVP) is adequate if this is the only imaging modality available and if no concomitant injuries to the abdominal structure are suspected. Ultrasound, although strongly advocated in some countries, can lead to some significant false negatives. The diagnosis and management of unusual problems such as the traumatic AV fistula, the patient with an absent kidney or injury to the congenitally abnormal kidney, the serendipitous renal tumor in a patient with trauma, or serious bleeding after an apparent minor injury (i.e., spontaneous hemorrhage) are also reviewed in this article.

Dialysis modality and the risk of allograft thrombosis in adult renal transplant recipients

Renal vascular thrombosis (RVT) is a rare but catastrophic complication of renal transplantation. Although a plethora of risk factors has been identified, a large proportion of cases of RVT is unexplained. Uremic coagulopathy and dialysis modality may predispose to RVT. We investigated the impact of the pretransplant dialysis modality on the risk of RVT in adult renal transplant recipients. Renal transplant recipients (age 18 years or more) who were enrolled in the national registry between 1990 and 1996 (N = 84,513) were evaluated for RVT occurring within 30 days of transplantation. Each case was matched with two controls from the same transplant center and with the year of transplantation. The association between RVT and 18 factors was studied with multivariate conditional logistic regression. Forty-nine percent of all cases of RVT (365 out of 743) occurred in repeat transplant recipients with an adjusted odds ratio (OR) of 5.72 compared with first transplants (P < 0.001). There were a significantly higher odds of RVT in peritoneal dialysis (PD)-compared with hemodialysis (HD)-treated patients (OR = 1.87, P = 0.001). Change in dialysis modality was an independent predictor of RVT: switching from HD to PD (OR = 3.59, P < 0.001) and from PD to HD (OR = 1.62, P = 0.047). Compared with primary transplant recipients on HD (OR = 1.00), the highest odds of RVT were in repeat transplant recipients treated with PD (OR = 12.95, P < 0.001) and HD (OR = 4.50, P < 0.001). Other independent predictors of RVT were preemptive transplantation, relatively young and old donor age, diabetes mellitus and systemic lupus erythematosus as causes of end-stage renal disease, recipient gender, and lower panel reactive antibody levels (PRAs). The strongest risk factors for RVT were retransplantation and prior PD treatment. Prevention of RVT with perioperative anticoagulation should be studied in patients who have a constellation of the identified risk factors.

The transgenic SAD mouse: A model of human sickle cell glomerulopathy

The transgenic SAD mouse which expresses a modified sickle hemoglobin, Hb SAD, displays in vivo hemoglobin polymerization and erythrocyte sickling. In the presence study functional and morphological renal analyses were performed in SAD mice in order to compare the renal pathology of SAD mice with the human disease. The SAD mice display renal hemosiderosis, microvascular occlusions, vascular thrombosis, cortical infarcts and papillary necrosis. In the medulla, hemoglobin polymers could be observed with infrequent erythrocyte sickling, which may explain the absence of significant renal concentration defect, whereas in humans, the difference in the vascularization network leads to more extensive sickling. Most animals develop glomerular hypertrophy and mesangial sclerosis which increases in frequency and severity with age. The glomerular damage is associated with functional defects, including increased blood urea nitrogen levels and non-selective proteinuria. The glomerular lesions of SAD mice strikingly mimic sickle cell glomerulosclerosis, the most severe renal complication of sickle cell disease in humans. In summary, the SAD mouse is a valuable model of the thrombotic and glomerulosclerotic complications of human sickle cell glomerulopathy and can serve for pathophysiologic studies, and, eventually, for prevention and therapy investigation.

Fibro-muscular renal artery disease treated by extracorporeal vascular reconstruction and renal autotransplantation: Short- and long-term results

Over a 16-year period (1973-1989), 63 renal autotransplants were performed in 59 patients for fibro-muscular dysplasia (FMD) with renal artery stenoses (42 kidneys) or aneurysms (21 kidneys). About two-thirds of the autotransplants were performed before percutaneous transluminal angioplasty (PTA) was established for clinical use. However, vascular disease at a site or type not suitable for PTA was present in 57 (90%) of the kidneys. Hypertension was the leading symptom in 56 patients, including four in whom renal autotransplantation was performed as an emergency for acute renal artery occlusion or malignant hypertension. Blood pressure returned to normal or improved in 51 (91%) and remained unchanged in five patients (9%) following autotransplantation. Three patients with renal artery aneurysm in whom haematuria and loin pain were the indications for treatment, became asymptomatic following surgical intervention. Bilateral renal autotransplantation was performed synchronously in one and sequentially in three patients. There were no operative deaths, but two kidneys were lost postoperatively in two 2-year-old children owing to renal vascular thrombosis. In the follow-up period (mean 4.3 years), one additional kidney was lost at 3 months owing to progressive FMD. Blood pressure and renal function remained stable in all other patients. Based on the excellent results achieved in this series, it is concluded that extracorporeal vascular repair and renal autotransplantation is a safe procedure for the patient as well as the kidney affected by FMD. The procedure is advocated as an alternative to in situ reconstruction in patients with renal artery disease not accessible to PTA, such as aneurysms and complex branch renal artery stenoses.

Pitfalls of “Bench Surgery” and Autotransplantation for Renal Cell Carcinoma

Under certain circumstances, extracorporeal surgical treatment ("bench surgery") followed by autotransplantation is indicated for renal cell carcinoma. During a 10-year period, 20 patients (16 men and 4 women) underwent bench surgery and attempted autotransplantation for renal cell carcinoma at our institution. The autotransplantation was successful in 16 patients but unsuccessful in 4 because of postoperative renal vascular thrombosis or extensive tumor involvement, which resulted in inadequate renal vein for anastomosis. Of the 16 patients who underwent successful autotransplantations, 4 (25%) subsequently had locally recurrent renal cell carcinoma (a mean of 35 months after initial autotransplantation). Only 6 of the 16 patients who underwent successful autotransplantation were ultimately free of both carcinoma and dialysis. Although an ex vivo surgical procedure can be beneficial for certain patients with renal cell carcinoma, computed tomographic scanning of the autotransplantation site should be performed every 3 to 6 months postoperatively for early detection of local tumor recurrence.