AN UNUSUAL CASE OF FLANK PAIN. F. Green 1 , R. Granieri 1 ; 1 University of Pittsburgh School of Medicine, Pittsburgh, PA LEARNING OBJECTIVE: Identify and treat acute renal infarction. CASE INFORMATION: J.C. is a 63 year old female with ischemic cardiomyopathy, mitral regurgitation, hypertension, and rheumatoid arthritis who developed spontaneous right flank pain that was constant, 8/10, sharp, and sufficient to wake her from sleep. The pain was associated with nausea, vomiting,and intermittent diaphoresis. There was no radiation to the groin, abdomen,or chest. There was no history of chest pain, palpitations, dysuria, abdominal trauma, vaginal discharge, or invasive vascular procedures. She has never had thromboembolic disease or atrial fibrillation. Medications included digoxin, losartan, prednisone, furosemide, hydroxychloroquine, aspirin, and methotrexate. Physical examination was notable only for compensated biventricular heart failure, mitral regurgitation, and right flank tenderness. Electrocardiogram revealed sinus tachycardia. Laboratory data was notable for BUN 35, Cr 1.2 WBC 14.1 (94% PMN), ALT 28, AST 37, GGT 180, Alk Phos 192, and LDH 386 . Urinalysis revealed 4 RBC, 0 WBC, and trace protein. CT scan of the abdomen and pelvis with contrast showed an acute infarct of the inferior pole of the right kidney. The patient was admitted and anticoagulated. Echocardiogram demonstrated an ejection fraction of 25% and severe mitral regurgitation with no evidence of mural thrombus. DISCUSSION: Renal infarction is an often overlooked clinical syndrome than can be mistaken for more common causes of flank pain. The etiology of most cases is embolic disease from underlying atrial fibrillation, valvular disease, or cardiomyopathy. No historical variable aside from risk factors for thromboembolic disease has been shown to be associated with renal infarction. Physical examination is non-specific although an incomplete infarction may cause a hyper-renin state with secondary hypertension. LDH is the best marker for renal infarction although initial measurements may be normal. Other lab abnormalities are inconsistently present. CT scans have replaced IVP and angiogram in making the diagnosis of renal infarct. While areas of infarction can be seen on non-contrasted CTs, contrast is necessary to increase sensitivity, better define the infarct, and distinguish acute from completed infarcts. Surgery, angioplasty, fibrinolysis, and conservative medical management are therapeutic options. Revascularization appears to be most successful in early infarction (first 3 hours). Conservative therapy with anticoagulation (and additional antihypertensive therapy if needed) is thought to have lower morbidity than invasive therapy in most cases. Although the mortality from the renal infarct itself is low, these patients have a dismal one year prognosis because of further embolic disease and underlying cardiac disease. year-old male roof repairman presented with shortness of breath for the past two weeks. He had no history of alcoholism, smoking or previous lung disease. He had been taking Azithromycin during the week prior to admission but had become worse. He had right-sided, pleuritic chest pain, fever, chills, yellow-greenish sputum, night sweats, and mild weight loss. Examination revealed moderate respiratory distress, a temperature of 101.1 8F and a pulse of 115. The mouth, teeth and oral pharynx were normal. The cardiac exam was normal except for tachycardia. Diminished breath sounds were noted on the right side of the chest. His WBC was 19.2 with 89% PMN's. A CXR and subsequent CT revealed a large loculated pleural effusion with right upper and middle lobe atelectasis. A sputum gram stain showed gram positive cocci in chains. A 2D echo showed a large peri-cardial effusion without evidence of tamponade. 1,200 cc of yellowish-greenish pus was drained following thoracentesis and placement of a chest tube. Cultures grew only Streptococcus constellatus which was sensitive to Clindamycin and Ampicillin. He recovered following these antibiotics with chest tube drainage. DISCUSSION: Streptococcus constellatus is a gram positive microaerophillic coccus that grows in chains or pairs and is a member of the Streptococcus intermedius group. It is usually present as a harmless commensal organism in the mouth and GI tract but like other members of the S. intermedius group has the propensity to form abscesses. Intrinsic virulence factors (hydrolytic enzymes, different adhesins on cell surfaces and a polysaccharide capsule) facilitate adherence, decrease phagocy-tosis and increase pathogenicity. S. constellatus is frequently associated with tho-racic infections and more prone to occur in males, alcoholics, people with previous pneumonia and in those at risk for aspiration. Mortality ranges between 15±30%. Although this patient had few risk factors for the development of this infection, the presence of a 3D Surface Shaded display showing high-grade stenosis of the celiac axis and superior dense empyema and pericardial effusion suggested S. costellatus or other organisms in the S. intermedius group as a possible cause.