Hindawi Publishing Corporation Case Reports in Medicine Volume 2011, Article ID 956089, 3 pages doi:10.1155/2011/956089 Case Report Cardiac Angiosarcoma-Associated Membranoproliferative Glomerulonephropathy Lokesh Shahani,1 Michael Beckmann,2 and Srikanth Vallurupalli1 1 Department of Internal Medicine, Southern Illinois University School of Medicine, 701 N. First Street, Springﬁeld, IL 62702, USA 2 Pathology Associates of Central Illinois LTD, Springﬁeld, IL 62702, USA Correspondence should be addressed to Srikanth Vallurupalli, svallurupalli@siumed.edu Received 21 September 2010; Accepted 24 March 2011 Academic Editor: Remo Panaccione Copyright © 2011 Lokesh Shahani et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Primary cardiac angiosarcoma is a rare cardiac tumor. The initial clinical course is often asymptomatic, and metastatic disease is present in a majority of aﬀected patients at diagnosis. We present a patient who presented with a hemorrhagic pericardial eﬀusion. No malignant cells were evident on cytological examination. He subsequently developed membranoproliferative glomerulonephritis requiring hemodialysis. Metastatic cardiac angiosarcoma was diagnosed 5 months later. To our knowledge, this is the ﬁrst reported case of paraneoplastic membranoproliferative glomerulopathy associated with cardiac angiosarcoma. 1. Introduction The occurrence of paraneoplastic glomerulopathies in pa- tients with cancer is well recognized [1]. We report a patient with cardiac angiosarcoma who initially presented with a pericardial eﬀusion and paraneoplastic glomerulopathy. 2. Case Report A 79-year-old Caucasian male presented with gradually worsening shortness of breath and fatigue. A chest X-ray revealed pulmonary congestion and cardiomegaly. Lab tests revealed normal kidney function. A transthoracic echocar- diogram revealed a large pericardial eﬀusion with features of cardiac tamponade. Hemorrhagic ﬂuid was obtained at pericardiocentesis, and around 400 milliliters were drained. Cytology was negative for malignant cells. Bacterial cultures grew Staphylococcus epidermidis. Though the clinical picture was not suggestive of bacterial pericarditis, he was treated with intravenous vancomycin for 4 weeks. A month later the patient developed shortness of breath and progressive pedal edema. Laboratory studies revealed a serum creatinine of 8.8 mg/dL. Spot urine protein to creatinine ratio was 3.1. He was found to have low comple- ment C3 and normal C4 levels. Serum ANA, ANCA, hep- atitis serology, and serum and urine protein electrophore- sis were negative. A repeat transthoracic echocardiogram revealed a small pericardial eﬀusion and normal cardiac function. A renal biopsy was performed. Light microscopy revealed hypercellular glomeruli with some prominence of mesangial matrix (Figure 1). Immunoﬂuorescence staining demonstrated granular glomerular basement membrane and variable mesangial staining with IgG, IgM, C3, C1q, kappa, and lambda. Tubular basement membranes and arterioles stained positive with C3. Electron microscopy demonstrated scattered small electron dense immune deposits within the mesangium and located primarily below the glomerular basement membrane reﬂection. There were no features sug- gestive of postinfectious glomerulonephritis or vancomycin- induced renal injury. Though C1q staining is not typical, the combined light, immunoﬂuorescence, and electron micro- scopic ﬁndings were felt to be consistent with a diagnosis of type 1 membranoproliferative glomerulonephritis. The patient was started on thrice weekly hemodialysis. Five months later, the patient developed gradually worsening diﬀuse abdominal and lower back pain. An abdominal and pelvis CT noted multiple hepatic and spinal lesions