Journal Browser

► Journal Browser

Pathophysiology of AKI from Sepsis to SARS-COV-2 Infection: Molecular Basis, Diagnosis and Treatment

Share This Special Issue

Special Issue Editors

Special Issue Information

Dear Colleagues,

Sepsis remains a major cause of morbidity and mortality worldwide, with more than 11 million deaths annually. The syndrome represents a life-threatening systemic disease associated with an overwhelmed host response due to invasion of the bloodstream by bacteria, viruses, fungi, or parasites. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causal agent of coronavirus disease 2019 (COVID-19), shares common features with sepsis as multiorgan dysfunction and is currently defined as “viral sepsis”. In recent years, these systemic inflammatory disorders have attracted the interest of several researchers because of their involvement in human health.

In critically ill patients, renal dysfunction is associated with an unacceptably high morbidity/mortality risk, progression toward chronic kidney disease, and increased health resource utilization. Patients with acute kidney injury (AKI) are twice as likely to require invasive mechanical ventilation and renal replacement therapies. Given the paucity of knowledge about optimal prevention and treatment strategies for sepsis and COVID-19-related AKI, specific biological markers for an early and reliable diagnosis of AKI and response to therapies should be defined. This last point is crucial in the management of severe forms of sepsis and COVID-19 and may have an immediate application in our daily approach to these patients. In addition, pre-clinical studies with animal models and in vitro experiments should provide additional insights into the physiopathological aspects of these systemic inflammatory disorders. Exploring new pathogenetic mechanisms, with special regard to the role of soluble and cellular components of innate immunity, would identify novel targets and innovative therapeutic approaches.

In this Special Issue, we will gather original research papers and reviews from different experts in the field that bring to the forefront new advances in pathophysiology and treatment of sepsis and COVID-19-associated AKI.

Prof. Dr. Giuseppe Castellano
Dr. Rossana Franzin
Dr. Alessandra Stasi
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

sepsis
SARS-CoV-2
Acute Kidney Injury (AKI)
experimental and clinical studies
molecular mechanisms
therapeutic targets
emerging biomarkers

Published Papers (2 papers)

Download All Papers

Research

Jump to: Review

11 pages, 1426 KiB

Open AccessArticle

Validation of a Prospective Urinalysis-Based Prediction Model for ICU Resources and Outcome of COVID-19 Disease: A Multicenter Cohort Study

by Oliver Gross, Onnen Moerer, Thomas Rauen, Jan Böckhaus, Elion Hoxha, Achim Jörres, Matthias Kamm, Amin Elfanish, Wolfram Windisch, Michael Dreher, Juergen Floege, Stefan Kluge, Christian Schmidt-Lauber, Jan-Eric Turner, Samuel Huber, Marylyn M. Addo, Simone Scheithauer, Tim Friede, Gerald S. Braun, Tobias B. Huber and Sabine Blaschke Show full author list Hide full author list

J. Clin. Med. 2021, 10(14), 3049; https://0-doi-org.brum.beds.ac.uk/10.3390/jcm10143049 - 09 Jul 2021

Cited by 12 | Viewed by 5468

Abstract

In COVID-19, guidelines recommend a urinalysis on hospital admission as SARS-CoV-2 renal tropism, post-mortem, was associated with disease severity and mortality. Following the hypothesis from our pilot study, we now validate an algorithm harnessing urinalysis to predict the outcome and the need for ICU resources on admission to hospital. Patients were screened for urinalysis, serum albumin (SA) and antithrombin III activity (AT-III) obtained prospectively on admission. The risk for an unfavorable course was categorized as (1) “low”, (2) “intermediate” or (3) “high”, depending on (1) normal urinalysis, (2) abnormal urinalysis with SA ≥ 2 g/dL and AT-III ≥ 70%, or (3) abnormal urinalysis with SA or AT-III abnormality. Time to ICU admission or death served as the primary endpoint. Among 223 screened patients, 145 were eligible for enrollment, 43 falling into the low, 84 intermediate, and 18 into high-risk categories. An abnormal urinalysis significantly elevated the risk for ICU admission or death (63.7% vs. 27.9%; HR 2.6; 95%-CI 1.4 to 4.9; p = 0.0020) and was 100% in the high-risk group. Having an abnormal urinalysis was associated with mortality, a need for mechanical ventilation, extra-corporeal membrane oxygenation or renal replacement therapy. In conclusion, our data confirm that COVID-19-associated urine abnormalities on admission predict disease aggravation and the need for ICU (ClinicalTrials.gov number NCT04347824). Full article

(This article belongs to the Special Issue Pathophysiology of AKI from Sepsis to SARS-COV-2 Infection: Molecular Basis, Diagnosis and Treatment)

► Show Figures

Figure 1

Review

Jump to: Research

17 pages, 396 KiB

Open AccessReview

Acute Kidney Injury and Blood Purification Techniques in Severe COVID-19 Patients

by Marianna Napoli, Michele Provenzano, Lilio Hu, Claudia Bini, Chiara Abenavoli, Gaetano La Manna and Giorgia Comai

J. Clin. Med. 2022, 11(21), 6286; https://0-doi-org.brum.beds.ac.uk/10.3390/jcm11216286 - 25 Oct 2022

Cited by 1 | Viewed by 2018

Abstract

Although most patients with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) experience respiratory manifestations, multi-organ dysfunction is frequent. Almost 20% of hospitalized patients with SARS-CoV-2 infection develop acute kidney injury (AKI). The pathophysiology of AKI is a result of both the direct and indirect effects of SARS-CoV-2 infection, including systemic inflammatory responses, the activation of the renin-angiotensin-aldosterone system (RAAS), and endothelial and coagulative dysfunction. Underlying SARS-CoV-2 infection-associated AKI, an immunological hyper-response with an unbalanced innate and adaptative response defined as a “cytokine storm” has emerged. Numerous agents have been tested in an effort to mitigate the cytokine storm, and a range of extracorporeal cytokine removal techniques have been proposed as potential therapeutic options. In the present review, we summarize the main pathogenetic mechanisms underlying COVID-19-related AKI in order to provide an appropriate individual therapeutic strategy to improve clinical outcomes and limit the progression of early disease. Full article

(This article belongs to the Special Issue Pathophysiology of AKI from Sepsis to SARS-COV-2 Infection: Molecular Basis, Diagnosis and Treatment)

► Show Figures