COVID-19 infection predisposes patients to a hypercoagulable state. The clin. significance of concomitantly pos. antiphospholipid antibodies as a risk factor for thrombus formation is unknown. We report a case of renal infarct secondary to COVID-19 infection with mildly elevated antiphospholipid antibodies. A 71-yr- old woman with a history of hypertension, supraventricular tachycardia, resected carcinoid tumor in remission, COVID-19 infection (20 days prior), presented to the hospital with acute onset severe left lower quadrant pain radiating to the left flank for one day. She reported a fever of 101 F. Vital signs were normal in the emergency room. Phys. exam showed left costovertebral angle tenderness, otherwise benign abdomen with no guarding or rigidity. Laboratory findings showed normal liver function tests, mildly elevated creatinine at 1.1 mg/dL (baseline 0.8 mg/dL), and leukocytosis (14.2 K/ul). Urinalysis showed no evidence of proteinuria or microscopic hematuria. CT scan of the abdomen demonstrated a large area of patchy hypoattenuation involving the upper pole and interpolar region of the left kidney with adjacent perinephric inflammation representing a sequela of an infarct. Hypercoagulable workup including HIV, hepatitis, ANA, ANCA, complements, B2 glycoprotein, homocysteine, factor V Leiden, anti-thrombin III, protein C, protein S were done. All tests resulted neg. except for mildly elevated anticardiolipin antibody, IgM 12.90 MPL (normal 0.00-12.49 MPL). Holter monitor was neg. for atrial fibrillation. An echocardiogram did not show any thrombus. Considering her neg. tests, renal infarct was believed to be secondary to a hypercoagulable state from COVID-19 infection. Antiphospholipid antibodies repeated 3 mo after this admission were mildly elevated. Renal infarction was treated with a heparin infusion and was subsequently transitioned to apixaban. Acute kidney injury resolved with i.v. fluid resuscitation. At a 3-mo follow-up, her renal function remained stable with a resolution of symptoms. Renal artery infarct is a possible thrombotic complication of COVID -19. Role of lupus anticoagulant antibodies in increasing this risk warrants further studies.