Acute kidney injury in patients with Covid-19 in a Brazilian ICU: incidence, predictors and in-hospital mortality

Costa, Rafael Lessa da; Sória, Taíza Corrêa; Salles, Eliene Ferreira; Gerecht, Ana Venâncio; Corvisier, Maurício Faria; Menezes, Márcia Adélia de Magalhães; Ávila, Carla da Silveira; Silva, Eduardo Costa de Freitas; Pereira, Sara Regina Neto; Simvoulidis, Luiz Fernando Nogueira

doi:10.1590/2175-8239-jbn-2020-0144

Cited by 36 publications

(18 citation statements)

References 26 publications

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“…After reviewing the full texts of 938 articles, 71 COVID-19 studies were included in the meta-analysis ( Figure 1A ). 1 - 3 , 13 , 27 …”

Section: Resultsmentioning

confidence: 99%

“…In critically ill patients, shock occurred in 24% (n = 1813/6621) of COVID-19 patients, whereas vasopressors were used in 26% (n = 9535/17 170) of patients (Table 1). In cohorts of patients infected with ACE2-associated viruses, 1813 (20) 9535 (29) 3441 (18) 4281 (8) 11159 (49) 18669 (35) 6562 (44) 6700 (40) 14227 ( 26) -Totals SARS-CoV-2 (KDIGO) 43257 16850 (39) 1200 (24) 7085 (26) 2801 (22) 3584 (8) 9769 (58) 16618 (38) 6041 (45) 3996 (40) 11064 ( 26…”

Section: Shock and Vasopressors In Covid-19 And Viruses That Are Or Are Not Associated With Ace2mentioning

confidence: 99%

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Acute Kidney Injury and Renal Replacement Therapy in COVID-19 Versus Other Respiratory Viruses: A Systematic Review and Meta-Analysis

Cau

Cheng

Lee

et al. 2021

Can J Kidney Health Dis

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Background: Acute kidney injury (AKI) is a potentially fatal complication of Coronavirus Disease-2019 (COVID-19). Binding of the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the virus responsible for COVID-19, to its viral receptor, angiotensin converting enzyme 2 (ACE2), results in viral entry and may cause AKI. Objectives: We performed a systematic review and meta-analysis of the frequencies of AKI and renal replacement therapy (RRT) in critically ill COVID-19 patients and compared those frequencies with patients who were infected by respiratory viruses that bind or downregulate ACE2 (ACE2-associated viruses) and viruses that do not bind nor downregulate ACE2 (non-ACE2-associated viruses). Design: Systematic review and meta-analysis. Setting: Observational studies on COVID-19 and other respiratory viral infections reporting AKI and RRT were included. The exclusion criteria were non-English articles, non-peer-reviewed articles, review articles, studies that included patients under the age of 18, studies including fewer than 10 patients, and studies not reporting AKI and RRT rates. Patients: Adult COVID-19, Severe Acute Respiratory Syndrome (SARS), Middle East Respiratory Syndrome (MERS), and influenza patients. Measurements: We extracted the following data from the included studies: author, year, study location, age, sex, race, diabetes mellitus, hypertension, chronic kidney disease, shock, vasopressor use, mortality, intensive care unit (ICU) admission, ICU mortality, AKI, and RRT. Methods: We systematically searched PubMed and EMBASE for articles reporting AKI or RRT. AKI was defined by authors of included studies. Critical illness was defined by ICU admission. We performed a random effects meta-analysis to calculate pooled estimates for the AKI and RRT rate within each virus group using a random intercept logistic regression model. Results: Of 23 655 hospitalized, critically ill COVID-19 patients, AKI frequencies were not significantly different between COVID-19 patients (51%, 95% confidence interval [CI]: 44%-57%) and critically ill patients infected with ACE2-associated (56%, 95% CI: 37%-74%, P = .610) or non-ACE2-associated viruses (63%, 95% CI: 43%-79%, P = .255). Pooled RRT rates were also not significantly different between critically ill, hospitalized patients with COVID-19 (20%, 95% CI: 16%-24%) and ACE2-associated viruses (18%, 95% CI: 8%-33%, P = .747). RRT rates for both COVID-19 and ACE2-associated viruses were significantly different ( P < .001 for both) from non-ACE2-associated viruses (49%, 95% CI: 44%-54%). After adjusting for shock or vasopressor use, AKI and RRT rates were not significantly different between groups. Limitations: Limitations of this study include the heterogeneity of definitions of AKI that were used across different virus studies. We could not match severity of infection or do propensity matching across studies. Most of the included studies were conducted in retrospective fashion. Last, we did not include non-English publications. Conclusions: Our findings suggest that viral ACE2 association does not significantly alter the rates of AKI and RRT among critically ill patients admitted to the ICU. However, the rate of RRT is lower in patients with COVID-19 or ACE2-associated viruses when compared with patients infected with non-ACE2-binding viruses, which might partly be due to the lower frequencies of shock and use of vasopressors in these two virus groups. Prospective studies are necessary to demonstrate whether modulation of the ACE2 axis with Renin-Angiotensin System inhibitors impacts the rates of AKI and whether they are beneficial or harmful in COVID-19 patients.

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“…After reviewing the full texts of 938 articles, 71 COVID-19 studies were included in the meta-analysis ( Figure 1A ). 1 - 3 , 13 , 27 …”

Section: Resultsmentioning

confidence: 99%

Section: Shock and Vasopressors In Covid-19 And Viruses That Are Or Are Not Associated With Ace2mentioning

confidence: 99%

Acute Kidney Injury and Renal Replacement Therapy in COVID-19 Versus Other Respiratory Viruses: A Systematic Review and Meta-Analysis

Cau

Cheng

Lee

et al. 2021

Can J Kidney Health Dis

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“…However, the onset of AKI in the US was observed much earlier—either upon admission or within 24 h of admission. Another study from Brazil also showed a high occurrence of AKI in 56% of COVID-19 patients, of which 67% developed stage 3 AKI [ 14 ].…”

Section: Epidemiologymentioning

confidence: 99%

“…Renal replacement therapy (RRT) is needed in up to 64% of critically ill COVID-19 patients who develop AKI ( Table 1 ) [ 6 , 12 , 13 , 14 , 15 ]. It is due to abnormal concentrations of electrolytes and volume overload resistance to pharmacological treatment.…”

Section: Renal Replacement Therapymentioning

confidence: 99%

Acute Kidney Injury in COVID-19

Głowacka

Lipka

Młynarska

et al. 2021

IJMS

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COVID-19 is mainly considered a respiratory illness, but since SARS-CoV-2 uses the angiotensin converting enzyme 2 receptor (ACE2) to enter human cells, the kidney is also a target of the viral infection. Acute kidney injury (AKI) is the most alarming condition in COVID-19 patients. Recent studies have confirmed the direct entry of SARS-CoV-2 into the renal cells, namely podocytes and proximal tubular cells, but this is not the only pathomechanism of kidney damage. Hypovolemia, cytokine storm and collapsing glomerulopathy also play an important role. An increasing number of papers suggest a strong association between AKI development and higher mortality in COVID-19 patients, hence our interest in the matter. Although knowledge about the role of kidneys in SARS-CoV-2 infection is changing dynamically and is yet to be fully investigated, we present an insight into the possible pathomechanisms of AKI in COVID-19, its clinical features, risk factors, impact on hospitalization and possible ways for its management via renal replacement therapy.

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“…Compared to previous pandemics with the same virus family, the current COVID-19 pandemic, just like the severe acute respiratory syndrome coronavirus 1 outbreak in 2005, yielded a higher incidence of AKI, opening thereafter a way for potential future research [ 40 ]. In a recent Brazilian cohort study, 55% of the patients developed AKI, and more than half of that progressed into stage 3 that was correlated with a high mortality rate compared to those without AKI [ 41 ]…”

Section: Renal Cellular Entry Of Sars-cov-2 and Cellular Damagementioning

confidence: 99%

Mechanisms of COVID-19-induced kidney injury and current pharmacotherapies

et al. 2021

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The COVID-19 pandemic created a worldwide debilitating health crisis with the entire humanity suffering from the deleterious effects associated with the high infectivity and mortality rates. While significant evidence is currently available online and targets various aspects of the disease, both inflammatory and noninflammatory kidney manifestations secondary to COVID-19 infection are still largely underrepresented. In this review, we summarized current knowledge about COVID-19-related kidney manifestations, their pathologic mechanisms as well as various pharmacotherapies used to treat patients with COVID-19. We also shed light on the effect of these medications on kidney functions that can further enhance renal damage secondary to the illness.

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Acute kidney injury in patients with Covid-19 in a Brazilian ICU: incidence, predictors and in-hospital mortality

Cited by 36 publications

References 26 publications

Acute Kidney Injury and Renal Replacement Therapy in COVID-19 Versus Other Respiratory Viruses: A Systematic Review and Meta-Analysis

Acute Kidney Injury and Renal Replacement Therapy in COVID-19 Versus Other Respiratory Viruses: A Systematic Review and Meta-Analysis

Acute Kidney Injury in COVID-19

Mechanisms of COVID-19-induced kidney injury and current pharmacotherapies

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