Outbreak of chronic renal failure: will this be a delayed heritage of COVID-19?
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EDITORIAL
Outbreak of chronic renal failure: will this be a delayed heritage of COVID‑19? Niloofar Khoshdel‑Rad1,2 · Ensieh Zahmatkesh1,2 · Anastasia Shpichka3,4 · Peter Timashev3,4,5 · Massoud Vosough1,2
© Italian Society of Nephrology 2020
Keywords Acute kidney injury · Chronic renal failure · COVID-19 · Renal damage · SARS-CoV-2 · Coronavirus Abbreviations ACE-2 Angiotensin-converting enzyme 2 AKI Acute kidney injury CRF Chronic renal failure ESRD End-stage renal disease RRT Renal replacement therapy SARS-CoV-2 Severe acute respiratory syndrome coronavirus 2 Outbreaks of newly emerging infectious diseases have always threatened human health and global stability. The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently causing a global pandemic of a disease now named COVID-19. While the common symptoms are influenza-like, SARS-CoV-2 infection may lead to multiorgan dysfunction and death; fragile patients have, as in other viral diseases, a higher risk of adverse events. To date, there is no agreed treatment for COVID-19 and a wide range of treatments has been proposed, including antiviral * Peter Timashev [email protected] * Massoud Vosough [email protected] 1
Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran
2
Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran
3
Institute for Regenerative Medicine, Sechenov University, Moscow, Russia
4
Chemistry Department, Lomonosov Moscow State University, Moscow, Russia
5
Department of Polymers and Composites, NN Semenov Institute of Chemical Physics, Moscow, Russia
drugs, immunotherapy, convalescent serum and monoclonal antibodies, cell-based therapies, and Chinese medicine [1]. The metallopeptidase angiotensin-converting enzyme 2 (ACE-2) is the functional receptor for SARS-CoV-2. It is present in various human organs such as heart, blood vessels, kidney, and gastrointestinal tract [2]. The kidneys are among the most common target organs of SARS-CoV-2. Several studies showed that renal deterioration is associated with 5.3 times in-hospital mortality risk in COVID-19 patients [3]. Computerized tomography (CT) scan of the kidneys showed that COVID-19 patients had renal interstitial inflammation and edema [3]. A broad range of clinical manifestations has been reported, including proteinuria (44–63%), hematuria (26.9–44%), urea (14.1–27%) and serum creatinine increase (10–19%). Moreover, up to 30% of hospitalized SARS-CoV2-infected patients developed acute kidney injury (AKI). As expected, pre-existing chronic kidney disease (CKD) was associated with a six-fold increased risk of AKI and severe COVID-19 infection [4]. Kidney involvement may in turn increase the risk of pulmonary edema, cardiopulmonary syndrome, circulatory insufficiency, and thromboembolic and hemorrhagic risks. The pathogenesis of kidney involvement
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