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Indian Heart Journal ; 73:S42-S43, 2021.
Article in English | EMBASE | ID: covidwho-1568741


Background: Nephrotic syndrome is known to be associated with hypercoagulable status. Pulmonary artery thromboembolism is one of the life- threatening complications in patients with nephrotic syndrome but rarely occurs before the diagnosis of nephrotic syndrome. Methods and Results: A 33-year-old man without any co-morbidities presented to a primary care clinic with sudden onset shortness of breath. An electrocardiogram showed sinus tachycardia with S1Q3T3. ECHO and CTPA revealed thrombi of the bilateral pulmonary arteries and he was COVID-19 negative by PCR analysis. Anticoagulant therapy was initiated immediately. Hypercoagulability workup showed normal levels of protein C, protein S, and AT III. He was ANA- and APLA negative and his homocysteine levels were normal. Lower limb Doppler showed multiple deep venous system thrombi. Three months following this episode, he presented with recurrence of acute worsening of breathlessness with pedal edema and abdominal distention. He was referred to our Cardiology emergency care. 2D Echocardiography showed classic Mc Connells sign with akinesia of RV free wall and RV systolic pressure of 60 mm Hg. CT pulmonary angiography definitively proved fresh (recurrence of) pulmonary embolism with large clots in both LPA and RPA and CXR showed classical signs of pulmonary embolism (Fig. 1). USG abdomen showed ascites, normal kidneys and no renal vein thrombosis. Laboratory examination showed he was COVID-19 negative again by PCR analysis. They also revealed low serum albumin (2.2g/dl) and nephrotic-range proteinuria (>10 gm in 24 hours) with transudative ascitic fluid. Since patient was on anticoagulation renal biopsy was deferred by the consultant nephrologist in view of possible bleeding complications. In view of possible primary membranous nephropathy, Serum Anti-Pla2r antibody was done which was strongly positive. The constellation of nephrotic-range proteinuria, pulmonary thromboembolic complications and associated serum anti-Pla2R antibody suggested primary membranous nephropathy. Immunosuppression was started as per modified Ponticelli regimen. Proteinuria resolved after three weeks and patient continues to be doing well on anticoagulation on oral VKA [Formula presented] Conclusion: Previous case reports of pulmonary artery thromboembolism associated with nephrotic syndrome are very few, particularly in adults. In the rare cases where they do occur, the patients initially present with the symptoms derived from nephrotic syndrome, unlike in our patient where the presentation was extremely rare and the investigation of the thromboembolic event led us “backwards” to the diagnosis of nephrotic syndrome. Awareness regarding the potential complications of hypercoagulable in nephrotic syndrome is thus essential.