IMPACT OF THE PATHOPHYSIOLOGY OF ACUTE KIDNEY INJURY IN PATIENTS AFFECTED BY COVID-19 ON CLINICAL OUTCOMES DIALYSIS AND DEATH - RETROSPECTIVE COHORT STUDY

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IMPACT OF THE PATHOPHYSIOLOGY OF ACUTE KIDNEY INJURY IN PATIENTS AFFECTED BY COVID-19 ON CLINICAL OUTCOMES DIALYSIS AND DEATH - RETROSPECTIVE COHORT STUDY
Daniela
Ponce
Pedro Andriolo Cardoso pedro.andriolo.cardoso@gmail.com State University of São Paulo Nephrology Botucatu
Bruna Kaori Yuasa bk.yuasa@unesp.br State University of São Paulo Nephrology Botucatu
Luis Eduardo Magalhães luis.magalhaes@unesp.br State University of São Paulo Nephrology Botucatu
Paula Gabriela Sousa de Oliveira paula.gs.oliveira@unesp.br State University of São Paulo Nephrology Botucatu
Ana Júlia Favarin ana.favarin@unesp.br State University of São Paulo Nephrology Botucatu
Welder Zamoner welder.zamoner@unesp.br State University of São Paulo Nephrology Botucatu
 
 
 
 
 
 
 
 
 

It is acknowledged that Acute Kidney Injury (AKI) is multifactorial in COVID-19, as the most relevant factors for its development are the cytokine storm, metabolic stress, medication use, rhabdomyolysis, renal viral tropism, and multiple organ dysfunction. However, little is known about the impact of AKI’s pathophysiology on its clinical outcome. Our aim is to identify the pathophysiological mechanisms of AKI in patients affected by COVID-19 and to associate them with death.

Retrospective cohort study that evaluated the medical records of patients diagnosed with SARS-COV-2 infection admitted to a Tertiary Reference Public Hospital for COVID-19, from 06/01/2020 to 07/31/2021 from their admission until the outcome (hospital discharge or death). Clinical and laboratory data were evaluated during hospitalization. The evaluation of renal function occurred through the variation of urinary output and serum creatinine measurement, and the diagnosis and classification of AKI followed the 2012 KDIGO criteria. The occurrence of AKI was  an inclusion criterion in the study. The nephrotoxic drug usage and the leak of clinical and laboratory data were exclusion criteria in the study. In addition to urine output and serum creatinine concentration, the creatine phosphokinase, type 1 urine test results especially concerning the presence of leukocyturia, proteinuria and hematuria, cardiocirculatory and ventilatory parameters, and vasoactive, diuretic, antihypertensive and corticoid drugs usage will be analyzed. Univariate analysis was performed to identify whether the pathophysiological mechanisms of AKI (ischemic, cytokine storm, endogenous nephrotoxic-rhabdomyolysis, renal viral tropism, or multiple organ dysfunction) are associated with death.

We have included 372 patients. There was a predominance of males (55.5%), Caucasian ethnicity (80.6%); median age was 64 years. Most patients were admitted to the ICU (85.1%). The predominant AKI was KDIGO 3 (56.9%). Regarding the different etiologies of AKI, Mixed (two or more viral injuries) was the most frequent (23.4%), followed by Renal Viral Tropism- RVT(19.9%), Multiple Organ Failure-MOF (18%), Septic (15.6%), Ischemic (12.9%) and Cytokine Storm-CS (10.2%). The Mixed AKI etiology markedly is the most lethal (90.5%) and mostly demands  dialysis (85.1%), followed by CS, MOF and RVT. Tests show an impressive mortality of 73.1%, which is associated with the AKI pathophysiological mechanisms (p<0.01). Logistic regression shows that APACHE II (OR=1.2, CI=[1.1-1,3], p=0,21.), ATN-ISS (OR=18.0, CI=[1.1-295.7], p=0.04.) and Sars-Cov2 Induced AKI (Mixed, CS, MOF and TVR) are associated with death (OR=4.8 , CI=[1.7-13.4], p=0.003). 

The mortality of AKI and COVID-19 patients and their need for dialysis depends on the pathophysiological mechanism their AKI, as Sars-Cov2 Induced AKI mechanisms are the most lethal

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