Kidney Week

Abstract: PUB158

Massive Pulmonary Embolism as the Initial Presentation of Minimal Change Disease

Session Information

• Publication Only

Category: Glomerular Diseases

• 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

• Burr, Madison, University of Utah Health Hospitals and Clinics, Salt Lake City, Utah, United States

Madison Burr, MMSc, PA-C

• Drury, Zachary, University of Utah Health Hospitals and Clinics, Salt Lake City, Utah, United States

Zachary Drury, APRN, CCRN, CNN-NP, DNP, NP, RN

• Shihab, Fuad, University of Utah Health Hospitals and Clinics, Salt Lake City, Utah, United States

Fuad Shihab, MD, FASN

• Al-Rabadi, Laith, University of Utah Health Hospitals and Clinics, Salt Lake City, Utah, United States

Laith Al-Rabadi, MD

• Barry, Marc, University of Utah Health Hospitals and Clinics, Salt Lake City, Utah, United States

Marc Barry, MD

• Abraham, Josephine, University of Utah Health Hospitals and Clinics, Salt Lake City, Utah, United States

Josephine Abraham, MD, MPH, FASN

Introduction

Minimal change disease (MCD) classically presents with edema and nephrotic-range proteinuria. While thromboembolic complications are a recognized sequelae of nephrotic syndrome, massive pulmonary embolism (PE) as the initial presentation is rare. We present a case in which massive PE led to the diagnosis of MCD.

Case Description

An 18-year-old female with a history of bipolar disorder, anxiety, and peptic ulcer disease presented with dyspnea and pleuritic chest pain. She was found to have massive PE complicated by acute right heart failure. Further evaluation revealed nephrotic syndrome with 24-hour urine protein of 39.4 g/day, serum albumin of 1.5 g/dL, and hypertriglyceridemia. Renal biopsy confirmed MCD with mild to moderate acute tubular injury, no global glomerulosclerosis or significant interstitial fibrosis/ tubular atrophy. Serologic workup and genetic testing for nephrotic syndrome were negative. Treatment with prednisone initiated at 100 mg daily and subsequently tapered, resulting in complete remission with normalization of proteinuria and renal function.

Discussion

Nephrotic syndrome confers a hypercoagulable state through urinary loss of anticoagulant proteins (e.g. antithrombin III, protein C, and protein S) and increased hepatic synthesis of prothrombotic factors. Although MCD carries a lower thrombotic risk than other nephrotic syndromes such as membranous nephropathy, severe thromboembolic events can occur. The severity of the patient’s hypoalbuminemia and high proteinuria likely contributed to increased thrombotic risk. Massive PE as the presenting event of MCD remains exceedingly rare. This case underscores the importance of evaluating for underlying nephrotic syndrome in young patients presenting with severe or unprovoked thromboembolism as early recognition may guide management and improve outcomes.

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