Saudi Journal of Kidney Diseases and Transplantation

: 2008  |  Volume : 19  |  Issue : 1  |  Page : 90--93

Extensive Cerebral Venous Thrombosis in a Renal Allograft Recipient

Shobhana G Nayak, Renuka Satish, Gokulnath 
 Department of Nephrology, St. John’s Medical College Hospital, Bangalore, India

Correspondence Address:
Renuka Satish
Department of Nephrology, St. John’s Medical College Hospital, Sarjapur Road, Bangalore-560034


An increased risk of venous thromboembolism has been demonstrated following renal transplantation. Commonly reported sites have been deep vein thrombosis, pulmonary thromboembolism and vascular thrombosis involving the graft. Cerebral venous thrombosis (CVT) has not been reported in literature so far. A 36-year-old male patient, transplanted in Jan 2005 with normal graft functions, was admitted with history of headache, blurring of vision and vomiting. Examination revealed papilledema and no neurological deficits. Baseline investigations and analysis of cerebrospinal fluid were normal. Cerebral magnetic resonance venogram revealed extensive CVT involving superior sagittal sinus, bilateral transverse sinuses and the right sigmoid sinus. He was investigated for a thrombophilic disorder; serum homocysteine, protein C and S levels, antiphospholipid antibody and antithrombin-III levels were done despite which no conclusive diagnosis could be arrived at. To our knowledge, this is the first report of extensive CVT described in a transplant recipient. No definite prothrombotic or predisposing factors could be identified in our patient and the cause of CVT remains unclear.

How to cite this article:
Nayak SG, Satish R, Gokulnath. Extensive Cerebral Venous Thrombosis in a Renal Allograft Recipient.Saudi J Kidney Dis Transpl 2008;19:90-93

How to cite this URL:
Nayak SG, Satish R, Gokulnath. Extensive Cerebral Venous Thrombosis in a Renal Allograft Recipient. Saudi J Kidney Dis Transpl [serial online] 2008 [cited 2021 Aug 5 ];19:90-93
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Full Text


Postoperative thromboembolism is a major complication after surgery that correlates with the duration and invasiveness of surgery. There is an increased risk of venous thrombo­embolism following renal transplantation. The incidence of reported deep venous thrombosis is between 6.2%-8.3% and about 25% of these patients suffer from pulmonary embolism.[1],[2],[3],[4],[5] The commonly reported sites of thrombosis after kidney transplantation have been deep venous thrombosis (mainly on the side of the transplant), pulmonary thromboembolism and renovascular throm­bosis involving the graft. Cerebral venous thrombosis (CVT) after renal transplantation has not been reported in literature so far as a thrombotic complication. We report herewith a case of isolated CVT in a renal allograft recipient, the diagnosis of which was confirmed by appropriate imaging.

 Case Report

A 36-year-old male patient had undergone living related kidney transplantation in Jan 2005, the donor being his haplomatched sister. His native kidney disease was right single ectopic kidney with vesicoureteric reflux. He was doing well on conventional triple immunosupppression with predisolone, cyclosporine and azathioprine and at last follow-up in July 2006 had a serum creatinine of 1.5 mg% with cyclosporine trough level of 160 ng/ml. He presented to us in early August 2006 with history of occipital headache, blurring of vision and vomiting of two days duration. The headache was continuous, diffuse and worsened on recumbent position and on coughing. He did not have fever, seizures or limb weakness. His past history was negative for tuberculosis.

On examination, he was afebrile with stable vitals; cardiovascular, respiratory and abdo­minal evaluation was negative. Neurological evaluation revealed a conscious though slightly irritable patient with no motor/sensory deficits. There were no meningeal signs; how­ever examination of optic fundi revealed features of early papilledema. With a suspicion of neuroinfection he was hospitalized. The relevant laboratory investigations done after admission are summarized in [Table 1]. He was empirically treated with cephalosporins. However, the patient continued to have persistent severe headache and a neurology opinion was sought. With a suspicion of cortical venous thrombosis, a magnetic reso­nance venogram (MRV) of the cerebral vessels was performed [Figure 1] which re­vealed extensive CVT with complete occlu­sion of the posterior aspect of the superior sagittal sinus, bilateral transverse sinuses and the right sigmoid sinus. In view of exten­sive thrombosis, he was investigated for a probable thrombophilic disorder [Table 2].


The incidence of venous thromboembolism following renal transplantation is increased in the range of 5-8% with pulmonary embolism being a common cause of death in these patients. [1],[3],[6] Cerebral venous thrombosis occurs primarily, but not exclusively, in patients with risk factors for thromboembolic disease inclu­ding hematological disorders, inherited and acquired thrombophilia, pregnancy and contra­ceptive medications. Headache is the most common presenting symptom in patients with CVT and in addition to thunderclap headache; patients can present with a combi­nation of papilledema, seizures, bilateral focal deficits and/or altered level of consciousness. Magnetic resonance venogram is the diag­nostic imaging of choice.

Our patient was investigated for inherited as well as acquired thrombophilic disorders. Monitoring of factor V Leiden mutation and prothrombin gene polymorphism could not be done due to the lack of diagnostic faci­lities. Congenital deficiency of protein C and protein S are inherited in an autosomal dominant manner and are usually asso­ciated with venous thrombosis in the deep veins of the legs, iliofemoral veins and the mesenteric veins. CVT has been associated with protein C and S deficiency particularly when combined with acquired risk factors for thrombosis such as oral contraceptives. [7],[8]

Our patient has levels of protein C and S in the slightly lower than normal ranges. How­ever, low levels have been documented in acute thrombosis, co-morbid illness and in patients on anticoagulant therapy. Dicou­marol therapy could therefore account for the low levels seen in our patient and may not be causative.

A strong correlation between hyperhomo­cysteinemia and increased risk of arterial vascular disease has been observed. Hyper­homocysteinemia also increases the risk of venous thrombosis; however, it has not been found to be an isolated risk factor for cerebral venous thrombosis. Serum homo­cysteine was elevated in our patient; however, is unlikely that it could have been the causative factor.

Cyclosporine A (CyA) has procoagulant properties and increases factor VIII levels and releases Von Willebrand factor and P­selectin from the endothelium. [9],[10] A prospec­tive multi-centre study did not however show a significant difference for the occurrence of thrombosis with the use of CyA vs. azathioprine. [11]

To the best of our knowledge, this is the first reported case of extensive CVT described after renal transplantation in a patient with preserved graft function. No definite pro­thrombotic and pre-disposing risk factors could be identified in our patient and the cause of CVT remains unclear.


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