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Case Vignette A young female patient presented with spontaneous right frontal 5x3x3cm parenchymal hemorrhage, seizure, and arteriovenous malformations (AVM). History was remarkable for remote history of seizure, rhabdomyolysis, and new liver cirrhosis with renal failure. At the time of her remote seizure, non-contrast CT and MRI brain with/without contrast are reported as only mild volume loss without identified lesions. Diagnostic angiogram demonstrated a left posterior frontal 16x13mm AVM supplied via left middle cerebral artery, 15x33mm right occipital AVM supplied via right posterior cerebral artery, and small bilateral cerebellar AVMs supplied via posterior inferior cerebellar arteries. Her case was managed conservatively. She recovered neurologically. She underwent liver and kidney transplantation and had good recovery of hepatic and renal function. Follow-up MRI / MRA / MRV completed two weeks after transplant due to significant headaches was concerning for atypical PRES but also showed only the occipital AVM. Edema improved on follow-up MRI. She recovered well and was able to be discharged home. A continued conservative management strategy was chosen for her AVM. For surveillance and consideration of treatment options, after recovery, a six-month follow-up diagnostic cerebral angiogram was completed. This showed complete resolution of all previously visualized AVMs, without new shunting or other vascular abnormalities.Case Discussion This case illustrates multiple apparent de novo cerebral AVMs in the context of liver cirrhosis, with subsequent spontaneous resolution after successful transplantation and restoration of hepatic function. While pathophysiologic mechanisms are not fully clear, cirrhotic hepatic cells release angiogenic factors (such as vascular endothelial growth factor, thymidine phosphorylase, basic fibroblast growth factor, acidic fibroblast growth factor), with increasing secretion as liver function worsens, and may create pro-angiogenic conditions. Treatment of these AVMs may consist largely of restoration of hepatic function, rather than intervention for AVM management, when appropriate.Disclosures T. Duda: None. D. Renedo: None. J. Haynes: None. N. Sujijantarat: None. R. Hebert: None.Abstract E-366 Figure 1Abstract E-366 Figure 2