An Abundance of Anything Is Harmful: Accessory Renal Arteries as a Rare Cause of Flash Pulmonary Edema

Introduction: Flash pulmonary edema (FPE) typically develops from bilateral renal artery stenosis (RAS) or unilateral RAS with a solitary functional kidney. In rare instances, unilateral RAS with both functional kidneys can also trigger FPE. We describe a novel case of FPE stemming from unilateral RAS and multiple accessory RAs (ARA) Case Description: A 68yo woman presented to ER with 3rd episode of FPE and HTN emergency Initial evaluation, including laboratory tests and RA ultrasound, showed no abnormalities. However, a CTA of the abdomen revealed a single heavily calcified L main RA with severe atherosclerosis extending into the lumen of the aorta and the proximal L main RA. Three RAs supply R kidney with questionable stenosis of superior, smaller R RA. Atherosclerotic plaque is present at the origin of the inferior R RA, but no definitive significant stenosis is detected Unilateral RAS and multiple ARAs were suspected as the cause of HTN and FPE. An aortogram with stenting was performed by vascular surgery. It confirmed > 75% stenosis in the L RA, prompting stent deployment. However, no significant stenosis was observed in R ARAs. BP control was achieved with a single agent Discussion: FPE is a life-threatening syndrome. It is usually accompanied by cardiac systolic or diastolic dysfunctions. Recurrent FPE due to bilateral RAS was described by Pickering et al. Although its exact mechanism is not completely understood, it is believed to result from hypervolemia due to decreased sodium excretion Could the presence of ARA mimic the pathophysiology of RAS? It has been theorized that ARA may lead to HTN due to reduced blood flow to kidneys, caused by its longer and narrower caliber, leading to high resistance, hypoperfusion, stenosis. The Poiseuille equation, rearranged to R=8μL/ΔPπR4 (where R=resistance, μ=viscosity, L=vessel's length, P=pressure, R=vessel's radius), suggests that radius and length of ARAs may play a role. In summary, ARAs are a common anatomical variation. Their specific characteristics may contribute to resistant HTN and FPE via renin-dependent hyperaldosteronism