Herein, we report a case of a young women aged 35 years with severe PE associated with SN. The patient was admitted to the Emergency Department of the University Hospital Sant’Andrea of Rome since she suffered of 3 syncopal episodes associated with the presence of lower limb edema and dyspnea. Laboratory examinations of blood and urine samples showed proteinuria (spot proteinuria 100 mg/dl) and hypoalbuminemia (2.2 g/dl),. She had no history of drug use including oral contraceptives. However, the patient reported a history of bacterial tonsillitis treated with fluoroquinolones 15 days before the admission to the Hospital. At the clinical examination, she was alert, and oriented, with pale skin (not sweaty). She also exhibited reduced blood pressure (100/60 mmHg), high heart rate (110 bpm), higher respiratory rate (24/min), grade 2 lower limb edema, and normal oxygen saturation (97%).
Blood tests showed normal levels of hemoglobin (15.7 g/dl), red blood cells (RBC) (5300000/ul), platelets (PLT) (250000/ul), and white blood cells (WBC) (7610/ul), liver and kidney markers in the normal range. Blood levels of D dimer were high (30670 ng/ml), with nearly normal level of troponin (350 pg/ml). During the stay in the emergency room, the patient underwent angio-computed tomography (CT) that showed the presence of thrombi in both right and left pulmonary arteries, suggestive of massive PE, areas of pulmonary infarctions along with deep venous thrombosis (DVT) with endoluminal thrombotic apposition of the common and left internal iliac vein (Fig. 1). Electrocardiogram (ECG) evaluation showed sinus tachycardia, normal intraventricular conduction, and normal ventricular repolarization. Echocardiogram exam showed normal left and right ventricular size and function, and diastolic D shape with a pulmonary artery systolic pressure value of 45 mmHg. The patient as treated with an intravenous heparin bolus of 80 UI/Kg followed by an intravenous infusion of 18 UI/Kg. The nephrologist consultant suggested to treat the patient with corticosteroids on the basis of PE diagnosis in the context of NS. The patient was admitted to the Intensive Care Coronary Unit (ICCU) to monitor vital signs and symptoms, and to continue the therapies. The patient was treated with prednisone 1 mg/kg/die; after 5 days of intravenous heparin infusion, the anti-coagulant therapy was shifted to edoxaban. The following laboratory tests were performed: complement C3 and C4, autoimmune markers including anti-nuclear antibodies (ANA), anti-cardiolipin IgG and IgM, anti-double strand or ds-DNA, extractable nuclear antigen (ENA), Factor II and V polymorphisms, JAK 2 mutation, anti-phospholipase A2 receptor (anti-PLA2R), and anti-thrombin (AT) III which resulted normal. A pharyngotonsillar culture showed absence of pathogenic bacteria growth. Blood levels of low density lipoprotein (LDL) cholesterol were 206 mg/dl, and triglycerides were 218 mg/dl. After 15 days of hospitalization, the lower limb edema was reduced, proteinuria decreased to 500 mg/24h, and blood albumin levels increased to 4.3 g/dl. At patient discharge, the following therapies were recommended: prednisolone, edoxaban, atorvastatin, and ramipril. Close follow-up by nephrologist was also recommended. The successful response to prednisone treatment and the negativity for PLA2R were suggestive for minimal change nephropathy, and, therefore, renal biopsy was not performed.