A 50-year-old woman presented to the emergency department of our hospital with a 2-day history of lower limb pain associated with unusual asthenia and diffuse arthralgia over the past 3 weeks. She was a native of Guinea and had lived in France for most of her life, working as a personal care assistant. Her only medical history of note was an occurrence of fetal death at 12 weeks gestation when she was 35 years old. She had bilateral lower limb swelling, without changes in skin temperature or color. All proximal and distal arterial pulses were felt. General physical examination findings were otherwise unremarkable. Her laboratory tests showed a decreased hemoglobin concentration of 8.9 g/dL (normal range, 12–16 g/dL), a decreased platelet count of 45  109/L (normal range, 150–400 3 109/L), a C-reactive protein level of 158 mg/L (normal range, ,5 mg/L) and a d-dimer level of 2000 mg/L (normal range, ,500 mg/L). Compression US of the lower limbs revealed bilateral calf vein thrombosis involving the fibular and posterior tibial veins. Curative anticoagulation using low-molecular-weight heparin (enoxaparin, subcutaneous injection of 100 units per kilogram of body weight twice a day) was started. The day after the start of anticoagulation therapy, the patient reported dyspnea and acute chest and abdominal pain. Her vital signs were assessed, and she had elevated blood pressure and increased heart rate and respiratory rate, but she remained afebrile. Her cardiac auscultation was unremarkable, besides tachycardia. Skin examination revealed small areas of necrosis on the fingertips of her right hand. Laboratory studies were repeated and showed an increase in serum creatinine level from a baseline value of 0.49 mg/dL to a new value of 1.01 mg/dL (normal range, 0.6–1.1 mg/dL), an apparition of low-grade proteinuria of 0.43 g per day (normal range, ,0.3 g/day), and a high serum troponin level of 1066 ng/L (normal range, ,14 ng/L), whereas electrocardiography showed no ST segment modification and echocardiography revealed a moderately altered left ventricular ejection fraction (45%). There was no coronary occlusion seen at emergency coronarography. Contrast-enhanced CT of the chest, abdomen, and pelvis was performed (Figs 1, 2) together with cardiac MRI (Figs 3, 4).Contrast-enhanced (90 mL of iomeprol, Iomeron 350; Bracco) axial CT image of the lung bases demonstrates a filling defect in the left lower lobe pulmonary artery, corresponding to an acute pulmonary embolism, associated with a left pleural effusion and left lower lobe consolidation consistent with compression atelectasis (Fig 1). On the abdominal images acquired at a later phase, a wedge-shaped perfusion defect of the left kidney is depicted, consistent with a kidney infarct. Low-abundance pericholecystic fluid is also present (Fig 2a). Coronal reformation demonstrates a highattenuation superior mesenteric vein wall surrounding a central filling defect, corresponding to an extensive superior mesenteric vein thrombosis (Fig 2b) and bilateral hypoattenuating swelling of both adrenal glands (Fig 2c), showing no contrast material uptake, consistent with adrenal infarction, probably due to thrombosis of the adrenal veins. The tail of the right adrenal vein thrombus can be seen at the posterior aspect of the inferior vena cava (Fig 2d). On cardiac MRI scans, subendocardial high signal intensity corresponding to ischemic edema is seen on the short-axis T2 short tau inversion-recovery image (Fig 3). Patchy subendocardial foci of delayed enhancement are observed in the late gadolinium enhancement sequence in the midanterior and midanterolateral segments. What is your diagnosis?