ACUTE TUBULOINTERSTITIAL NEPHRITIS ASSOCIATED WITH CLOPIDOGREL. N. Palanichamy 1 , C. Kumar 1 ; 1 Oakwood Healthcare System, Dearborn, MI (Tracking  ID #76611) LEARNING OBJECTIVES: To describe clopidogrel induced acute renal failure, a previously unreported drug reaction. CASE INFORMATION: An 89 year-old white male presented with hematuria and acute renal failure. His Medications were aspirin, plavix, metaprolol, prinivil, lasix and flomax. He was placed on clopidogrel two weeks prior. He stopped the drug the day before admission. His creatinine level was 3.9 mg/dl (baseline creatinine 1.3 mg/dl). Urinalysis showed proteinuria, leukocytes and erythrocytes. 24-hour protein excretion was 756 mg. A renal ultrasound showed no obstruction. Over the course of the next week his renal function deteriorated (creat 8.9 mg/ dl). Renal biopsy showed a widened, edematous interstitium with moderate lymphocytosis, plasma cells and regenerative tubules and was compatible with tubulointerstitial nephritis (AIN). Dialysis was started and the patient was placed on steroids. With treatment the creatinine decreased to 2.6 mg/dl, the dialysis stopped and the steroids tapered. Based on the history and presentation clopidogrel was thought to be the etiology of the nephritis in this case. IMPLICATIONS/DISCUSSION: To our knowledge, this is the first case of clopidogrel induced acute tubulointerstitial nephritis. The rapid deterioration in the renal function two weeks after starting clopidogrel and the absence of confounding factors suggests the diagnosis in the presence of the biopsy findings. Clopidogrel affects platelet aggregation by inhibiting the ADP receptor and the subsequent ADP-mediated activation of the glycoprotein GPIIb/IIIa complex. The precise mechanism of the renal dysfunction is unknown but, like ticlopidine, a chemically similar drug with known adverse renal effects, may be caused by cell-mediated injury. Guerciolini et al. (1985) demonstrated a positive lymphocyte stimulation test in explaining agranulocytosis associated with ticlopidine. The other known mechanism of drug induced AIN, antibody mediated injury and circulating immune complexes are less likely causes insofar as the immunoflorescent studies in our case were nonspecific. In addition to the more commonly known side effects of clopidogrel physicians now need to realize that in rare instances it may cause renal dysfunction. LEARNING OBJECTIVES: Think about malignancy in the differential diagnosis of leukemoid reaction. CASE INFORMATION: A 68 year old Caucasian male with no significant past medical history presented with complaints of swelling of both legs, vague abdominal pain, watery diarrhea and increased urinary frequency of 6 weeks duration. He also reported a weight gain of 50 pounds over the past 6 months. On physical examination, he was afebrile, pulse was 81/min and blood pressure was 145/82 mm Hg. He had pallor and massive lower extremity edema extending upto the scrotum. There was no lymphadenopathy. Abdominal examination revealed a large hard mass extending anteriorly from the right lumbar region to the opposite flank and pelvis. Laboratory data-Hb 8.7gm/dl, Total WBC 74,800/cu mm, Differential±40% neutrophils, 56% bands and 4% monocytes, platelets 195 K/cu mm, LAP score 217. Urinalysis was normal. Alkaline phosphatase 144 IU/L, total serum protein 6.3 g/dl, C-reactive protein 13.3 mg/dl. Both blood and urine cultures were negative. Peripheral smear±leukocytosis, mature granulocytes and band forms, no blasts. CT scan of the abdomen showed a large, lobulated retroperitoneal mass extending to the posterior aspect of the right kidney, measuring 9Â8Â15 cm and another left sided pelvic mass, 14Â10Â17 cm, contiguous with the urinary bladder and pressing on the IVC. Multiple low-density lesions were also noted in the liver and spleen. Bone marrow biopsy revealed a myeloid predominant hypercellular marrow, no blast cells. A CT guided biopsy from the hypodense lesion in the liver revealed a metastatic, poorly differentiated malignant fibrous histiocytoma (MFH), pleomorphic type, positive for vimentin and negative for cytokeratin and alpha-fetoprotein on immunostaining. The IL-6 and IL-2 levels were normal. The patient was started on chemotherapy with cyclophosphamide, dexamethasone, adriamycin and dacarbazine. He developed disseminated intravascular coagulation on the 5th day of chemotherapy and expired. IMPLICATIONS/DISCUSSION: This case is unique because of the association of malignant fibrous histiocytoma with leukemoid reaction (LR). Several cases of soft tissue sarcomas with leukocytosis have been reported, but less than 15 cases of MFH with this phenomenon were found in the review of literature. The relationship between cytokine levels and LR has not been consistently demonstrated in the cases reported. Although, in our patient, serum cytokine levels were noninformative and histologically, the metastatic component of the tumor was not significantly different from the``non-inflammatory'' fibroxanthosarcomas, the absence of any other cause of leukocytosis highlights its association with MFH. The prognostic significance of leukocytosis with these tumors is yet to be defined, an added survival benefit of the inflammatory component is debatable. year-old male with a history of 30 pack-year tobacco use and positive tuberculin test, presented with nonproductive cough and night sweats for several months. Physical exam was normal. Serum immunofixation tests and acid fast stains of sputum were normal. Pulmonary function test (PFTs) showed moderate obstructive airway disease, and transthoracic echocardiogram was unremarkable. Chest x-ray (CXR) exam revealed a rounded opacity in the right lung apex. Computed tomography (CT) showed a 2.5 cm right apical mass and multiple small nodules seen in both lung fields. Transbronchial biopsy of the apical mass was consistent with pulmonary nodular amyloidosis. Follow-up CT imaging showed no significant change after one year. Case 2: A 73 year-old Caucasian male with a history of 40 pack-year tobacco use, had a CXR for preoperative evaluation for blepharoplasty. He denied cough, weight loss, and night sweats. Physical exam and laboratories were all within normal limits. PFTs were consistent with mild obstructive airway disease. CXR exam showed an incidental finding of a round density in the right middle lung field. CT revealed a 1.5 cm round opacity in the right middle lobe. Transbronchial lung biopsy of the mass was consistent with pulmonary nodular amyloidosis. Follow-up CT imaging showed no significant change after one year. IMPLICATIONS/DISCUSSION: Pulmonay amyloidosis may present in one of three ways: