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BackgroundThe COVID-19 pandemic has led to widespread vaccination with effective results and a great safety profile. However, as the vaccination rate has increased, more cases of autoimmune diseases after the COVID-19 vaccine have been described. We present a systematic review of ANCA-associated glomerulonephritis after the COVID-19 vaccine.ObjectivesTo summarize the existing evidence on ANCA-associated glomerulonephritis after the COVID-19 vaccine.MethodsWe searched all studies from inception till January 27, 2022, that described ANCA-associated biopsy-proven glomerulonephritis after COVID-19 vaccine through Embase and Medline. Methodological quality was evaluated with the 4 domains tool. We included 13 patients from 2 case series and 9 case reports. We extracted demographics, history, lab results, outcomes. We then applied descriptive statistics.Results46% of the patients were males and 54% were females. The median age was 74 years. 54% developed symptoms after the second dose of the 2-dose vaccine. The median interval between the vaccine and the symptom onset was 10.5 days. 85% had anti-MPO antibodies, and the rest – anti-PR3 antibodies. 31% of patients had persistent creatinine (Cr) elevation on follow-up, and 3 patients were requiring hemodialysis. Of those 3 patients, 1 patient had normal renal function prior to presentation, and the rest had chronic kidney disease. The summary of the cases is presented in Table 1.Table 1.Gender, ageDe novo (1) or relapse (2)AZD1222 (1), or mRNA-1273 (2), or BNT162b2 (3)OutcomeM, 75121HemodialysisM, 74121Improved CrF, 82212Improved CrF, 70312Improved CrF, 78413Improved CrF, 79513RemissionF, 54613Improved CrF, 78623HemodialysisM, 58712RemissionM, 63811Improved CrF, 29913RemissionM, 521012HemodialysisM, 841113Worsened CrConclusionAlthough the causality cannot be established on current evidence, the COVID-19 vaccine can probably trigger glomerulonephritis associated with ANCA, primarily anti-MPO type. We need a bigger cohort to identify patients predisposed for disease development or relapse after the COVID-19 vaccine.References[1]David R, Hanna P, Lee K, et al. Relapsed ANCA associated vasculitis following Oxford AstraZeneca ChAdOx1-S COVID-19 vaccination: A case series of two patients. Nephrol. 2021;27(1):109-110.[2]Klomjit N, Alexander MP, Fervenza FC, et al. COVID-19 Vaccination and Glomerulonephritis. Kidney Int Rep. 2021;6(12):2969-2978.[3]Chen C-C, Chen H-Y, Lu C-C, et al. Case Report: Anti-neutrophil Cytoplasmic Antibody-Associated Vasculitis With Acute Renal Failure and Pulmonary Hemorrhage May Occur After COVID-19 Vaccination. Front Med. 2021;8.[4]Shakoor MT, Birkenbach MP, Lynch M. ANCA-Associated Vasculitis Following Pfizer-BioNTech COVID-19 Vaccine. Am J Kidney Dis. 2021;78(4):611-613.[5]Hakroush S, Tampe B. Case Report: ANCA-Associated Vasculitis Presenting With Rhabdomyolysis and Pauci-Immune Crescentic Glomerulonephritis After Pfizer-BioNTech COVID-19 mRNA Vaccination. Front Immunol. 2021;12.[6]Davidovic T, Schimpf J, Sprenger-Mahr H, et al. De Novo and Relapsing Glomerulonephritis following SARS-CoV-2 mRNA Vaccination in Microscopic Polyangiitis. Case Reports Nephrol. 2021.[7]Feghali EJ, Zafar M, Abid S, et al. De-novo Antineutrophil Cytoplasmic Antibody-Associated Vasculitis Following the mRNA-1273 (Moderna) Vaccine for COVID-19. Cureus. 2021;13(11).[8]Villa M, Diaz-Crespo F, Perez de Jose A, et al. A case of ANCA-associated vasculitis after AZD1222 (Oxford–AstraZeneca) SARS-CoV-2 vaccination: casualty or causality? Kidney Int. 2021;100(4):937-938.[9]Dube GK, Benvenuto L, Batal I. Antineutrophil Cytoplasmic Autoantibody-Associated Glomerulonephritis Following the Pfizer-BioNTech COVID-19 Vaccine. Kidney Int Rep. 2021;6(12):3087-3089.[10]Sekar A, Campbell R, Tabbara J, et al. ANCA glomerulonephritis after the Moderna COVID-19 vaccination. Kidney Int. 2021;100(2):473-474.[11]Obata S, Hidaka S, Yamano M, et al. MPO-ANCA-associated vasculitis after the Pfizer/BioNTech SARS-CoV-2 vaccination. Clin Kidney J. 2021.Disclosure of InterestsNone declared

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Case Presentation A 28 year old male with a past medical history of diabetes mellitus type 2 (T2DM) and hypertension presented to the emergency room with acute onset, progressive epigastric pain associated with nausea. The pain suddenly started earlier that day after a large meal. He denied alcohol use. He was previously on insulin Glargine 55 units nightly but was not using it for several months. Vitals signs were within normal limits, BMI was 38.5 kg/m 2 . Physical examination revealed marked epigastric tenderness and multiple yellow papules on the abdomen and extensor surfaces of extremities. Lab findings revealed WBC 14.3 k/mm cu, lipase 437 IU/L, triglycerides greater than 3000 mg/dl with VLDL greater than 3000 mg/dl. Computerized tomography of the abdomen was consistent with acute pancreatitis. He was diagnosed with familial hypertriglyceridemia presenting with hypertriglyceridemia-induced pancreatitis and was admitted to the intensive care unit (ICU). Treatment with regular insulin infusion was started. On day 3, triglyceride levels decreased to 543 mg/dl and insulin infusion was stopped. He reported symptomatic improvement and was able to tolerate oral diet. He was counseled on significance of lifestyle modifications and medication compliance and was discharged on Niacin, Omega 3, Fenofibrate, Ezetimibe, and Pravastatin with plans to follow up with an Endocrinologist. Discussion This case of a young male presenting with hypertriglyceridemia-induced pancreatitis due to underlying familial hypertriglyceridemia emphasizes the significance of comprehensive history taking and work up for patients initially presenting to the clinic with risk factors such as obesity and insulin resistance. Our patient classically had a history of T2DM, and as cardiovascular complications are the leading cause of mortality in diabetic patients, screening for and managing dyslipidemia is pivotal. Eruptive xanthomas are erythematous-yellow papules typically located on extensor surfaces which appear when triglyceride levels exceed 1500-2000 mg/dl. This characteristic skin finding led to a prompt suspicion for familial hypertriglyceridemia in our patient. Our patient was stabilized in the ICU and subsequently discharged on multiple oral agents. The current consensus is that single statin therapy is not recommended; however, further research is indicated to specify the optimal combination of triglyceride lowering agents based on the severity of hypertriglyceridemia. Presentation: No date and time listed

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