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Systemic Capillary Leak Syndrome Secondary to COVID-19 Infection: Case Report

Systemic Capillary Leak Syndrome Secondary to COVID-19 Infection: Case Report

作     者:Mariam El Galiou N’mili Manal Benamar Loubna Ouzeddoun Naima Bayahia Rabia Madani Naoufel Bouattar Tarik Mariam El Galiou;N’mili Manal;Benamar Loubna;Ouzeddoun Naima;Bayahia Rabia;Madani Naoufel;Bouattar Tarik

作者机构:Department of Nephrology Dialysis and Transplantation Ibn Sina University Hospital Center Faculty of Medicine and Pharmacy Mohamed V University Rabat Morocco Department of Emergency Medicine Ibn Sina University Hospital Center Faculty of Medicine and Pharmacy Mohamed V University Rabat Morocco 

出 版 物:《Open Journal of Nephrology》 (肾脏病(英文))

年 卷 期:2023年第13卷第3期

页      面:226-233页

学科分类:1002[医学-临床医学] 100201[医学-内科学(含:心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

主  题:Hemoconcentration Low Blood Pressure COVID-19 Tubulointerstitial Nephritis 

摘      要:Introduction: Systemic capillary leak syndrome (SCLS) is an increasingly recognized rare syndrome. Its diagnosis is suggested by the occurrence of edema with arterial hypotension, hemoconcentration, and paradoxical hypoalbuminemia. SCLS can be idiopathic (Clarkson syndrome) or secondary. Secondary SCLS (SSCLS) is mainly triggered by infections (especially viruses), drugs (antitumor therapy), malignancies, and inflammatory diseases. We report a case of systemic capillary leak syndrome secondary to the COVID-19 infection. Observation: A 74-year-old chronic smoker with no particular history was initially admitted to the intensive care unit (ICU) with a picture of respiratory distress secondary to a COVID-19 infection with favorable evolution, hence his transfer to the emergency services. On Day 8 of hospitalization, following the installation of arterial hypotension, not responding to filling, associated with hypoalbuminemia, and generalized edematous syndrome, and in the absence of any other explanation for this clinical picture, a SCLS secondary to COVID-19 infection was suggested. On the balance sheet, after the discovery of acute renal failure, serum creatinine went from 7.9 mg/l to 16.6 mg/l with microalbuminuria at 420 mg/24h and leukocyturia at 20 elements/mm3 without germ-evoked tubulointerstitial nephritis (TIN) secondary to a viral infection with COVID-19. The evolution was marked by the spontaneous regression of the edema and the normalization of the blood pressure figures. Discussion: The classic triad combining hypotension, hemoconcentration, and hypoalbuminemia suggests the diagnosis of SCLS once all other causes of shock have been ruled out. Hemoconcentration is less constant in SSCLS than in ISCLS. This is the case with our patient. The exact pathophysiological process of SCLS is largely unknown. Viral infections are the most common infectious cause of SCLS. The kidneys are the second-most common organs affected by the SARS-Cov-2 coronavirus

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