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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2016  |  Volume : 27  |  Issue : 6  |  Page : 1256-1259
Multiple visceral venous thromboses associated with oral contraceptive use

1 Department of Medicine, Faculty of Medicine, Kuwait University, Safat, Kuwait
2 Department of Medicine, Al-Amiri Hospital, Kuwait City, Kuwait
3 Department of Radiology, Hadi Hospital, Hawally, Kuwait

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Date of Web Publication28-Nov-2016


Peripheral venous thromboembolism (VTE) is a known complication of oral contraceptive drugs (OCs), yet its association with visceral VTE is rarely reported. We describe a 21-year-old female patient who presented with sudden left loin pain. Plain computed tomography (CT) urography did not show kidney lesion but was suspicious of left renal vein thrombosis. Contrast study confirmed the diagnosis and also disclosed thrombosis of the splenic and left ovarian veins. The patient did not have a family history or laboratory evidence of hypercoagulable disorder. An OC was the only medication she had received in the previous three months. The OC was discontinued, and the patient was anticoagulated with heparin and discharged home on warfarin for a total period of six months. Subsequent CT study with contrast, one month later, showed complete resolution of the thrombosis without any visceral abnormality.

How to cite this article:
El-Reshaid K, Al-Bader S, Sallam H. Multiple visceral venous thromboses associated with oral contraceptive use. Saudi J Kidney Dis Transpl 2016;27:1256-9

How to cite this URL:
El-Reshaid K, Al-Bader S, Sallam H. Multiple visceral venous thromboses associated with oral contraceptive use. Saudi J Kidney Dis Transpl [serial online] 2016 [cited 2023 Jan 29];27:1256-9. Available from: https://www.sjkdt.org/text.asp?2016/27/6/1256/194683

   Introduction Top

During their lifetimes, women may face several unique situations with an increased risk of venous thromboembolism (VTE), namely, the use of oral contraceptives (OCs), hormone replacement therapy, pregnancy, and the need for tamoxifen in breast cancer. The relative risk of VTE increases up to 6-fold higher in these conditions even with the modern "lowdose OCs." [1] The association of OCs with peripheral VTE has been documented, [2] yet its association with visceral VTE has been reported in only two patients with overt and concealed renal vein thrombosis (RVT). [3],[4] In this case report, we describe a multiparous woman who presented with multiple visceral venous thromboses shortly after starting treatment with an OC.

   Case Report Top

A 29-year-old woman presented with severe and persistent left loin pain for three days. She did not have past history of significant medical illness, surgery, allergy, or chronic intake of medications except for an OC for the past three months. On her initial examination, the patient was conscious, oriented, and without shortness of breath. Blood pressure was 120/80 mm Hg. She was afebrile with a body weight of 77 kg. Systemic examination did not show any abnormality. Laboratory investigations showed normal peripheral leukocyte and platelet counts. Hemoglobin was normal. Erythrocyte sedimentation rate was 20 mm/h. Serum sugar, urea, creatinine, electrolytes, and liver functions were normal. Urine routine and microscopy showed 25 red blood cells/high power field but no pyuria or proteinuria. Serum complements (C3 and C4) and protein electrophoresis were normal. Antineutrophil antibody, antineutrophil cytoplasmic antibody, and hepatitis B and C serology were negative. Chest X-ray, plain X-ray of abdomen and pelvis were normal. Abdominal and pelvic ultrasound was normal. A computed tomography (CT) urography showed enlarged left kidney with perirenal stranding (collaterals) and a hyperdense area inside the left renal vein suggestive of a thrombus [Figure 1]a. CT urography with contrast confirmed such thrombosis [Figure 1]b. Moreover, the contrast study showed an additional thrombosis in the splenic and the left ovarian veins [Figure 2] and [Figure 3]. The OC was discontinued, thrombophilia workup was collected, and the patient was treated with heparin. The loin pain disappeared within two days, and heparin was replaced with warfarin for a total period of six months. Repeat CT study with contrast, one month later, showed complete resolution of the thrombosis [Figure 1]c. Thrombophilia screening was done for PT and APTT, lupus anticoagulant, fibrinogen, D-dimer, factor VIII-c, functional protein C and S activity, antithrombin and activated protein C resistance, factor V Leiden, and prothrombin 20210A gene mutation. The results were negative for all.
Figure 1: (a) Plain computed tomography showing enlarged left kidney with perirenal stranding (collaterals) and a hyperdense area inside the left renal vein suggestive of thrombus, (b) postcontrast study showing a filling defect in the left renal vein (thrombus), (c) postcontrast study, 1 month after anticoagulation, showing patent renal vein and healthy kidney.

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Figure 2: Initial postcontrast study showing large filling defects in the splenic vein (white arrow).

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Figure 3: Initial postcontrast study of the left ovarian vein showing it thrombosis (white arrow).

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   Discussion Top

VTE is a serious complication. If occult, misdiagnosed, or late in presentation, it can lead to visceral infarction and potentially fatal pulmonary emboli. [5] RVT is an early sign of disease and fortunately rarely silent. It can present with loin pain simulating renal colic with its acute onset and hematuria. [3] Ultrasound examination is useful in excluding hydronephrosis and in infarcts and a Doppler study may be useful detecting suspected cases. [6] Fortunately, plain CT study which became a useful study in renal colics and nephrolithiasis can reveal it as well. [3] However, the contrast study is the gold standard, and it may even further disclose concealed thrombosis in other organs as in our patient. If misdiagnosed, RVT can lead to renal damage, hypertension, or both. [4] Moreover, thrombosis in the ovarian vein can lead to organ loss while the splenic one can extend to the portal and mesenteric veins leading to catastrophic hepatic failure and mesenteric infarction. [5] Trauma, severe dehydration, infection, malignancies, myeloproliferative disorders, autoimmune diseases, hypercoagulable states, hyperhomocysteinemia as well as nephrotic syndrome, especially membranous glomerulopathy and amyloidosis are considered to be causes of this vascular thrombosis in children and adults. [7] Our patient did not have any of those acquired or inherited conditions by detailed assessment. Her only risk factor was a recent use of an OC. These drugs have long been incriminated as a cause of VTE. The pathogenesis of thrombophilia with OC use has been extensively studied. [2] OC use can perpetuate the coagulation cascade and alters the hemostatic system. They increase levels of certain factors such as fibrinogen, factors II, VII, IX, X, and XII and decreases in antithrombin III levels. [8],[9] OCs can also cause activation of the fibrinolytic system as evidenced by increased levels of D-dimer, plasmin- antiplasmin complexes (PAP), and tissue plasminogen activator (t-PA) activity and decreased levels of plasminogen activator inhibitor-1 activity, t-PA antigen, and u-PA antigen. [8] Although peripheral venous thrombosis is a known complication of OCs, the visceral ones are rarely reported and mainly as an isolated RVT. [3],[4] Our case report indicated that such phenomenon is not localized to RVT, yet it can involve multiple visceral veins with potential catastrophic complications if misdiagnosed. Interestingly, in unilateral cases of RVT, the left renal vein is affected more commonly than the right as in our case. The left ovarian vein may have affected more than the right as it has a longer and more tortuous path. This vein is difficult to see by imaging but becomes evident when thrombosed as in [Figure 2]. Previous reports indicated that the highest incidence of peripheral VTE is associated with OC use is in the 1 st year. The duration of anticoagulant therapy recommended is three months since their hypercoagulable potential disappears after that. [9] We elected to continue her anticoagulation for six months since there was a visceral involvement. Alone, OC increases the risk of VTE, and they amplify the effect of other risk factors. OC use alone confers a relative risk of about four to six for VTE. [10] In comparison, patients heterozygous for factor V Leiden have a relative risk of three to 10 for the same. The combined risk of both OCs and factor V Leiden heterozygosity increases the relative risk for VTE to 35-40. [11] Similarly, patients homozygous for factor V Leiden alone have a relative risk of 79. Adding OCs increases the relative risk to almost 100. [12] Prothrombin mutation with OC use increases the relative risk of VTE by 16, whereas protein C or S or antithrombin III deficiency with oral contraceptive use has a relative risk of 9.7. [11]

Conflict of interest: None declared.

   References Top

Kujovich JL. Hormones and pregnancy: Thromboembolic risks for women. Br J Haematol 2004;126:443-54.  Back to cited text no. 1
Stegeman BH, de Bastos M, Rosendaal FR, et al. Different combined oral contraceptives and the risk of venous thrombosis: Systematic review and network meta-analysis. BMJ 2013;347:f5298.  Back to cited text no. 2
Ajmera A, Joshi A, Kamat B, Germaine P, Weisberg L. Idiopathic acute renal vein thrombosis in a young healthy woman with no hypercoagulable state taking oral contraceptives. Am J Med Sci 2010;339:380-2.  Back to cited text no. 3
Slick GL, Schnetzler DE, Kaloyanides GJ. Hypertension, renal vein thrombosis and renal failure (occurring in a patient on an oral contraceptive agent). Clin Nephrol 1975;3:70-4.  Back to cited text no. 4
De Stefano V, Martinelli I. Abdominal thromboses of splanchnic, renal and ovarian veins. Baillieres Best Pract Res Clin Haematol 2012;25:253-64.  Back to cited text no. 5
Kraft JK, Brandão LR, Navarro OM. Sonography of renal venous thrombosis in neonates and infants: Can we predict outcome? Pediatr Radiol 2011;41:299-307.  Back to cited text no. 6
Brenner BM. Disorders of renal arteries and veins. In: The Kidney. 7th ed. Pennsylvania: Saunders; 2004. p. 1584.  Back to cited text no. 7
Quehenberger P, Kapiotis S, Pärtan C, et al. Studies on oral contraceptive-induced changes in blood coagulation and fibrinolysis and the estrogen effect on endothelial cells. Ann Hematol 1993;67:33-6.  Back to cited text no. 8
Miller J, Chan BK, Nelson HD. Postmenopausal estrogen replacement and risk for venous thromboembolism: A systematic review and meta-analysis for the U.S. Preventive Services Task Force. Ann Intern Med 2002;136:680-90.  Back to cited text no. 9
Venous thromboembolic disease and combined oral contraceptives: results of international multi center case-control study: World Health Organization Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception. Lancet 1995;346:1575-82.  Back to cited text no. 10
Douketis JD, Ginsberg JS, Holbrook A, Crowther M, Duku EK, Burrows RF. A reevaluation of the risk for venous thromboembolism with the use of oral contraceptives and hormone replacement therapy. Arch Intern Med 1997;157:1522-30.  Back to cited text no. 11
Dalen JE. Should patients with venous thromboembolism be screened for thrombophilia? Am J Med 2008;121:458-63.  Back to cited text no. 12

Correspondence Address:
Kamel El-Reshaid
Department of Medicine, Faculty of Medicine, Kuwait University, P. O. Box 24923, 13110 Safat
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.194683

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