MO240A FATAL CASE OF VASCULITIS AFTER SARS-COV-2 NEGATIVIZATION

Abstract Background and Aims Spectrum of acute severe respiratory syndrome Coronavirus 2 (SARS-CoV-2) ranges from mild to critical and probably mortality rate is largely underestimated. Complications may represent different manifestation of a profound endothelial dysfunction and injury. Biopsies rev...

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Published in:Nephrology, dialysis, transplantation dialysis, transplantation, 2021-05, Vol.36 (Supplement_1)
Main Authors: Bracaccia, Maria Elena, De Cicco, Nicolò, Moioli, Alessandra, Barberi, Simona, Fofi, Claudia, Mene', Paolo
Format: Article
Language:English
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Summary:Abstract Background and Aims Spectrum of acute severe respiratory syndrome Coronavirus 2 (SARS-CoV-2) ranges from mild to critical and probably mortality rate is largely underestimated. Complications may represent different manifestation of a profound endothelial dysfunction and injury. Biopsies reveal macro and microvascular thrombosis involving larger and smaller vessels. Different Authors described accumulation of inflammatory cells across vascular bed, viral inclusions and apoptotic bodies across vascular bed. Endotheliitis leads to loss of vessel integrity with bleedings and lumen restriction with tissue ischemia and necrosis. SARS-CoV-2 also can cause vasculitis and a systemic inflammatory vascular disease with COVID-19-associated coagulopathy. Several cases of vasculitis have been described during COVID-19 pandemy but in literature, to our knowledge, there are few cases of patients developing vasculitis after SARS-CoV-2 infection. Method A 59-year-old male patient in chronic haemodialysis with hypertension, chronic thrombocytopenia, uncertain history of type 2 diabetes mellitus and recent COVID-19 pneumonia (1 month before) was admitted to our E.R. with psycho-motor slowdown, dyspnoea, profound hypotension, diffuse and extensive purpura especially on extremities and nose with petechiae and ecchymoses, thrombocytopenia, widespread arthritis and myalgia and atrial fibrillation with high ventricular response. Laboratory tests revealed leucocytosis with elevation of inflammatory markers (GB 15.6 x 103/µL CRP 6.61 mg/dl, procalcitonin 2.64 ng/ml), thrombocytopenia (PLTs 55 x 103/µL), Hb 11.2 g/dl, increased amylase (444 UI/L) and lipase (608 UI/L), hyperkaliaemic metabolic acidosis, mild impaired blood clotting with normal fibrinogen and severe D-Dimer elevation (3453 mcg/ml), normal haptoglobin and bilirubin. SARS-CoV-2 rapid antigen test and three molecular swab tests (at admission and during recovery) were negative. Contrast-enhanced chest-abdomen CT did not demonstrate relevant findings. Results We suspected thrombotic thrombocytopenic purpura, COVID-19 related vasculitis or an autoimmune disease reactivation after SARS-CoV-2 or other concurrent viral infections. A peripheral blood smear excluded presence of schistocytes, HBV, HCV, HIV, c-ANCA, p-ANCA, LAC anti-mitochondrial and ENA antibodies were negative, such as complement factor C4 (C3 at low limits). IgA immunoglobulins resulted increased (952 mg/dl). We administered intravenous (IV) hydration,
ISSN:0931-0509
1460-2385
DOI:10.1093/ndt/gfab092.00118