1. bookVolume 1 (2021): Issue 2 (September 2021)
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2719-3500
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30 Jun 2021
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access type Open Access

Diabetic kidney disease, a potentially serious issue resulting from collision of the coronavirus disease 2019 and diabetes global pandemics

Published Online: 01 Apr 2022
Volume & Issue: Volume 1 (2021) - Issue 2 (September 2021)
Page range: 63 - 66
Received: 17 Dec 2020
Accepted: 27 Jan 2021
Journal Details
License
Format
Journal
eISSN
2719-3500
First Published
30 Jun 2021
Publication timeframe
4 times per year
Languages
English

Diabetic kidney disease (DKD) is a progressive chronic kidney condition that occurs in the context of both type 1 and type 2 diabetes. DKD is a leading cause of end-stage renal disease (ESRD), a devastating condition that requires either kidney transplantation or life-long regular dialysis for the affected person to survive. Approximately 30%–50% of subjects with diabetes develop DKD. Diabetes is estimated to have affected 463 million people in 2019 globally [1], arguably one of the greatest pandemics in human history.

In late 2019, coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2), was initially diagnosed in Wuhan, China [2,3,4]. This disease rapidly became a global pandemic. At the time that this article was written, >67 million confirmed COVID-19 cases have been recorded globally. The pandemic is still widely prevalent in many countries including both developing and developed nations with >500,000 new cases per day being diagnosed in December 2020 [5].

In COVID-19 patients, particularly those hospitalized with severe COVID-19, diabetes has been a major comorbidity and is associated with a deleterious outcome [6, 7]. It has also been observed that Covid-19 is associated with increased severity of preexisting diabetes manifesting in some individuals as diabetic ketoacidosis [8,9,10,11]. Specific recommendations have been proposed to guide the management of diabetes in COVID-19 patients in the early stage of the COVID-19 pandemic [12].

The consequence of the collision of these two great pandemics and the long-term effects on the affected subjects are largely unknown. Whether COVID-19 associated severe complications of preexisting diabetes and new-onset diabetes (see below) make them more prone to DKD, or whether this could lead to a new form of kidney injury is currently unknown. DKD was already a leading cause of death in people with diabetes in the pre-COVID-19 era. Therefore, understanding whether COVID-19 influences the onset and progression of DKD in people with both COVID-19 and diabetes would be important and may require more specific guidelines for monitoring and managing the individuals affected.

Indeed, COVID-19 can cause multi-organ injury leading to severe complications and death [13,14,15,16]. SARS-Cov-2, the virus causing COVID-19, and SARS-Cov-1 responsible for the SARS outbreak in 2003, both being coronaviruses, use the same cell surface enzyme protein, angiotensin-converting enzyme 2 (ACE2) as their receptor to enter host cells [17,18,19]. ACE2 was initially found to be expressed mainly in the heart, kidney, and testis [20], and subsequently confirmed to also be expressed in other tissues such as the nasal airway, lung, gastrointestinal tract, liver, and pancreas [19, 21,22,23,24,25,26,27,28,29,30]. Therefore, these ACE2 expressing organs can be the targets of SARS-Cov-2 infection and their physiological functions could potentially be impaired as a result of virus infection, due to viral protein interactions with host cellular proteins as well as due to the anti-viral response including inflammation.

Some of these vulnerable organs such as the pancreas and liver may be involved in and thus could affect glucose metabolism. Thus, impairment of the function of such organs could lead to a deterioration of preexisting diabetes, or cause new-onset diabetes. In some subjects with COVID-19, it has been noted that they develop features of diabetes, such as hyperglycemia, even when they had no prior history of diabetes. This would imply that new-onset diabetes can be caused as a result of SARS-Cov-2 infection. The extent and pathophysiology of this phenomenon are currently being investigated by an international team of experts through the global COVIDIAB Registry led by Monash University and King's College, London [31]. Indeed, SARS-Cov-2 has been demonstrated to infect pancreatic endocrine cells, including insulin-producing beta cells in pancreatic organoids, leading to robust chemokine induction and increased cellular apoptosis [32]. The relevance of this finding in humans is further supported by the presence of ACE2, the receptor for SARS-Cov-2, in the human pancreas including in the insulin-producing pancreatic beta cells [27]. This is consistent with the finding reported >15 years ago that ACE2 is expressed in rat pancreatic islets [30]. It is highly likely that SARS-Cov-2, when it reaches the pancreas, would be able to infect pancreatic beta cells and other cells within the islets, either triggering an anti-viral inflammatory response within the pancreas or directly injuring these pancreatic endocrine cells. The virus-induced impairment of beta cell functions such as insulin synthesis and secretion or loss of insulin-producing cells would ultimately lead to acute new-onset diabetes manifested by severe hyperglycaemia.

Virus-induced new-onset diabetes or increased severity of preexisting diabetes in people with COVID-19 would presumably harm the kidney, an organ that is sensitive to increased ambient glucose levels. This would increase the risk of onset of DKD or increase the severity of existing chronic kidney disease in affected subjects. COVID-19 per se is also considered to be a direct causal factor for acute renal injury [33,34,35,36,37,38,39]. The kidney, with a high level of ACE2 expression, can be directly infected by SARS-Cov-2 and directly impacted as a result of virus infection and/or the anti-viral inflammatory response, such as cytokine storm as has been observed in COVID-19, particularly in those with severe COVID-19 [40, 41]. Proteomics analysis of urinary proteins from people with COVID-19 has recently confirmed that the cytokine storm occurs in a later stage of COVID-19 with increased severity following an initial stage of immunosuppression [42].

Hypoxia is considered to be a key final common pathway for chronic kidney disease to progress to end-stage renal disease [43, 44]. With pneumonia being a major condition seen in severe COVID-19, often with associated systemic hypoxia, it could promote a renal hypoxic response. Thrombosis is another major complication seen in severe COVID-19 patients [45] and the clots in the circulation can block the small blood vessels and capillaries in the kidney.

Furthermore, the renin-angiotensin system (RAS) plays a pivotal role in injuring the kidney due to increased activity of the Angiotensin II/AT1 receptor axis, including in DKD [46]. ACE2 plays a protective role by specifically cleaving Angiotensin II into Angiotensin 1–7, leading to inactivation of Angiotensin II, the major effector hormone of the RAS. Furthermore, the newly formed Angiotensin 1–7 has anti-inflammatory and antifibrotic effects via its receptor Mas [46, 47]. SARS-Cov-1 and other similar coronaviruses, such as SARS-Cov-2, bind to ACE2 to enter cells, leading to increased shedding of ACE2 and downregulation of cell surface ACE2 levels [48, 49]. When this occurs in the kidney, increased renal RAS activity due to ACE2 downregulation would presumably promote renal injury. All these factors together would significantly increase the risk of kidney injury, either increasing the severity of existing chronic kidney disease such as DKD or promoting a new form of kidney injury.

Taken together, diabetes worsens the outcome of COVID-19 and vice versa COVID-19 can further worsen preexisting diabetes or cause new-onset diabetes, leading to fatal multi-organ injury including renal damage. DKD is already a leading cause of death in people with diabetes, with diabetes arguably the greatest non-communicable disease pandemic in human history.

The current collision between diabetes and COVID-19 has generated major new challenges for affected individuals and health providers, including potentially serious and as yet unknown adverse consequences for those with COVID-19. Therefore, more research needs to be carried out to understand the pathophysiology and mechanisms of the interactions among these diseases. This can provide the direction for an optimized management strategy, including evidence-based guidelines for managing COVID-19 patients already affected by or at risk of diabetes and/or renal disease.

Saeedi P, Petersohn I, Salpea P, Malanda B, Karuranga S, Unwin N, et al. Global and regional diabetes prevalence estimates for 2019 and projections for 2030 and 2045: Results from the International Diabetes Federation Diabetes Atlas, 9(th) edition. Diabetes Res Clin Pract 2019; 157: 107843 SaeediP PetersohnI SalpeaP MalandaB KarurangaS UnwinN Global and regional diabetes prevalence estimates for 2019 and projections for 2030 and 2045: Results from the International Diabetes Federation Diabetes Atlas, 9(th) edition Diabetes Res Clin Pract 2019 157 107843 10.1016/j.diabres.2019.107843 Search in Google Scholar

Wang C, Horby PW, Hayden FG, Gao GF. A novel coronavirus outbreak of global health concern. Lancet 2020; 395: 470–3. WangC HorbyPW HaydenFG GaoGF A novel coronavirus outbreak of global health concern Lancet 2020 395 470 3 10.1016/S0140-6736(20)30185-9 Search in Google Scholar

Zhu N, Zhang D, Wang W, Li X, Yang B, Song J, et al. A novel coronavirus from patients with pneumonia in China, 2019. N Engl J Med 2020; 382: 727–3. ZhuN ZhangD WangW LiX YangB SongJ A novel coronavirus from patients with pneumonia in China, 2019 N Engl J Med 2020 382 727 3 10.1056/NEJMoa2001017709280331978945 Search in Google Scholar

Munster VJ, Koopmans M, van Doremalen N, van Riel D, de Wit E. A novel coronavirus emerging in China-Key Questions for Impact Assessment. N Engl J Med 2020; 382: 692–4. MunsterVJ KoopmansM van DoremalenN van RielD de WitE A novel coronavirus emerging in China-Key Questions for Impact Assessment N Engl J Med 2020 382 692 4 10.1056/NEJMp200092931978293 Search in Google Scholar

Johns Hopkins University Coronavirus Resource Center. 2020 Available at: https://coronavirusjhuedu/. Accessed December 8, 2020. Johns Hopkins University Coronavirus Resource Center 2020 Available at: https://coronavirusjhuedu/. Accessed December 8, 2020. Search in Google Scholar

Wang S, Ma P, Zhang S, Song S, Wang Z, Ma Y, et al. Fasting blood glucose at admission is an independent predictor for 28-day mortality in patients with COVID-19 without previous diagnosis of diabetes: A multi-centre retrospective study. Diabetologia 2020; 63: 2102–11. WangS MaP ZhangS SongS WangZ MaY Fasting blood glucose at admission is an independent predictor for 28-day mortality in patients with COVID-19 without previous diagnosis of diabetes: A multi-centre retrospective study Diabetologia 2020 63 2102 11 10.1007/s00125-020-05209-1734740232647915 Search in Google Scholar

Obukhov AG, Stevens BR, Prasad R, Calzi SL, Boulton ME, Raizada MK, et al. SARS-CoV-2 infections and ACE2: Clinical outcomes linked with increased morbidity and mortality in individuals with diabetes. Diabetes 2020; 69: 1875–86. ObukhovAG StevensBR PrasadR CalziSL BoultonME RaizadaMK SARS-CoV-2 infections and ACE2: Clinical outcomes linked with increased morbidity and mortality in individuals with diabetes Diabetes 2020 69 1875 86 10.2337/dbi20-0019745803532669391 Search in Google Scholar

Chee YJ, Ng SJ, Yeoh E. Diabetic ketoacidosis precipitated by Covid-19 in a patient with newly diagnosed diabetes mellitus. Diabetes Res Clin Pract 2020; 164: 108166. CheeYJ NgSJ YeohE Diabetic ketoacidosis precipitated by Covid-19 in a patient with newly diagnosed diabetes mellitus Diabetes Res Clin Pract 2020 164 108166 10.1016/j.diabres.2020.108166719458932339533 Search in Google Scholar

Reddy PK, Kuchay MS, Mehta Y, Mishra SK. Diabetic ketoacidosis precipitated by COVID-19: A report of two cases and review of literature. Diabetes Metab Syndr 2020; 14: 1459–62. ReddyPK KuchayMS MehtaY MishraSK Diabetic ketoacidosis precipitated by COVID-19: A report of two cases and review of literature Diabetes Metab Syndr 2020 14 1459 62 10.1016/j.dsx.2020.07.050739522832771918 Search in Google Scholar

Smati S, Mahot PM, Bourdiol A, Ploteau S, Hadjadj S, Cariou B. Euglycaemic ketoacidosis during gestational diabetes with concomitant COVID-19 infection. Diabetes Metab 2020; 47: 101181. SmatiS MahotPM BourdiolA PloteauS HadjadjS CariouB Euglycaemic ketoacidosis during gestational diabetes with concomitant COVID-19 infection Diabetes Metab 2020 47 101181 10.1016/j.diabet.2020.07.008738791932738403 Search in Google Scholar

Meza JL, Triana A, De Avila I, Del Rio-Pertuz G, Viasus D. Diabetic ketoacidosis precipitated by COVID-19 in patients without respiratory symptoms: Case reports. Cureus 2020; 12: e10031. MezaJL TrianaA De AvilaI Del Rio-PertuzG ViasusD Diabetic ketoacidosis precipitated by COVID-19 in patients without respiratory symptoms: Case reports Cureus 2020 12 e10031 10.7759/cureus.10031751579932983724 Search in Google Scholar

Bornstein SR, Rubino F, Khunti K, Mingrone G, Hopkins D, Birkenfeld AL, et al. Practical recommendations for the management of diabetes in patients with COVID-19. Lancet Diabetes Endocrinol 2020; 8: 546–50. BornsteinSR RubinoF KhuntiK MingroneG HopkinsD BirkenfeldAL Practical recommendations for the management of diabetes in patients with COVID-19 Lancet Diabetes Endocrinol 2020 8 546 50 10.1016/S2213-8587(20)30152-2 Search in Google Scholar

Wang T, Du Z, Zhu F, Cao Z, An Y, Gao Y, et al. Comorbidities and multi-organ injuries in the treatment of COVID-19. Lancet 2020; 395: e52. WangT DuZ ZhuF CaoZ AnY GaoY Comorbidities and multi-organ injuries in the treatment of COVID-19 Lancet 2020 395 e52 10.1016/S0140-6736(20)30558-4 Search in Google Scholar

Zaim S, Chong JH, Sankaranarayanan V, Harky A. COVID-19 and multiorgan response. Curr Probl Cardiol 2020; 45: 100618. ZaimS ChongJH SankaranarayananV HarkyA COVID-19 and multiorgan response Curr Probl Cardiol 2020 45 100618 10.1016/j.cpcardiol.2020.100618718788132439197 Search in Google Scholar

Mokhtari T, Hassani F, Ghaffari N, Ebrahimi B, Yarahmadi A, Hassanzadeh G. COVID-19 and multiorgan failure: A narrative review on potential mechanisms. J Mol Histol 2020; 51: 613–8. MokhtariT HassaniF GhaffariN EbrahimiB YarahmadiA HassanzadehG COVID-19 and multiorgan failure: A narrative review on potential mechanisms J Mol Histol 2020 51 613 8 10.1007/s10735-020-09915-3753304533011887 Search in Google Scholar

Collange O, Tacquard C, Delabranche X, Leonard-Lorant I, Ohana M, Onea M, et al. Coronavirus disease 2019: Associated multiple organ damage. Open Forum Infect Dis 2020; 7: ofaa249. CollangeO TacquardC DelabrancheX Leonard-LorantI OhanaM OneaM Coronavirus disease 2019: Associated multiple organ damage Open Forum Infect Dis 2020 7 ofaa249 10.1093/ofid/ofaa249733654832661498 Search in Google Scholar

Li W, Moore MJ, Vasilieva N, Sui J, Wong SK, Berne MA, et al. Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus. Nature 2003; 426: 450–4. LiW MooreMJ VasilievaN SuiJ WongSK BerneMA Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus Nature 2003 426 450 4 10.1038/nature02145709501614647384 Search in Google Scholar

Zhou P, Yang XL, Wang XG, Hu B, Zhang L, Zhang W, et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature 2020; 579: 270–3. ZhouP YangXL WangXG HuB ZhangL ZhangW A pneumonia outbreak associated with a new coronavirus of probable bat origin Nature 2020 579 270 3 10.1038/s41586-020-2012-7709541832015507 Search in Google Scholar

Hoffmann M, Kleine-Weber H, Schroeder S, Kruger N, Herrler T, Erichsen S, et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell 2020; 181: 271–80.e8. HoffmannM Kleine-WeberH SchroederS KrugerN HerrlerT ErichsenS SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor Cell 2020 181 271 80.e8 10.1016/j.cell.2020.02.052710262732142651 Search in Google Scholar

Donoghue M, Hsieh F, Baronas E, Godbout K, Gosselin M, Stagliano N, et al. A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1–9. Circ Res 2000; 87: e1–9. DonoghueM HsiehF BaronasE GodboutK GosselinM StaglianoN A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1–9 Circ Res 2000 87 e1 9 10.1161/01.RES.87.5.e1 Search in Google Scholar

Sungnak W, Huang N, Becavin C, Berg M, Queen R, Litvinukova M, et al. SARS-CoV-2 entry factors are highly expressed in nasal epithelial cells together with innate immune genes. Nat Med 2020; 26: 681–7. SungnakW HuangN BecavinC BergM QueenR LitvinukovaM SARS-CoV-2 entry factors are highly expressed in nasal epithelial cells together with innate immune genes Nat Med 2020 26 681 7 10.1038/s41591-020-0868-6863793832327758 Search in Google Scholar

Harmer D, Gilbert M, Borman R, Clark KL. Quantitative mRNA expression profiling of ACE 2, a novel homologue of angiotensin converting enzyme. FEBS Lett 2002; 532: 107–10. HarmerD GilbertM BormanR ClarkKL Quantitative mRNA expression profiling of ACE 2, a novel homologue of angiotensin converting enzyme FEBS Lett 2002 532 107 10 10.1016/S0014-5793(02)03640-2 Search in Google Scholar

Jia H. Pulmonary angiotensin-converting enzyme 2 (ACE2) and inflammatory lung disease. Shock 2016; 46: 239–48. JiaH Pulmonary angiotensin-converting enzyme 2 (ACE2) and inflammatory lung disease Shock 2016 46 239 48 10.1097/SHK.000000000000063327082314 Search in Google Scholar

Jia HP, Look DC, Hickey M, Shi L, Pewe L, Netland J, et al. Infection of human airway epithelia by SARS coronavirus is associated with ACE2 expression and localization. Adv Exp Med Biol 2006; 581: 479–84. JiaHP LookDC HickeyM ShiL PeweL NetlandJ Infection of human airway epithelia by SARS coronavirus is associated with ACE2 expression and localization Adv Exp Med Biol 2006 581 479 84 10.1007/978-0-387-33012-9_85712364117037581 Search in Google Scholar

Jia HP, Look DC, Shi L, Hickey M, Pewe L, Netland J, et al. ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia. J Virol 2005; 79: 14614–21. JiaHP LookDC ShiL HickeyM PeweL NetlandJ ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia J Virol 2005 79 14614 21 10.1128/JVI.79.23.14614-14621.2005128756816282461 Search in Google Scholar

Wu SJ, Huo LJ, Zhang J, Wang JJ, Jia H. Differential expression in ACE2, Ang(1–7) and Mas receptor during progression of liver fibrosis in a rat model. Zhonghua Gan Zang Bing Za Zhi 2014; 22: 118–21. WuSJ HuoLJ ZhangJ WangJJ JiaH Differential expression in ACE2, Ang(1–7) and Mas receptor during progression of liver fibrosis in a rat model Zhonghua Gan Zang Bing Za Zhi 2014 22 118 21 Search in Google Scholar

Fignani D, Licata G, Brusco N, Nigi L, Grieco GE, Marselli L, et al. SARS-CoV-2 receptor angiotensin I-converting enzyme type 2 (ACE2) is expressed in human pancreatic beta-cells and in the human pancreas microvasculature. Front Endocrinol (Lausanne) 2020; 11: 596898. FignaniD LicataG BruscoN NigiL GriecoGE MarselliL SARS-CoV-2 receptor angiotensin I-converting enzyme type 2 (ACE2) is expressed in human pancreatic beta-cells and in the human pancreas microvasculature Front Endocrinol (Lausanne) 2020 11 596898 10.3389/fendo.2020.596898769142533281748 Search in Google Scholar

Lukassen S, Chua RL, Trefzer T, Kahn NC, Schneider MA, Muley T, et al. SARS-CoV-2 receptor ACE2 and TMPRSS2 are primarily expressed in bronchial transient secretory cells. EMBO J 2020; 39: e105114. LukassenS ChuaRL TrefzerT KahnNC SchneiderMA MuleyT SARS-CoV-2 receptor ACE2 and TMPRSS2 are primarily expressed in bronchial transient secretory cells EMBO J 2020 39 e105114 10.15252/embj.2020105114 Search in Google Scholar

Zhang H, Kang Z, Gong H, Xu D, Wang J, Li Z, et al. Digestive system is a potential route of COVID-19: An analysis of single-cell coexpression pattern of key proteins in viral entry process. Gut 2020; 69: 1010–18. ZhangH KangZ GongH XuD WangJ LiZ Digestive system is a potential route of COVID-19: An analysis of single-cell coexpression pattern of key proteins in viral entry process Gut 2020 69 1010 18 10.1136/gutjnl-2020-320953 Search in Google Scholar

Tikellis C, Wookey PJ, Candido R, Andrikopoulos S, Thomas MC, Cooper ME. Improved islet morphology after blockade of the renin-angiotensin system in the ZDF rat. Diabetes 2004; 53:989–97. TikellisC WookeyPJ CandidoR AndrikopoulosS ThomasMC CooperME Improved islet morphology after blockade of the renin-angiotensin system in the ZDF rat Diabetes 2004 53 989 97 10.2337/diabetes.53.4.98915047614 Search in Google Scholar

Rubino F, Amiel SA, Zimmet P, Alberti G, Bornstein S, Eckel RH, et al. New-onset diabetes in covid-19. N Engl J Med 2020; 383: 789–90. RubinoF AmielSA ZimmetP AlbertiG BornsteinS EckelRH New-onset diabetes in covid-19 N Engl J Med 2020 383 789 90 10.1056/NEJMc2018688730441532530585 Search in Google Scholar

Yang L, Han Y, Nilsson-Payant BE, Gupta V, Wang P, Duan X et al. A human pluripotent stem cell-based platform to study SARS-CoV-2 tropism and model virus infection in human cells and organoids. Cell Stem Cell 2020; 27: 125–36.e7. YangL HanY Nilsson-PayantBE GuptaV WangP DuanX A human pluripotent stem cell-based platform to study SARS-CoV-2 tropism and model virus infection in human cells and organoids Cell Stem Cell 2020 27 125 36.e7 10.1016/j.stem.2020.06.015730362032579880 Search in Google Scholar

Batlle D, Soler MJ, Sparks MA, Hiremath S, South AM, Welling PA, et al. Acute kidney injury in COVID-19: Emerging evidence of a distinct pathophysiology. J Am Soc Nephrol 2020; 31: 1380–3. BatlleD SolerMJ SparksMA HiremathS SouthAM WellingPA Acute kidney injury in COVID-19: Emerging evidence of a distinct pathophysiology J Am Soc Nephrol 2020 31 1380 3 10.1681/ASN.2020040419 Search in Google Scholar

Cheruiyot I, Henry B, Lippi G, Kipkorir V, Ngure B, Munguti J, et al. Acute kidney injury is associated with worse prognosis in COVID-19 patients: A systematic review and meta-analysis. Acta Biomed 2020; 91: e2020029. CheruiyotI HenryB LippiG KipkorirV NgureB MungutiJ Acute kidney injury is associated with worse prognosis in COVID-19 patients: A systematic review and meta-analysis Acta Biomed 2020 91 e2020029 Search in Google Scholar

Hirsch JS, Ng JH, Ross DW, Sharma P, Shah HH, Barnett RL, et al. Acute kidney injury in patients hospitalized with COVID-19. Kidney Int 2020; 98: 209–18. HirschJS NgJH RossDW SharmaP ShahHH BarnettRL Acute kidney injury in patients hospitalized with COVID-19 Kidney Int 2020 98 209 18 10.1016/j.kint.2020.05.006 Search in Google Scholar

Izzedine H, Jhaveri KD. Acute kidney injury in patients with COVID-19: An update on the pathophysiology. Nephrol Dial Transplant 2020; 36: 224–6. IzzedineH JhaveriKD Acute kidney injury in patients with COVID-19: An update on the pathophysiology Nephrol Dial Transplant 2020 36 224 6 10.1093/ndt/gfaa184 Search in Google Scholar

Kolhe NV, Fluck RJ, Selby NM, Taal MW. Acute kidney injury associated with COVID-19: A retrospective cohort study. PLoS Med 2020; 17: e1003406. KolheNV FluckRJ SelbyNM TaalMW Acute kidney injury associated with COVID-19: A retrospective cohort study PLoS Med 2020 17 e1003406 10.1371/journal.pmed.1003406 Search in Google Scholar

Nadim MK, Forni LG, Mehta RL, Connor MJ, Jr., Liu KD, Ostermann M, et al. COVID-19-associated acute kidney injury: Consensus report of the 25th Acute Disease Quality Initiative (ADQI) Workgroup. Nat Rev Nephrol 2020; 16: 747–64. NadimMK ForniLG MehtaRL ConnorMJJr. LiuKD OstermannM COVID-19-associated acute kidney injury: Consensus report of the 25th Acute Disease Quality Initiative (ADQI) Workgroup Nat Rev Nephrol 2020 16 747 64 10.1038/s41581-020-00356-5 Search in Google Scholar

Rudnick MR, Hilburg R. Acute kidney injury in COVID-19: Another challenge for nephrology. Am J Nephrol 2020; 51:761–3. RudnickMR HilburgR Acute kidney injury in COVID-19: Another challenge for nephrology Am J Nephrol 2020 51 761 3 10.1159/000511161 Search in Google Scholar

Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 2020; 395: 497–06. HuangC WangY LiX RenL ZhaoJ HuY Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China Lancet 2020 395 497 06 10.1016/S0140-6736(20)30183-5 Search in Google Scholar

Chen G, Wu DI, Guo W, Cao Y, Huang D, Wang H, et al. Clinical and immunological features of severe and moderate coronavirus disease 2019. J Clin Invest 2020; 130: 2620–9. ChenG WuDI GuoW CaoY HuangD WangH Clinical and immunological features of severe and moderate coronavirus disease 2019 J Clin Invest 2020 130 2620 9 10.1172/JCI137244719099032217835 Search in Google Scholar

Tian W, Zhang N, Jin R, Feng Y, Wang S, Gao S, et al. Immune suppression in the early stage of COVID-19 disease. Nat Commun 2020; 11: 5859. TianW ZhangN JinR FengY WangS GaoS Immune suppression in the early stage of COVID-19 disease Nat Commun 2020 11 5859 10.1038/s41467-020-19706-9767311233203833 Search in Google Scholar

Fine LG, Norman JT. Chronic hypoxia as a mechanism of progression of chronic kidney diseases: From hypothesis to novel therapeutics. Kidney Int 2008; 74: 867–72. FineLG NormanJT Chronic hypoxia as a mechanism of progression of chronic kidney diseases: From hypothesis to novel therapeutics Kidney Int 2008 74 867 72 10.1038/ki.2008.35018633339 Search in Google Scholar

Fine LG, Orphanides C, Norman JT. Progressive renal disease: The chronic hypoxia hypothesis. Kidney Int Suppl 1998; 65: S74–8. FineLG OrphanidesC NormanJT Progressive renal disease: The chronic hypoxia hypothesis Kidney Int Suppl 1998 65 S74 8 Search in Google Scholar

Mondal S, Quintili AL, Karamchandani K, Bose S. Thromboembolic disease in COVID-19 patients: A brief narrative review. J Intensive Care 2020; 8: 70. MondalS QuintiliAL KaramchandaniK BoseS Thromboembolic disease in COVID-19 patients: A brief narrative review J Intensive Care 2020 8 70 10.1186/s40560-020-00483-y748744732939266 Search in Google Scholar

Mezzano S, Droguett A, Burgos ME, Ardiles LG, Flores CA, Aros CA, et al. Renin-angiotensin system activation and interstitial inflammation in human diabetic nephropathy. Kidney Int Suppl 2003; 64: S64–70. MezzanoS DroguettA BurgosME ArdilesLG FloresCA ArosCA Renin-angiotensin system activation and interstitial inflammation in human diabetic nephropathy Kidney Int Suppl 2003 64 S64 70 10.1046/j.1523-1755.64.s86.12.x12969130 Search in Google Scholar

Gheblawi M, Wang K, Viveiros A, Nguyen Q, Zhong JC, Turner AJ, et al. Angiotensin-converting enzyme 2: SARS-CoV-2 receptor and regulator of the renin-angiotensin system: Celebrating the 20th Anniversary of the Discovery of ACE2. Circ Res 2020; 126: 1456–74. GheblawiM WangK ViveirosA NguyenQ ZhongJC TurnerAJ Angiotensin-converting enzyme 2: SARS-CoV-2 receptor and regulator of the renin-angiotensin system: Celebrating the 20th Anniversary of the Discovery of ACE2 Circ Res 2020 126 1456 74 10.1161/CIRCRESAHA.120.317015718804932264791 Search in Google Scholar

Kuba K, Imai Y, Rao S, Gao H, Guo F, Guan B, et al. A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury. Nat Med 2005; 11: 875–9. KubaK ImaiY RaoS GaoH GuoF GuanB A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury Nat Med 2005 11 875 9 10.1038/nm1267709578316007097 Search in Google Scholar

Glowacka I, Bertram S, Herzog P, Pfefferle S, Steffen I, Muench MO, et al. Differential downregulation of ACE2 by the spike proteins of severe acute respiratory syndrome coronavirus and human coronavirus NL63. J Virol 2010; 84: 1198–205. GlowackaI BertramS HerzogP PfefferleS SteffenI MuenchMO Differential downregulation of ACE2 by the spike proteins of severe acute respiratory syndrome coronavirus and human coronavirus NL63 J Virol 2010 84 1198 205 10.1128/JVI.01248-09279838019864379 Search in Google Scholar

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