ABSTRACT
Background: Numerous studies have suggested a possible role for acute kidney injury (AKI) biomarkers in predicting renal recovery after kidney replacement therapy (KRT) with poor performance. In this study, we investigated urinary SerpinA3 (USerA3) as a biomarker to predict renal recovery (RR) after AKI in critically ill COVID-19 patients with invasive mechanical ventilation (IMV). Method(s): Prospective cohort study of patients with critical COVID-19 in ICU with IMV and who required KRT, admitted to our Institute in Mexico City (Mar 2020 -Feb 2022). Patients with CKD stages 4 or 5 and kidney transplant were excluded. SerpinA3, KIM-1, NGAL and HSP-72 were measured in urine on day 0 (start of KRT) and days 1, 3, 7 and 14. We performed log10 transformation only for urinary USerA3 and, subsequently performed repeated sample ANOVA for each one of the biomarkers. Result(s): Sixty patients were included, 52% died before discharge, 38% had complete RR after 90 days and 10% partial RR. Characteristics at baseline for KRT are shown in Table 1. No differences or trends were found in KIM-1 (p=0.380), NGAL (p=0.956), or HSP-72 (p=0.899). In Figure 1 appears USerA3 behavior along the study, showing a clear tendency to be different among the groups. We can observe that the patients who died presented lower amount of USerA3 compared to those who survived. On the other hand, patients with partial RR exhibited USerA3 excretion with a tendency to be lower than those with complete RR, especially in measurements 4 and 5 (day 7 and day 14, respectively). Conclusion(s): In this study, we observed that USerA3 seems to be a predictor of RR and survival, which probably reflects a greater renal functional reserve.
ABSTRACT
Martinez-Rojas MA, Vega-Vega O, Bobadilla NA. Is the kidney a target of SARS-CoV-2? Am J Physiol Renal Physiol 318: F1454-F1462, 2020. First published May 15, 2020;doi:10.1152/ajprenal.00160.2020.-The new disease produced by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) represents a major pandemic event nowadays. Since its origin in China in December 2019, there is compelling evidence that novel SARS-CoV-2 is a highly transmissible virus, and it is associated to a broad clinical spectrum going from subclinical presentation to severe respiratory distress and multiorgan failure. Like other coronaviruses, SARS-CoV-2 recognizes human angiotensin-converting enzyme 2 as a cellular receptor that allows it to infect different host cells and likely disrupts renin-angiotensin-aldosterone system homeostasis. Particularly, a considerable incidence of many renal abnormalities associated to COVID-19 has been reported, including proteinuria, hematuria, and acute kidney injury. Moreover, it has been recently demonstrated that SARS-CoV-2 can infect podocytes and tubular epithelial cells, which could contribute to the development of the aforementioned renal abnormalities. In this review, we discuss the biological aspects of SARSCoV-2 infection, how understanding current knowledge about SARS-CoV-2 infection may partly explain the involvement of the kidneys in the pathophysiology of COVID-19, and what questions have arisen and remain to be explored.