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Acute Unilateral Renal Infarction in the Setting of an Inherited Thrombophilia and Atrial Septal Defect.

1. Introduction

Paradoxical embolism is a rare but increasingly recognized cause of embolic events. An atrial septal abnormality such as a patent foramen ovale (PFO) or an atrial septal defect (ASD) serves as a pathway for a thrombus from the peripheral veins, bypassing the lungs, and entering the systemic circulation [1]. Cryptogenic stroke is the most commonly described presentation in patients with paradoxical embolism [2]. Renal infarction secondary to paradoxical embolism has rarely been described. Here, we report a case of a paradoxical embolism caused by ASD involving only one kidney in the setting of an inherited thrombophilia.

2. Case Presentation

A 43-year-old female was seen in consultation at our thrombosis clinic. She had a stroke at age 14 and had presented with collapse and left sided hemiparesis. Her thrombophilia work-up was positive for a prothrombin G20210A gene mutation in heterozygous form. She had been on aspirin 81 mg daily since age 14.

Prior to being diagnosed with a renal infarct at age 42, the patient presented with nausea, vomiting, hematuria, and left flank pain and was initially diagnosed as renal colic. She subsequently had a computerized tomography scan of the abdomen and pelvis, which showed evidence of a wedge-shaped area in the lower pole of the left kidney consistent with a renal infarction. She was not on an oral contraceptive. We started treatment with intravenous heparin and transitioned to warfarin for 15 months without any further thromboembolic events.

Given that cardioembolic sources are well-documented causes of renal infarction [3], the patient had loop monitoring for two weeks and electrocardiograms, which did not detect atrial fibrillation. She also had two echocardiograms, none of which showed any evidence of cardiac thrombus. A transthoracic echocardiogram was performed with agitated saline at rest and after valsalva maneuver, which showed mild to moderate degree of shunting at rest that increased significantly with the release phase of a valsalva maneuver. This was suspicious for a PFO. A follow-up transesophageal echocardiogram showed a small left to right shunt due to a small ASD rather than a PFO. The patient had device closure of the ASD with no evidence of any remaining shunt on a transthoracic echocardiogram. It is likely that the patient's renal infarction was related to paradoxical embolism caused by small deep vein thrombosis migrating through the ASD shunt.

After 4 months of being off of anticoagulation, patient had a D-dimer test, which was positive at 591 [micrp]g/L. There were no other reasons for the elevated D-dimer. Based on an annual risk of recurrence of approximately ten percent in females with a first unprovoked venous thromboembolism (VTE) event and a positive D-dimer, the patient was restarted back of warfarin [4].

3. Discussion

Prothrombin gene mutation is the second most common inherited thrombophilia with a prevalence of approximately 2% [5]. The risk of VTE in individuals who are heterozygous for the prothrombin G20210A mutation is approximately 3-4-fold compared with a control group [6, 7]. It is unclear if the prothrombin gene mutation increases the risk of VTE recurrence, with some studies suggesting an increased risk [8] while others not [9, 10]. It is generally known that the prothrombin gene mutation is not associated with an increased risk of arterial thrombosis. However, a 2017 meta-analysis reported a slightly increased risk of stroke in children and young adults with the prothrombin gene mutation [11].

There are several case reports of paradoxical embolism causing renal infarction through a PFO in presence or absence of a thrombophilia (Table 1) [12-17]. However, to our knowledge, this is the first report of a renal infarction due to paradoxical embolism in the setting of an ASD and thrombophilia. Paradoxical embolism is a rare cause of renal infarction; however the role of an atrial septal abnormality as a source of embolic events in various organs is increasingly recognized.

4. Conclusions

Our case report identifies paradoxical embolism causing renal infarction through an ASD and highlights the need for immediate identification of a paradoxical embolism so that anticoagulation can be started and device closure can be considered to prevent further embolic events in other organs.

https://doi.org/10.1155/2017/3159363

Received 18 May 2017; Accepted 31 July 2017; Published 27 August 2017

Academic Editor: Kate Khair

Consent

Informed consent was obtained from the patient to publish the case report.

Conflicts of Interest

Siavash Piran has nothing to disclose; Sam Schulman reports receiving consulting fees from Boehringer Ingelheim, Bristol-Myer-Squibb, Bayer, and Daichii and grant support from Boehringer Ingelheim, Baxter, and Octapharma.

References

[1] C. N. Dao and J. M. Tobis, "PFO and paradoxical embolism producing events other than stroke," Catheterization and Cardiovascular Interventions, vol. 77, no. 6, pp. 903-909, 2011.

[2] C. Lamy, C. Giannesini, M. Zuber et al., "Clinical and imaging findings in cryptogenic stroke patients with and without patent foramen ovale: the PFO-ASA study," Stroke, vol. 33, no. 3, pp. 706-711, 2002.

[3] Y. K. Oh, C. W. Yang, Y. Kim et al., "Clinical Characteristics and Outcomes of Renal Infarction," American Journal of Kidney Diseases, vol. 7, no. 2, pp. 243-250, 2016.

[4] J. Douketis, A. Tosetto, M. Marcucci et al., "Patient-level meta-analysis: Effect of measurement timing, threshold, and patient age on ability of D-dimer testing to assess recurrence risk after unprovoked venous thromboembolism," Annals of Internal Medicine, vol. 153, no. 8, pp. 523-531, 2010.

[5] F. R. Rosendaal, C. J. Doggen, A. Zivelin et al., "Geographic distribution of the 20210 G to A prothrombin variant," Thromb Haemost, vol. 79, no. 4, p. 706, 1998.

[6] C. Leroyer, B. Mercier, E. Oger et al., "Prevalence of 20210 A allele of the prothrombin gene in venous thromboembolism patients," Thrombosis and Haemostasis, vol. 80, no. 1, pp. 49-51, 1998.

[7] M. Margaglione, V. Brancaccio, N. Giuliani et al., "Increased risk for venous thrombosis in carriers of the prothrombin G->A20210 gene variant," Annals of Internal Medicine, vol. 129, no. 2, pp. 89-93, 1998.

[8] P. Simioni, P. Prandoni, and A. W. Lensing, "Risk for subsequent venous thromboembolic complications in carriers of the prothrombin or the factor V gene mutation with a first episode of deep-vein thrombosis," Blood, vol. 96, no. 10, p. 3329, 2000.

[9] S. Eichinger, E. Minar, M. Hirschl et al., "The risk of early recurrent venous thromboembolism after oral anticoagulant therapy in patients with the G20210A transition in the prothrombin gene," Thrombosis and Haemostasis, vol. 81, no. 1, pp. 14-17, 1999.

[10] V. De Stefano, I. Martinelli, P. M. Mannucci et al., "The risk of recurrent venous thromboembolism among heterozygous carriers of the G20210a prothrombin gene mutation," British Journal of Haematology, vol. 113, no. 3, pp. 630-635, 2001.

[11] B. Sarecka-Hujar, I. Kopyta, M. Skrzypek, and J. Sordyl, "Association Between the 20210G>A Prothrombin Gene Polymorphism and Arterial Ischemic Stroke in Children and Young Adults--Two Meta-analyses of 3586 Cases and 6440 Control Subjects in Total," Pediatric Neurology, vol. 69, p. 93, 2017

[12] A. Garachemani, P. Eshtehardi, and B. Meier, "Paradoxical emboli through the patent foramen ovale as the suspected cause of myocardial and renal infarction in a 48-year-old woman," Catheterization and Cardiovascular Interventions, vol. 70, no. 7, pp. 1010-1012, 2007.

[13] M. Iwasaki, N. Joki, Y. Tanaka, H. Hara, M. Suzuki, and H. Hase, "A suspected case of paradoxical renal embolism through the patent foramen ovale," Clinical and Experimental Nephrology, vol. 15, no. 1, pp. 147-150, 2011.

[14] H. Jeong, H. Woo Lee, J. Young Joung et al., "Renal infarction caused by paradoxical embolism through a patent foramen ovale," Kidney Research and Clinical Practice, vol. 31, no. 3, pp. 196-199, 2012.

[15] I. Ekinci, S. A. Dae, E. Asoglu et al., "A rare cause of renal infarct: Paradoxical embolism through the patent foramen ovale," Int J Urol Nephrol, vol. 2, no. 3, pp. 55-58, 2014.

[16] E. M. Vilbert and S. V Franciosa, "Acute Renal Infarction With Heritable Coagulopathy and Patent Foramen Ovale," Radiology Case Reports, vol. 4, no. 2, p. 260, 2016.

[17] O. Khoma, A. Suppiah, and D. Martin, "Case report: Renal infarction by paradoxical embolism through the patent foramen ovale as an unusual cause of post-operative abdominal pain after sleeve gastrectomy," International Journal of Surgery Case Reports, vol. 26, pp. 47-49, 2016.

Siavash Piran and Sam Schulman

Department of Medicine, Division of Hematology and Thromboembolism and Thrombosis and Atherosclerosis Research Institute, McMaster University, Hamilton, ON, Canada

Correspondence should be addressed to Siavash Piran; siavash.piran@medportal.ca
TABLE 1: Case reports of renal infarction associated with
paradoxical embolism in the setting of a patent foramen ovale.

Study                 Garachemani      Iwasaki      Jeong et al.
                        et al.          et al.

Year of                2007 [12]       2011 [13]     2012 [14]
  publication
  [Ref]
Renal                Unilateral,      Unilateral,   Unilateral,
  (unilateral          left side         right         right
  versus                                 side           side
  bilateral,
  side)
Venous                    No            No DVTs       No DVTs
  thromboembolism   investigations     detected        or PE
  detected             performed                      detected
Thrombophilia             No           Negative      Negative
                    investigations      screen         screen
                       performed
Other VTE risk           None            None           None
  factors
Other organ           Myocardial         None           None
  involvement         infarction
Anticoagulation          Oral          Secondary        IV
                    anticoagulation   prevention      heparin
                       type and          with
                       duration        aspirin
                      unspecified       100 mg
                                         daily
Device closure            Yes            Not          Planned
                                       specified

Study                  Ekinci        Vilbert and      Khoma
                        et al.        Franciosa       et al.

Year of               2014 [15]       2016 [16]      2016 [17]
  publication
  [Ref]
Renal                Unilateral,     Unilateral,    Unilateral,
  (unilateral            left            left          left
  versus                 side            side          side
  bilateral,
  side)
Venous                    No           No DVTs        No DVTs
  thromboembolism   investigations     detected      detected
  detected            performed
Thrombophilia          Negative      Prothrombin     Negative
                        screen         G20210A        screen
                                       mutation
Other VTE risk           None            OCP          After
  factors                                            bariatric
                                                      surgery
Other organ              None            None          None
  involvement
Anticoagulation       Enoxaparin      IV heparin     Warfarin,
                        60 mg        transitioned     6-month
                        twice             to         duration
                        daily         warfarin,
                                       6-month
                                       duration
Device closure           Not             Not          Planned
                      specified        planned

DVT: deep vein thrombosis; IV: intravenous; OCP: oral
contraceptive pill; PE: pulmonary embolism.
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Title Annotation:Case Report
Author:Piran, Siavash; Schulman, Sam
Publication:Case Reports in Hematology
Article Type:Clinical report
Date:Jan 1, 2017
Words:1607
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