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 Table of Contents  
REVIEW ARTICLE
Year : 2020  |  Volume : 20  |  Issue : 4  |  Page : 204-210

Acute kidney injury in patients with coronavirus disease 2019 – how much do we know?


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 Submission02-Jun-2020
Date of Acceptance26-Jun-2020
Date of Web Publication16-Oct-2020

Correspondence Address:
Dr. Mohamed Abdalbary
Department of Internal Medicine (Nephrology), Faculty of Medicine, Mansoura University, Saleh Elesawi Street, Hay Algamaa, West District, Mansoura, Dakahliya 35516
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jesnt.jesnt_21_20

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  Abstract 


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 2020 Oct 23];20:204-10. Available from: http://www.jesnt.eg.net/text.asp?2020/20/4/204/298252




  Introduction Top


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 [1],[2]. 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 [3],[4].

SARS-CoV-2 is a single-stranded RNA virus belonging to the β-coronavirus cluster [5]. Fever and respiratory manifestations are the most common symptoms with COVID-19; however, multiple organ dysfunction including kidney affection is noted [6].

Acute kidney injury (AKI) is strongly related to higher rates of morbidity and mortality in seriously ill patients [7]. 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 [8]. Interestingly, AKI was noted as an important complication in hospitalized patients with COVID-19 [9],[10].

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 [11],[12],[13]. 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 [14]. According to published data, the length of time between the detection of SARS-CoV-2 in blood samples and AKI occurrence was ∼7 days [11].

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 [15]. 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 [16]. Further analysis showed that severe or critical COVID-19 was associated with a higher risk of proteinuria and dipstick hematuria [17].

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 [18].

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 [19].

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 [20]. 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 [3] and urine samples of COVID-19-infected patients [13],[20]. The clearance of viral RNA in patients’ urine was delayed compared with that in oropharyngeal swabs in recovering patients [21]. Of note, the presence of viral RNA in urine has not been linked to AKI and is only sporadically demonstrated [15].

Similar to SARS-CoV, the spike protein of SARS-CoV-2 binds to ACE2 receptor, which is highly expressed in the kidney [22],[23]. The spike protein is activated and cleaved by cellular transmembrane serine proteases. This allows fusion to host cell membrane [24]. ACE2 is mainly expressed in human kidney on the brush border of the proximal tubule and podocytes [23],[25]. SARS-CoV-2 nucleocapsid protein was demonstrated in renal tubules in an autopsy study using immunohistochemistry [26]. Farkash et al. [27] 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 [18].

Hemodynamic instability and organ cross-talks

Nearly half of critically ill patients would develop AKI at some point during their ICU admission [28].

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’ [29],[30]. 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 [30],[31].

Acute tubular necrosis (ATN) was noted in an autopsy study of COVID-19-infected patients [26]. ATN can occur owing to many contributing factors including volume depletion, cytokine storm, hypoxia, shock, or rhabdomyolysis [13],[18],[32].

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 [33].

Hypercoagulability and microthrombi

COVID-19 is associated with macrophage activation and cytokine storm. This can result in activation of coagulation factors and hypercoagulability [34]. 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 [35]. COVID-19 was also associated with an increased myocardial injury that mimics myocardial infarction, probably from myocarditis and microangiopathy [9]. 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 Top


In SARS-CoV-1-infected patients, ATN was the most common pathological feature of AKI without evidence of glomerular pathology [36],[37]. 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. [26]. 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 [38]. 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 [26].

On the contrary, collapsing glomerulopathy was noticed by two case reports of patients presented with severe AKI and nephrotic-range proteinuria [39],[40].

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 Top


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 [41]. All these recommendations are based on weak evidences and may differ a bit from Infectious Diseases Society of America (IDSA) guideline [42] or Surviving Sepsis Campaign (SSC) guideline [43].

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 [44]. 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 [43].

COVID-19-infected patients with severe AKI requiring renal replacement therapy (RRT) have a very poor prognosis [18]. 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 [6],[13]. 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 [45]. RRT may be required sooner in oliguric patients with difficulty to achieve conservative fluid balance [6],[13].

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 [46].

Pathophysiological rationale of COVID-19 might support the use of high cutoff or medium cutoff membranes to increase cytokine removal [33]. However, there are no established treatment options yet.

Peritoneal dialysis (PD) could be considered when available hemodialysis or CRRT machines are scarce [47]. 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 [48]. 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 [49]. 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 [50]. Blood purification therapy had proven its capability in removing pathogenic antibodies or cytokines in multiple scenarios [51]. 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 [52],[53],[54]. Adeli et al. [55] 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 [56],[57].

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 [33].

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 [58].

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 Top


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 [14]. In a study by Cheng et al. [18], 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. [59] in a preprint also found that AKI was associated with 5.3 times increased risk of mortality in an unadjusted analysis.


  Conclusion Top


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

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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