Pulmonary Vascular Disease |

Failure of Anticoagulation in a Case of Nephrotic Syndrome With Recurrent Thromboembolism FREE TO VIEW

Aparna Basu, MD; Shriyanka Jain, MD; Dhruvan Patel, MD; Geeta Bodapati, MD; Neethi Venkatappa, MD; Priyanka Bhattacharya, MD
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Mercy Catholic Medical Center, Philadelphia, PA

Chest. 2015;148(4_MeetingAbstracts):983A. doi:10.1378/chest.2280343
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SESSION TITLE: Pulmonary Vascular Disease Student/Resident Case Report Posters

SESSION TYPE: Student/Resident Case Report Poster

PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM

INTRODUCTION: Nephrotic syndrome is a hypercoagulable state which can lead to arterial and venous thromboembolism. Here we report a case of arterial and venous thrombosis who presented with extension of clot despite anticoagulation

CASE PRESENTATION: 21 female who was diagnosed with a pulmonary embolism two years ago prior to the presentation to our hospital. At that time she was treated with Warfarin. Six months later while on warfarin she was diagnosed with thrombosis in the inferior vena cava. At that time as she was pregnant she was treated with Low Molecular Weight Heparin. Following the completion of her pregnancy she was switched to Rivaroxaban. Two months later presented to our hospital with acute abdominal pain. CT scan of the abdomen revealed a new splenic infarct while on Rivaroxaban. On questioning she claimed compliance with medication. She found to have an albumin level of 2.1 gm/dl. 24 hour urine collection revealed a 3 gm proteinuria. She had peripheral edema on physical exam. Her triglyceride level was 428 mg/dl and total cholesterol level of 270 mg/dl. Her ANA screen was positive with a titre of 1:320 with a speckled pattern. She was found to have Hemoglobin of 6.9 g/dl with COOMBS test positive for antibodies. C4 complement level was low at 6 mg/dl. A diagnosis of nephrotic syndrome likely secondary to Lupus was made though she is still awaiting a kidney biopsy.

DISCUSSION: Increased activity of factors II, V, VII, VIII, X and XII is seen in nephrotic syndrome. This is due to compensatory increase in hepatic production secondary to hypoallbuminemia. LMWH acts through antithrombin III to inhibit Factor II and X, Warfarin inhibits factors II, VII, IX and X and Rivaroxaban is a direct Factor X inhibitor. Therefore increased factor levels can make these anticoagulants ineffective. Also all three anticoagulants are highly protein bound which can lead to increased plasma clearance of the drug in nephrotic syndrome leading to sub therapeutic levels of the medications in the blood.

CONCLUSIONS: Therefore our case proves anticoagulation in itself may not always be effective to prevent thromboembolism in nephrotic syndrome. Normalization of albumin levels is also essential as it decreases the level of clotting factors making anticoagulation more effective

Reference #1: Fahal IH, McClelland P, Hay CR, Bell GM. Arterial thrombosis in the nephrotic syndrome. Postgrad Med J. 1994;70:905-9.

DISCLOSURE: The following authors have nothing to disclose: Aparna Basu, Shriyanka Jain, Dhruvan Patel, Geeta Bodapati, Neethi Venkatappa, Priyanka Bhattacharya

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