|Year : 2020 | Volume
| Issue : 4 | Page : 204-210
Acute kidney injury in patients with coronavirus disease 2019 – how much do we know?
Mohamed Abdalbary1, Hussein Sheashaa2
1 Nephrology and Dialysis Unit, Department of Internal Medicine, Faculty of Medicine, Mansoura University, Mansoura, Egypt
2 Department of Nephrology, Urology and Nephrology Center, Faculty of Medicine, Mansoura University, Mansoura, Egypt
|Date of Submission||02-Jun-2020|
|Date of Acceptance||26-Jun-2020|
|Date of Web Publication||16-Oct-2020|
Dr. Mohamed Abdalbary
Department of Internal Medicine (Nephrology), Faculty of Medicine, Mansoura University, Saleh Elesawi Street, Hay Algamaa, West District, Mansoura, Dakahliya 35516
Source of Support: None, Conflict of Interest: None
By the end of 2019, coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a new RNA virus belonging to the β-coronavirus cluster, started spreading in China. A few months later, it was declared a pandemic, and it is spreading all over the world causing millions of patients and hundreds of thousands of deaths. Despite respiratory manifestations being the most common symptoms with coronavirus disease 2019 (COVID-19), kidney affection was noted in many studies. There is noticeable heterogeneity in the available literature about the incidence of acute kidney injury (AKI) in COVID-19-infected patients. However, AKI was associated with higher rates of mortality. SARS-CoV-2 uses angiotensin-converting enzyme 2 receptor to enter target organs. Angiotensin-converting enzyme 2 is highly expressed in kidney tubules, which suggests that tubular injury is the main consequence of SARS-CoV-2. It remains unclear whether AKI in COVID-19-infected patients is a direct viral cytopathic effect or a part of a cytokine storm, hemodynamic instability, or hypercoagulability. It is more likely that the etiology of AKI is multifactorial. The available evidence for treatment of COVID-19 is either from observational studies or small limited controlled trials. Moreover, limited data are suggesting specific strategies for AKI management in COVID-19-infected patients. However, earlier detection and management of renal abnormalities, involving hemodynamic support, avoidance of nephrotoxic medications, and extracorporeal modalities, may help to mitigate the hazardous effect of AKI on COVID-19-infected patients. We tried to highlight the possible mechanism, management options, and magnitude of AKI in patients with COVID-19 infection.
Keywords: acute kidney injury, coronavirus disease 2019, kidney, severe acute respiratory syndrome coronavirus 2
|How to cite this article:|
Abdalbary M, Sheashaa H. Acute kidney injury in patients with coronavirus disease 2019 – how much do we know?. J Egypt Soc Nephrol Transplant 2020;20:204-10
|How to cite this URL:|
Abdalbary M, Sheashaa H. Acute kidney injury in patients with coronavirus disease 2019 – how much do we know?. J Egypt Soc Nephrol Transplant [serial online] 2020 [cited 2021 May 17];20:204-10. Available from: http://www.jesnt.eg.net/text.asp?2020/20/4/204/298252
| Introduction|| |
By the end of 2019, coronavirus disease 2019 (COVID-19), caused by a novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), started spreading in Wuhan, a city in the Hubei Province of China ,. Months later, it was declared a pandemic by WHO, and it is still spreading at extreme rates, causing millions of patients and thousands of death all over the world ,.
SARS-CoV-2 is a single-stranded RNA virus belonging to the β-coronavirus cluster . Fever and respiratory manifestations are the most common symptoms with COVID-19; however, multiple organ dysfunction including kidney affection is noted .
Acute kidney injury (AKI) is strongly related to higher rates of morbidity and mortality in seriously ill patients . Information about AKI during the COVID-19 pandemic is still limited. Some studies reported a common presence of AKI, whereas other studies reported it is just a rare incident among COVID-19-infected patients. SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) receptor to facilitate viral entry to target organs. ACE2 receptor is highly expressed in kidney cells, which may consequently increase the incidence of AKI episodes . Interestingly, AKI was noted as an important complication in hospitalized patients with COVID-19 ,.
Incidence of acute kidney injury in coronavirus disease 2019-infected patients
There is a wide variation in the reported incidence of AKI in COVID-19-infected patients ranging from 0.5 to 7% of cases and 2.9 to 23% of ICU patients ,,. The earlier evidence showed a lower incidence of AKI; however, there is growing evidence that AKI in COVID-19-infected patients is related to mortality. AKI is an important complication, observed in 22% of patients who died owing to COVID-19 in Italy . According to published data, the length of time between the detection of SARS-CoV-2 in blood samples and AKI occurrence was ∼7 days .
AKI was uncommon in a relatively small study involving 160 COVID-19-infected patients in Wuhan. Overall, 10% of patients showed a mild increase in blood urea nitrogen or creatinine. Moreover, SARS-CoV-2 RNA in urine sediments was positive in only 6% of examined samples . In a retrospective study including COVID-19 patients from two cohorts in Sichuan Province, proteinuria and hematuria were noted in 18.4 and 17.4% of patients, respectively, whereas AKI only occurred in one patient. The incidence of proteinuria and hematuria was higher than the general population . Further analysis showed that severe or critical COVID-19 was associated with a higher risk of proteinuria and dipstick hematuria .
Kidney disease was associated with in-hospital mortality of COVID-19-infected patients in a prospective study in Wuhan that included 701 consecutive patients. On admission, proteinuria and hematuria were reported in 44 and 27% of patients, respectively, and hematuria AKI occurred in 5% of patients during the study period. Elevated serum creatinine, high blood urea nitrogen, AKI, proteinuria, and hematuria were independent risk factors for in-hospital death .
In a meta-analysis of 11 cohort studies involving 5336 patients with COVID-19 infection, AKI incidence in hospitalized patients was 4%. However, the in-hospital mortality with AKI was up to 32%, and the mortality rate with AKI was 16 times higher than without AKI .
We should give more attention to AKI in the COVID-19 pandemic, because it may be a strong red flag to death risk. Larger studies are needed to clarify the relationship between COVID-19 and renal damage, and long-term follow-up for COVID-19 patients should be conducted to explore its effect on the renal outcome.
Possible mechanisms of acute kidney injury in coronavirus disease 2019-infected patients
It remains unclear whether AKI in COVID-19-infected patients is a direct viral effect or a part of a systemic response. The etiology of AKI is likely to be multifactorial. The postulated mechanisms include hemodynamic changes, direct viral cytopathic effect, cytokine storm-induced systemic inflammatory response, and hypercoagulability . Mechanisms of AKI in COVID-19-infected patients are illustrated in [Figure 1].
|Figure 1 Mechanisms of AKI in COVID-19-infected patients. It explains the possible mechanisms of AKI in COVID-19-infected patients and the current evidence supporting each one of them. AKI in COVID-19-infected patients is likely to be multifactorial. ACE2, angiotensin-converting enzyme 2; AKI, acute kidney injury; ARDS, acute respiratory distress syndrome; ATN, acute tubular necrosis; COVID-19, coronavirus disease 2019; DIC, disseminated intravascular coagulation; SARS-COV-2, severe acute respiratory syndrome coronavirus 2.|
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Rationale/evidence of direct viral cytopathic effect
SARS-CoV-2 was isolated from blood  and urine samples of COVID-19-infected patients ,. The clearance of viral RNA in patients’ urine was delayed compared with that in oropharyngeal swabs in recovering patients . Of note, the presence of viral RNA in urine has not been linked to AKI and is only sporadically demonstrated .
Similar to SARS-CoV, the spike protein of SARS-CoV-2 binds to ACE2 receptor, which is highly expressed in the kidney ,. The spike protein is activated and cleaved by cellular transmembrane serine proteases. This allows fusion to host cell membrane . ACE2 is mainly expressed in human kidney on the brush border of the proximal tubule and podocytes ,. SARS-CoV-2 nucleocapsid protein was demonstrated in renal tubules in an autopsy study using immunohistochemistry . Farkash et al.  performed an autopsy on a single COVID-19-infected patient who died with oliguric renal failure. They noticed presence of viral particles identical to SARS-CoV-2 in the renal tubular epithelium. It can be confirmatory evidence of direct renal infection in the setting of AKI in COVID-19.
Viral replication in podocytes and the ensuing damage could in theory account for the proteinuria that has been reported in patients with COVID-19 .
Hemodynamic instability and organ cross-talks
Nearly half of critically ill patients would develop AKI at some point during their ICU admission .
Impaired function of one organ can cause dysfunction of other organs via complex mechanisms. This is evident especially in critical illness and has been called ‘organ cross-talk’ ,. AKI in critical COVID-19-infected patients is a typical example of that. AKI in patients with acute respiratory distress syndrome (ARDS) is a kind of lung–kidney interactions. It may be attributed to hemodynamic changes and multiple different causes such as impairment of blood gas exchange, including right heart failure, fluid overload, kidney and systemic congestion, detrimental mechanic ventilation strategies, and secondary infections/sepsis ,.
Acute tubular necrosis (ATN) was noted in an autopsy study of COVID-19-infected patients . ATN can occur owing to many contributing factors including volume depletion, cytokine storm, hypoxia, shock, or rhabdomyolysis ,,.
In addition, there might be direct kidney effects of SARS-CoV-2-related cytokine storm and sepsis that lead to tubular and endothelial injury, which may also be potential pathways of kidney damage .
Hypercoagulability and microthrombi
COVID-19 is associated with macrophage activation and cytokine storm. This can result in activation of coagulation factors and hypercoagulability . Recent clinical and autopsy reports of COVID-19 from China and the United States reported an increase in clotting and disseminated intravascular coagulation with small vessel thrombosis and pulmonary infarction . COVID-19 was also associated with an increased myocardial injury that mimics myocardial infarction, probably from myocarditis and microangiopathy . Detailed studies to examine the potential role of innate immune and coagulation dysfunction as a mechanism of AKI are still needed.
There is a scarcity of data regarding clinical and laboratory characteristics of AKI in patients with COVID-19. Thus, although AKI may be attributable to hypotension and decreased kidney perfusion secondary to hemodynamic or hemostatic factors or associated sepsis, one needs to consider that viral infection of the kidneys with viral replication directly in kidney parenchyma also plays a role.
| Pathology|| |
In SARS-CoV-1-infected patients, ATN was the most common pathological feature of AKI without evidence of glomerular pathology ,. The expression of ACE2 in kidney tubules is higher than glomeruli, which suggests that tubular injury is the main consequence of SARS-CoV-2. Macrophage infiltration and acute tubular damage without any severe glomerular injury were observed by Diao et al. . This indicates that SARS-CoV-2 could directly infect human kidney tubules and induce cytoplasmic renal tubular inclusions, a feature observed in other virus-associated nephropathies.
Diffuse acute tubular injury was evident in an autopsy of 26 COVID-19-infected patients. Prominent erythrocyte clusters obstructing capillaries without platelet or fibrinoid material were reported. There was no evidence of vasculitis, interstitial inflammation, or hemorrhage. Particles resembling coronaviruses were identified in seven of the nine samples tested for intracellular virus. SARS-CoV-2 nucleoprotein antibody was positive by immunostaining in three of them . Moreover, a preprint in medRxiv reported severe ATN with lymphocyte and macrophage infiltration in autopsies of six patients who had AKI. It is not clear from this report if these patients had actually developed cortical necrosis .
On the contrary, collapsing glomerulopathy was noticed by two case reports of patients presented with severe AKI and nephrotic-range proteinuria ,.
The kidney pathology of patients with COVID-19-related AKI needs more research to define the direct viral effect from the effect of other disease-related multiorgan dysfunction, shock, and sepsis.
| Acute kidney injury management in coronavirus disease 2019-infected patients|| |
Data regarding the safety of antiviral agents for the treatment of COVID-19 among patients with kidney disease remain unknown. The Current Canadian Medical Association Panel suggests not using convalescent plasma, ribavirin, umifenovir, favipiravir, lopinavir-ritonavir, hydroxychloroquine, interferon-α, and interferon-β in patients with COVID-19. The panel made a weak recommendation suggesting the use of corticosteroids only in patients with ARDS . All these recommendations are based on weak evidences and may differ a bit from Infectious Diseases Society of America (IDSA) guideline  or Surviving Sepsis Campaign (SSC) guideline .
The available evidence for treatment of COVID-19 is either indirect or from observational studies. Randomized controlled trials in patients with COVID-19 are still limited with small sample sizes. Moreover, there are limited data in the published literature regarding specific strategies for AKI management in COVID-19-infected patients.
Patients with AKI who do not require dialysis should be managed in the standard way like other critically ill patients with limited contact as much as possible and strict adherence to infection control practices. Most patients are expected to have a variable degree of hypoxia with different needs of oxygen requirement and/or airway control. Fluid resuscitation should be individualized and based on the assessment of dynamic measures with cautious monitoring of the volume status. A fluid conservative strategy was the preferred way to manage patients with ARDS . Surviving Sepsis Campaign: guidelines on the management of critically ill adults with COVID-19 recommended conservative fluid strategy with crystalloids rather than colloids, nor-epinephrine for shock management followed by vasopressin or epinephrine and avoidance of dopamine, and steroids to be used for refractory septic shock .
COVID-19-infected patients with severe AKI requiring renal replacement therapy (RRT) have a very poor prognosis . Indications of RRT in COVID-19 patients are likely to be the same as non-COVID-19-infected patients. If possible, patients with suspected or confirmed COVID-19 requiring RRT should be dialyzed in their isolation room rather than being transported to the dialysis unit. This should be done with the minimum numbers of medical stuff. Remote monitoring with audio and video streams can be used to minimize the need for the dialysis nurse or the nephrologist to enter the isolation room.
Continuous renal replacement therapy (CRRT) was the most used method in most studies. It remains the preferred modality among critically ill patients with AKI ,. However, some patients can tolerate intermittent hemodialysis, or prolonged intermittent RRT (sustained low-efficiency dialysis).
With lack of evidence showing the superiority of any mode of RRT in terms of patient survival, choice of dialysis modality should be based on machine availability and stuff experience . RRT may be required sooner in oliguric patients with difficulty to achieve conservative fluid balance ,.
In the absence of contraindications, patients with COVID-19 should receive anticoagulation during RRT. This is based upon the growing incidence of thrombotic complications in critically ill COVID-19-infected patients .
Pathophysiological rationale of COVID-19 might support the use of high cutoff or medium cutoff membranes to increase cytokine removal . However, there are no established treatment options yet.
Peritoneal dialysis (PD) could be considered when available hemodialysis or CRRT machines are scarce . Patients with AKI who are treated with PD have similar rates of all-cause mortality, kidney function recovery, and infectious complications compared with patients treated with other modalities . PD requires relatively less equipment, infrastructure, and resources relative to other forms of RRT. However, it can increase intra-abdominal pressure, interfere with respiratory mechanics, and may theoretically worsen respiratory failure, particularly among mechanically ventilated patients . Data suggesting that PD or CRRT effluent is infectious are lacking.
Therapeutic plasma exchange (TPE) was used earlier in the course of septic shock with multiple organ failure and ARDS . Blood purification therapy had proven its capability in removing pathogenic antibodies or cytokines in multiple scenarios . There are some case reports of patients with COVID-19 treated successfully with TPE. Most of them were in severe condition, and some were given intravenous immunoglobulin after TPE ,,. Adeli et al.  reported a case series of eight patients with severe COVID-19. All of them presented with shock stage and ARDS, which was nonresponsive to antiviral and corticosteroid therapy. They were treated with TPE. The first patient died, but the other seven patients had a dramatic improvement after starting of TPE earlier in the course of the disease. The evidence of using TPE still needs to be appropriately studied through well-designed clinical trials, but theoretically, it can offer benefits to patients with severe COVID-19 by eliminating inflammatory cytokines, stabilizing endothelial membranes, and resetting the hypercoagulable state ,.
Extracorporeal hemoperfusion devices for cytokine removal, such as Cytosorb, had no clear role in the management of sepsis before the COVID-19 pandemic. However, it might prevent cytokine-induced kidney damage in cases with evident immune dysregulation, or when inflammatory parameters or cytokines are elevated. Although encouraging results have been reported, the evidence is limited at present, so they should be applied only in the context of a clinical trial to determine their safety and efficacy .
Extracorporeal treatments do not compromise the experimental antibody-based therapies used in COVID-19, such as tocilizumab, intravenous immunoglobulin, and convalescent plasma administration. Neither hemodialysis filters nor hemadsorption cartridges remove antibodies, as their size far exceeds the upper size of molecules that can be removed with RRT or hemadsorption .
Management of AKI and the use of extracorporeal modalities in COVID-19 patients is summarized in [Table 1].
|Table 1 Management of acute kidney injury and the use of extracorporeal modalities in coronavirus disease 2019-infected patients|
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| Prognosis|| |
AKI especially in advanced stages has a strong effect on patient outcomes in published literature. In the Italian report of more than 20 000 deaths related to COVID-19, 22% of patients who died had different degrees of AKI. It was the second observed complication in deceased patients after ARDS . In a study by Cheng et al. , AKI was independently associated with increased mortality. In addition, elevated blood urea nitrogen, creatinine, proteinuria, and hematuria at admission were also found to be independent predictors of mortality. Li et al.  in a preprint also found that AKI was associated with 5.3 times increased risk of mortality in an unadjusted analysis.
| Conclusion|| |
The research on COVID-19, especially its renal implications, is still evolving. In the rush to report medical complications of COVID-19 and because of the magnitude and accelerated pace of the COVID-19 pandemic, we are missing valuable clinical information. We encourage further studies analyzing the clinical course of patients with COVID-19 including kidney injury markers, urine microscopy, quantified urine protein, urine output, and urine electrolytes. Rigorous randomized controlled trials are immediately required to determine the advantages and dangers of possible interventions.
There is cumulative evidence that AKI is associated with decreased survival in COVID-19-infected patients. We need to increase the awareness of AKI and pay more attention to the early monitoring of renal function in hospitalized COVID-19-infected patients.
Early detection and treatment of renal abnormalities, including adequate hemodynamic support, avoidance of nephrotoxic drugs, and different extracorporeal modalities, may help to improve the prognosis of COVID-19-infected patients.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Zhou P, Yang X-L, Wang XG, Hu B, Zhang L, Zhang W et al.
A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature 2020; 579:270–273.
Xu Z, Shi L, Wang Y, Zhang J, Huang L, Zhang C et al.
Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med 2020; 8:420–422.
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; 382:727–733.
World Health Organization. Coronavirus disease (COVID-2019) situation reports. Situation report-64; (29 March 2020). 2020.
Cui J, Li F, Shi Z-L. Origin and evolution of pathogenic coronaviruses. Nat Rev Microbiol 2019; 17: 181–192.
Chen N, Zhou M, Dong X, Qu J, Gong F, Han Y et al.
Epidemiological and clinical characteristics of 99 cases of2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet 2020; 395:507–513.
Vanmassenhove J, Kielstein J, Jörres A, Van Biesen W. Management of patients at risk of acute kidney injury. Lancet 2017; 389:2139–2151.
Letko M, Marzi A, Munster V. Functional assessment of cell entry and receptor usage for SARS-CoV-2 and other lineage B betacoronaviruses. Nat Microbiol 2020; 5: 562–569.
Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z et al.
Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet 2020; 395:1054–1062.
Yang X, Yu Y, Xu J, Shu H, Xia J, Liu H et al.
Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study. Lancet Respir Med 2020; 8:475–481.
Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y et al.
Clinical features of patients infected with2019 novel coronavirus in Wuhan, China. Lancet 2020; 395:497–506.
Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J et al.
Clinical characteristics of 138 hospitalized patients with2019 novel coronavirus–infected pneumonia in Wuhan, China. JAMA 2020; 323:1061–1069.
Guan W-J, Ni Z-Y, Hu Y, Liang W-H, Ou C-Q, He J-X et al.
Clinical characteristics of coronavirus disease2019 in China. N Engl J Med 2020; 382:1708–1720.
Group S-C-S. Characteristics of SARS-CoV-2 patients dying in Italy. Report based on available data on May 14th , 2020. 2020.
Wang L, Li X, Chen H, Yan S, Li D, Li Y et al.
Coronavirus disease 19 infection does not result in acute kidney injury: an analysis of 116 hospitalized patients from Wuhan, China. Am J Nephrol 2020; 51:343–348.
Zhang L, Wang F, Wang L, Wang W, Liu B, Liu J et al.
Prevalence of chronic kidney disease in China: a cross-sectional survey. Lancet 2012; 379:815–822.
Hong D, Long L, Wang AY, Lei Y, Tang Y, Zhao JW et al.
Kidney manifestations of mild, moderate and severe coronavirus disease 2019: a retrospective cohort study. Clin Kidney J 2020.
Cheng Y, Luo R, Wang K, Zhang M, Wang Z, Dong L et al.
Kidney disease is associated with in-hospital death of patients with COVID-19. Kidney Int 2020; 97:829–838.
Mou Z, Zhang X. AKI during COVID-19 infection: low incidence, high risk of death. medRxiv 2020 (Preprint).
Naicker S, Yang C-W, Hwang S-J, Liu B-C, Chen J-H, Jha V. The novel coronavirus2019 epidemic and kidneys. Kidney Int 2020; 97:824–828.
Ling Y, Xu S, Lin Y, Tian D, Zhu Z, Dai F et al.
Persistence and clearance of viral RNA in2019 novel coronavirus disease survivors. Chin Med J (Engl) 2020; 133:1039–1043.
Serfozo P, Wysocki J, Gulua G, Schulze A, Ye M, Liu P et al.
Ang II (angiotensin II) conversion to angiotensin-(1-7) in the circulation is POP (prolyloligopeptidase)-dependent and ACE2 (angiotensin-converting enzyme 2)-independent. Hypertension 2020; 75:173–182.
Ye M, Wysocki J, William J, Soler MJ, Cokic I, Batlle D. Glomerular localization and expression of angiotensin-converting enzyme 2 and angiotensin-converting enzyme: implications for albuminuria in diabetes. J Am Soc Nephrol 2006; 17:3067–3075.
Zhang H, Penninger JM, Li Y, Zhong N, Slutsky AS. Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target. Intensive Care Med 2020; 46:586–590.
Pan X-W, Da Xu HZ, Zhou W, Wang L-H, Cui X-G. Identification of a potential mechanism of acute kidney injury during the COVID-19 outbreak: a study based on single-cell transcriptome analysis. Intensive Care Med 2020; 46:1114–1116.
Diao B, Feng Z, Wang C, Wang H, Liu L, Wang C et al.
Human kidney is a target for novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. MedRxiv 2020 (Preprint).
Farkash EA, Wilson AM, Jentzen JM. Ultrastructural evidence for direct renal infection with SARS-CoV-2. J Am Soc Nephrol 2020.
Hoste EA, Bagshaw SM, Bellomo R, Cely CM, Colman R, Cruz DN et al.
Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Med 2015; 41:1411–1423.
Vincent J-L, Sakr Y, Sprung CL, Ranieri VM, Reinhart K, Gerlach H et al.
Sepsis in European intensive care units: results of the SOAP study. Crit Care Med 2006; 34:344–353.
Husain-Syed F, Ricci Z, Brodie D, Vincent J-L, Ranieri VM, Slutsky AS et al.
Extracorporeal organ support (ECOS) in critical illness and acute kidney injury: from native to artificial organ crosstalk. Intensive Care Med 2018; 44:1447–1459.
Joannidis M, Forni LG, Klein SJ, Honore PM, Kashani K, Ostermann M et al.
Lung–kidney interactions in critically ill patients: consensus report of the Acute Disease Quality Initiative (ADQI) 21 Workgroup. Intensive Care Med 2020; 46:654–672.
Valizadeh R, Baradaran A, Mirzazadeh A, Bhaskar L. Coronavirus-nephropathy; renal involvement in COVID-19. J Ren Inj Prev Coronavirus-Nephropathy 2020; 9:3–4.
Ronco C, Reis T. Kidney involvement in COVID-19 and rationale for extracorporeal therapies. Nat Rev Nephrol 2020; 16:308–310.
Delvaeye M, Conway EM. Coagulation and innate immune responses: can we view them separately? Blood 2009; 114:2367–2374.
Tang N, Li D, Wang X, Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost 2020; 18:844–847.
Chu KH, Tsang WK, Tang CS, Lam MF, Lai FM, To KF et al.
Acute renal impairment in coronavirus-associated severe acute respiratory syndrome. Kidney Int 2005; 67:698–705.
Gu J, Gong E, Zhang B, Zheng J, Gao Z, Zhong Y et al.
Multiple organ infection and the pathogenesis of SARS. J Exp Med 2005; 202:415–424.
Su H, Yang M, Wan C, Yi LX, Tang F, Zhu HY et al.
Renal histopathological analysis of 26 postmortem findings of patients with COVID-19 in China. Kidney Int 2020; 98:219–227.
Larsen CP, Bourne TD, Wilson JD, Saqqa O, Sharshir MA. Collapsing glomerulopathy in a patient with coronavirus disease2019 (COVID-19). Kidney Int Rep 2020; 5:935–939.
Kissling S, Rotman S, Gerber C, Halfon M, Lamoth F, Comte D et al.
Collapsing glomerulopathy in a COVID-19 patient. Kidney Int 2020; 98:228–231.
Ye Z, Rochwerg B, Wang Y, Adhikari NK, Murthy S, Lamontagne F et al.
Treatment of patients with nonsevere and severe coronavirus disease 2019: an evidence-based guideline. CMAJ 2020; 192:E536–E545.
Bhimraj A, Morgan RL, Shumaker AH, Lavergne V, Baden L, Cheng VC et al.
Infectious Diseases Society of America guidelines on the treatment and management of patients with COVID-19. Clin Infect Dis 2020.
Alhazzani W, Møller MH, Arabi YM, Loeb M, Gong MN, Fan E et al.
Surviving Sepsis Campaign: guidelines on the management of critically ill adults with Coronavirus Disease 2019 (COVID-19). Intensive Care Med 2020; 46:854–887.
Matthay MA, Aldrich JM, Gotts JE. Treatment for severe acute respiratory distress syndrome from COVID-19. Lancet Respir Med 2020; 8:433–434.
Wang AY, Bellomo R. Renal replacement therapy in the ICU: intermittent hemodialysis, sustained low-efficiency dialysis or continuous renal replacement therapy? Curr Opin Crit Care 2018; 24:437–442.
Klok FA, Kruip M, van der Meer NJM, Arbous MS, Gommers D, Kant KM et al.
Confirmation of the high cumulative incidence of thrombotic complications in critically ill ICU patients with COVID-19: an updated analysis. Thromb Res 2020; 191:148–150.
El Shamy O, Sharma S, Winston J, Uribarri J. Peritoneal dialysis during the coronavirus2019 (COVID-19) pandemic: acute inpatient and maintenance outpatient experiences. Kidney Med 2020.
Chionh CY, Soni SS, Finkelstein FO, Ronco C, Cruz DN. Use of peritoneal dialysis in AKI: a systematic review. Clin J Am Soc Nephrol 2013; 8:1649–1660.
Almeida CP, Ponce D, de Marchi AC, Balbi AL. Effect of peritoneal dialysis on respiratory mechanics in acute kidney injury patients. Perit Dial Int 2014; 34:544–549.
Keith P, Day M, Perkins L, Moyer L, Hewitt K, Wells A. A novel treatment approach to the novel coronavirus: an argument for the use of therapeutic plasma exchange for fulminant COVID-19. BioMed Central 2020; 24:128.
Schwindenhammer V, Girardot T, Chaulier K, Grégoire A, Monard C, Huriaux L et al.
oXiris® use in septic shock: experience of two French centres. Blood Purif 2019; 47:29–35.
Lin J-H, Chen YC, Lu CL, Hsu YN, Wang WJ. Application of plasma exchange in association with higher dose CVVH in cytokine storm complicating COVID-19. J Formos Med Assoc 2020; 119:1116–1118.
Ma J, Xia P, Zhou Y, Liu Z, Zhou X, Wang J et al.
Potential effect of blood purification therapy in reducing cytokine storm as a late complication of severe COVID-19. Clin Immunol 2020; 214:108408.
Shi H, Zhou C, He P, Huang S, Duan Y, Wang X et al.
Successful treatment of plasma exchange followed by intravenous immunogloblin in a critically ill patient with2019 novel coronavirus infection. Int J Antimicrob Agents 2020; 13:105974.
Adeli SH, Asghari A, Tabarraii R, Shajari R, Afshari S, Kalhor N et al.
Using therapeutic plasma exchange as a rescue therapy in CoVID-19 patients: a case series. Pol Arch Intern Med 2020; 130:455–458.
Chang JC. Sepsis and septic shock: endothelial molecular pathogenesis associated with vascular microthrombotic disease. Thromb J 2019; 17:10.
Knaup H, Stahl K, Schmidt BM, Idowu TO, Busch M, Wiesner O et al.
Early therapeutic plasma exchange in septic shock: a prospective open-label nonrandomized pilot study focusing on safety, hemodynamics, vascular barrier function, and biologic markers. Crit Care 2018; 22:285.
Honore PM, Hoste E, Molnár Z, Jacobs R, Joannes-Boyau O, Malbrain ML et al.
Cytokine removal in human septic shock: where are we and where are we going? Ann Intensive Care 2019; 9:56.
Li Z, Wu M, Guo J, Yao J, Liao X, Song S et al.
Caution on kidney dysfunctions of 2019-nCoV patients. MedRxiv 2020 (Preprint).