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Table of Contents
Year : 2019  |  Volume : 13  |  Issue : 1  |  Page : 42-45

Deep vein thrombosis occurring early postrenal transplant

1 Department of Nephrology, Sri Ramachandra Medical College and Research Institute, Chennai, Tamil Nadu, India
2 Department of Nephrology, Dr. Pinnamaneni Siddhartha Institute of Medical Sciences and RF, Gannavaram, Andhra Pradesh, India

Date of Web Publication29-Mar-2019

Correspondence Address:
Dr. Manikantan Shekar
Department of Nephrology, Sri Ramachandra Institute of Higher Education and Research, Porur, Chennai - 600 056, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijot.ijot_64_18

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In kidney transplant recipients (KTRs), there can be an increased risk of thrombotic diseases. Here, we report a case of KTR, who developed ipsilateral acute iliofemoral deep vein thrombosis (DVT). A 38-year-old male with end-stage renal disease underwent deceased donor renal transplantation. He received antithymocyte globulin induction (2 mg/kg) and was maintained on tacrolimus, mycophenolate mofetil, and steroids. He had delayed graft function. One month posttransplant, the patient presented with right lower limb edema, with Doppler showing DVT of the right external iliac, common femoral, and proximal superficial femoral veins. He was treated with unfractionated heparin and underwent placement of retrieval filter in the infrarenal inferior vena cava (IVC) through the right internal jugular vein approach. Heparin was overlapped and switched to oral acenocoumarol. At 3 months postoperative, the patient is stable with no limb edema and serum creatinine of 0.8 mg/dl. A follow-up venous Doppler demonstrated the resolution of the thrombus. In conclusion, our patient developed DVT within 30-day postoperative period with no apparent risk factor and was successfully treated with anticoagulation and placement of IVC filter. Venography, thrombolysis, and thrombectomy pose challenges in the KTRs because of increased risk of adverse effects such as bleeding, contrast-induced nephropathy, and pulmonary embolism.

Keywords: Deep venous thrombosis, inferior vena cava filter, renal transplant

How to cite this article:
Makkena VK, Shekar M, Mamidi V, Bandi VK, Matcha J. Deep vein thrombosis occurring early postrenal transplant. Indian J Transplant 2019;13:42-5

How to cite this URL:
Makkena VK, Shekar M, Mamidi V, Bandi VK, Matcha J. Deep vein thrombosis occurring early postrenal transplant. Indian J Transplant [serial online] 2019 [cited 2022 Oct 4];13:42-5. Available from: https://www.ijtonline.in/text.asp?2019/13/1/42/255188

  Introduction Top

Deep vein thrombosis (DVT) is one of the major medical problems affecting 2.5 million people in the United States each year with an incidence of approximately 1 per 100.[1] Incidence of DVT in India is not known. In kidney transplant recipients (KTRs), there is an imbalance of the hemostatic system, leading to persistent hypercoagulable state and increased risk of thrombotic diseases.[2],[3] The reported incidence of DVT in KTRs is between 1.6% and 8.3%.[4],[5] Ipsilateral DVT in a KTR can lead to allograft loss, graft rupture, and death.[6],[7] DVTs have been conventionally treated with anticoagulation, but the use of retrieval filter in the early posttransplant period is not common. Here, we report a case of KTR, who developed ipsilateral acute iliofemoral DVT, which was treated successfully with anticoagulation and inferior vena cava (IVC) filter placement.

  Case Report Top

A 38-year-old male with end-stage renal disease secondary to presumed chronic glomerulonephritis with a dialysis (hemodialysis) vintage of 36 months underwent deceased donor renal transplantation with the graft kidney transplanted into the right iliac fossa with the graft vessels being anastomosed to the internal iliac vessels. He received antithymocyte globulin for induction (2 mg/kg) and was maintained on triple immunosuppression with tacrolimus, mycophenolate mofetil, and steroids. There were no intraoperative complications. Postoperatively, he had delayed graft function (DGF) and underwent five sessions of hemodialysis. In view of DGF, transplant kidney Doppler was done, which was normal, and he underwent allograft renal biopsy on postoperative day (POD) 5, which showed the presence of acute tubular necrosis and no evidence of rejection. His serum creatinine decreased from a peak of 5.4 mg/dl on day 5 to discharge creatinine of 1.8 mg/dl on day 15.

The patient had no history of leg edema or pain. All laboratory values and imaging studies of the renal vessels before transplant, including prothrombin time, activated partial thromboplastin time, and international normalized ratio (INR), were within normal limits. The patient had a steady improvement in graft function, with creatinine improving to 1.8 mg/dl by POD 15 and hemoglobin of 10.8 g/dl.

One month posttransplant, the patient developed gradual swelling of the right lower limb, which was extending from the right thigh to the foot, with no erythema or local rise of temperature. Doppler of the right lower limb was done which revealed the presence of a DVT involving the right external iliac, common femoral, and proximal superficial femoral veins [Figure 1]. Although venography is the gold standard for confirmation of DVT, we used duplex Doppler ultrasound to confirm the diagnosis of DVT. Venography was not done in view of posttransplant status with DGF and the risk of contrast-induced nephropathy.[7]
Figure 1: Doppler image of the right lower limb showing deep vein thrombosis involving right external iliac, common femoral, and proximal superficial femoral veins

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There was no evidence of cytomegalovirus (CMV) infection with the CMV DNA polymerase chain reaction in blood showing undetectable copies, while his preoperative serology was IgM negative and IgG positive. Serum homocysteine levels were mildly elevated at 20.43 μmol/l and he was started on folic acid supplements. His workup for antiphospholipid antibodies (APLAs) was negative, as also antinuclear antibodies. Another workup for procoagulant statuses such as protein C, protein S, and Factor V Leiden mutations could not be done due to logistic reasons.

The patient was started on intravenous unfractionated heparin 5000 units 8th hourly and was planned for IVC filter. He underwent fluoroscopy guided placement of retrieval filter in the infrarenal IVC through the right internal jugular vein. Unfractionated heparin was continued intravenous up to 48-h postfilter placement and then overlapped and switched to oral acenocoumarol 2 mg once a day. He was discharged after 2 weeks with decrease in edema of the right leg, a urine output of 6 l/day, serum creatinine of 1.1 mg/dl, and hemoglobin of 11.2 g/dl. His anticoagulation was adjusted to maintain INR between 2 and 2.5.

At 3 months postoperative, the patient is stable with no limb edema and serum creatinine of 0.8 mg/dl. A follow-up venous Doppler demonstrated the resolution of the thrombus. Fluoroscopy pictures confirmed the position of the IVC filter [Figure 2].
Figure 2: Fluoroscopy pictures showing the position of the inferior vena cava filter (a) preinsertion and (b) postinsertion

Click here to view

  Discussion Top

More than 90% of the DVT in general surgical patients occur within the 1st week after surgery.[8] Most of the early thrombotic events that occur in this setting can be attributed to technical failures, external compression, preexisting asymptomatic DVT, or thrombophilia. In our case, the patient developed DVT 30 days after the procedure although there was no apparent risk factor.[6]

KTRs per se have been shown to have a procoagulable state in the absence of any additional complication.[3] This risk of hypercoagulability is highest during the initial 6 months, but it is present throughout life. The hypercoagulable risk in the 1st month can be attributed to general risk for any major surgery, while several other factors have been proposed to operate in the posttransplant patient.[5],[9]

In a study by Humar et al.,[5] the authors reported that more DVT episodes were seen in the 3rd–5th month after transplant. They also observed that in the initial month posttransplant, the risk of DVT was more than two times higher on the side of the graft surgery, in accordance with the risk due to local surgical manipulation. However, over the time frame of study, the risk equalized on both sides, suggesting that the later risk was not related to surgical factors.

The cause of hypercoagulable state in KTRs is multifactorial. It includes the use of immunosuppressive agents, presence of APLAs, native kidney disease, and infections. Among the immunosuppressive drugs, the use of steroids,[10] cyclosporin,[11] and sirolimus[12] has been shown to be associated with increased risk of thrombosis, while few studies have demonstrated a decreased risk with tacrolimus.[13] The KTRs with DVT should also be evaluated for APLAs whose incidence has been reported to be as high as 28.1% in a report.[14] The native kidney disease of the patient also plays a role, with patients having lupus nephritis (due to APLAs)[15] and Fabry's disease[16] having increased risk of thrombotic events.

There is growing evidence that homocysteine is associated with increased thrombotic risk, and the levels of homocysteine have been found to be elevated in KTRs, with one study reporting a prevalence of about 70%.[17] Another risk factor to consider is the posttransplant polycythemia. It has been assumed that as the hematocrit increases, the risk of DVT increases.[18] However, a study by Verhave et al.[19] showed that anemia was associated with increased risk of DVT. The authors suggested that this could probably reflect an increased state of inflammation leading to anemia and DVT. Nephrotic syndrome developing posttransplant is also an established risk factor for DVT, as it promotes a procoagulant milieu.[20]

Our patient was successfully treated with anticoagulation and placement of IVC filter. We did not proceed with thrombolysis in view of recent transplant surgery. Many authors have reported thrombolytic therapy as the treatment of choice for acute DVT in KTR.[21] It is clinically effective in approximately 85% of the patients. However, the incidence of hemorrhagic complication is approximately 10%. Recent surgery is a relative contraindication for thrombolytic therapy.[22] Surgical thrombectomy is also an option but can be associated with significant perioperative risk of pulmonary embolism and high risk of DVT.

In patients with DVT, IVC filter has been used in high-risk patients to prevent pulmonary embolism. The filter can be placed either through a femoral approach or a right jugular venous approach depending on the position of the thrombus.[23] Here, IVC filter was placed in the infrarenal IVC through internal jugular approach.

  Conclusion Top

Acute iliofemoral DVT is a rare event after renal transplant. We report a case of early postrenal transplant acute iliofemoral DVT, which was successfully treated with anticoagulation and IVC filter placement. Venography, thrombolysis, and thrombectomy pose challenges in the KTRs because of increased risk of adverse effects such as bleeding, contrast-induced nephropathy, and pulmonary embolism.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

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Malyszko J, Malyszko JS, Pawlak K, Mysliwiec M. The coagulo-lytic system and endothelial function in cyclosporine-treated kidney allograft recipients. Transplantation 1996;62:828-30.  Back to cited text no. 2
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Muraki T, Taka T, Noguchi T, Ishii H, Seki J, Yamamoto J, et al. Effects of cyclosporine and FK506 onin vitro high shear-induced platelet reactivity in rat and human non-anticoagulated blood. Transplantation 1998;65:1132-4.  Back to cited text no. 13
Ducloux D, Bourrinet E, Motte G, Chalopin JM. Antiphospholipid antibodies as a risk factor for atherosclerotic events in renal transplant recipients. Kidney Int 2003;64:1065-70.  Back to cited text no. 14
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Friedman GS, Wik D, Silva L, Abdou JC, Meier-Kriesche HU, Kaplan B, et al. Allograft loss in renal transplant recipients with Fabry's disease and activated protein C resistance. Transplantation 2000;69:2099-102.  Back to cited text no. 16
Ducloux D, Motte G, Challier B, Gibey R, Chalopin JM. Serum total homocysteine and cardiovascular disease occurrence in chronic, stable renal transplant recipients: A prospective study. J Am Soc Nephrol 2000;11:134-7.  Back to cited text no. 17
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Verhave JC, Tagalakis V, Suissa S, Madore F, Hébert MJ, Cardinal H, et al. The risk of thromboembolic events in kidney transplant patients. Kidney Int 2014;85:1454-60.  Back to cited text no. 19
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Hirota S, Matsumoto S, Yoshikawa T, Tomita M, Kono M, Sako M, et al. Inferior vena cava filter placement for prevention of pulmonary tumor emboli of renal cancer with renal vein or vena caval tumor thrombus: Prophylactic usage prior to transcatheter arterial embolization. Radiat Med 1998;16:335-9.  Back to cited text no. 23


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