An unforeseen complication: left ventricular thrombus formation in a patient with membranous nephropathy

Abstract

Membranous nephropathy (MN) is an autoimmune glomerulopathy and one of the leading causes of adult nephrotic syndrome (NS). It is characterized by subepithelial immune complex deposition, complement activation, and podocyte injury, leading to proteinuria, hypoalbuminemia, hyperlipidaemia, and systemic oedema. A major complication of NS is a hypercoagulable state due to urinary loss of anticoagulants, hepatic overproduction of clotting factors, endothelial dysfunction, and platelet hyperactivity. Thromboembolic events are well-documented in MN, with venous thromboses predominating, whereas arterial thrombosis such as left ventricular thrombus (LVT) remains a rare but clinically significant event. We report the case of a 57-year-old male with type 2 diabetes mellitus who presented with generalized anasarca, dyspnoea on exertion, productive cough, weakness, and cutaneous lesions. Laboratory evaluation revealed nephrotic-range proteinuria (urine protein-creatinine ratio 19.78), hypoalbuminemia (2.0 g/dL), elevated serum creatinine (2.0-2.4 mg/dL). Renal biopsy demonstrated Stage II membranous nephropathy with characteristic basement membrane thickening and IgG-dominant immune deposits. Cardiac evaluation revealed a left ventricular apical clot with mildly reduced ejection fraction (45-50%), in the absence of prior cardiac disease history. Importantly, physicians promptly initiated a target-specific treatment approach addressing the glomerular pathology with immunosuppressive therapy, mitigating hypercoagulability with anticoagulation, and relieving fluid overload with diuretics. This individualized, timely strategy directly targeted the dual pathology of MN and its thrombotic complication, preventing further morbidity and demonstrating the value of precision-based decision-making. This case highlights LVT as a rare but severe thromboembolic complication of MN-induced nephrotic syndrome, even in the absence of pre-existing cardiac disease. Early recognition of hypercoagulability, prompt anticoagulation, and multidisciplinary management are crucial to prevent life-threatening embolic events in such patients.