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Special Issue "Pathobiology of Acute Kidney Injury"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 1 July 2021.

Special Issue Editors

Dr. Amandeep Bajwa
E-Mail Website1 Website2
Guest Editor
Transplant Research Institute, James D. Eason Transplant Institute, Department of Surgery, School of Medicine, University of Tennessee Health Science Center, Memphis, TN; USA
Dr. Navjot Pabla
Guest Editor
Comprehensive Cancer Center & School of Pharmacy Ohio State University, Columbus, OH 43210, USA

Special Issue Information

Dear Colleagues,

Acute kidney injury (AKI) is a common clinical condition associated with diverse etiologies and abrupt loss of renal function. In patients with sepsis, rhabdomyolysis, cancer, as well as cardiovascular disorders, the underlying disease or associated therapeutic interventions can cause hypoxic, cytotoxic, and inflammatory insults to renal parenchymal cells (endothelial and epithelial) resulting in the onset of AKI. Furthermore, the pathogenesis of kidney injury following AKI involves a complex interaction between altered microcirculatory hemodynamics, renal parenchymal cells, and infiltrating innate and adaptive immune cells. Considerable data support that the immune system mediates AKI, yet many of the underlying mechanisms still remain unclear. Furthermore, lack of clinical data supporting the involvement of the immune system in AKI pathogenesis have hindered the development of clinically tenable anti-inflammatory options. Therefore, as of now, dialysis remains the only treatment option available to AKI patients, underscoring the need to develop novel approaches to tackle this hurdle to ultimately improve patient quality of life. Thus, in order to better understand these comlexities of AKI, it is necessary to clarify these interplays. In this Special Issue on “Pathobiology of Acute Kidney Injury”, we will discuss various mediators of inflammation to further understand their interactions that result in AKI. 

Dr. Amandeep Bajwa
Dr. Navjot Pabla
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 papers will be 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.


  • acute kidney injury
  • inflammation
  • tubular epithelial cells
  • immune cells
  • macrophages
  • neutrophils
  • innate immunity
  • adaptive immunity
  • mitochondria
  • apoptosis
  • necrosis

Published Papers (1 paper)

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Open AccessReview
Acute Tubulointerstitial Nephritis in Clinical Oncology: A Comprehensive Review
Int. J. Mol. Sci. 2021, 22(5), 2326; https://doi.org/10.3390/ijms22052326 - 26 Feb 2021
Viewed by 378
Acute kidney injury in patients who suffer a malignancy is a common complication. Due to its high prevalence and effective treatment, one of the most frequent causes that both oncologists and nephrologists must be aware of is acute tubulointerstitial nephritis (ATIN). ATIN is [...] Read more.
Acute kidney injury in patients who suffer a malignancy is a common complication. Due to its high prevalence and effective treatment, one of the most frequent causes that both oncologists and nephrologists must be aware of is acute tubulointerstitial nephritis (ATIN). ATIN is an immunomediated condition and the hallmark of the disease, with the presence of a tubulointerstitial inflammatory infiltrate in the renal parenchyma. This infiltrate is composed mainly of T lymphocytes that can be accompanied by macrophages, neutrophils, or eosinophils among other cells. One of the major causes is drug-related ATIN, and some antineoplastic treatments have been related to this condition. Worthy of note are the novel immunotherapy treatments aimed at enhancing natural immunity in order to defeat cancer cells. In the context of the immunosuppression status affecting ATIN patients, some pathogen antigens can trigger the development of the disease. Finally, hematological malignancies can also manifest in the kidney leading to ATIN, even at the debut of the disease. In this review, we aim to comprehensively examine differential diagnosis of ATIN in the setting of a neoplastic patient. Full article
(This article belongs to the Special Issue Pathobiology of Acute Kidney Injury)
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