The Predictive Role of the Biomarker Kidney Molecule-1 (KIM-1) in Acute Kidney Injury (AKI) Cisplatin-Induced Nephrotoxicity

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Abstract

Acute kidney injury (AKI) following platinum-based chemotherapeutics is a frequently reported serious side-effect. However, there are no approved biomarkers that can properly identify proximal tubular injury while routine assessments such as serum creatinine lack sensitivity. Kidney-injury-molecule 1 (KIM-1) is showing promise in identifying cisplatin-induced renal injury both in vitro and in vivo studies. In this review, we focus on describing the mechanisms of renal tubular cells cisplatin-induced apoptosis, the associated inflammatory response and oxidative stress and the role of KIM-1 as a possible biomarker used to predict cisplatin associated AKI.

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Mechanisms of Cisplatin Nephrotoxicity

Ronald Miller, Raghu K. Tadagavadi, Ganesan Ramesh … (2010)

Cisplatin is a widely used and highly effective cancer chemotherapeutic agent. One of the limiting side effects of cisplatin use is nephrotoxicity. Research over the past 10 years has uncovered many of the cellular mechanisms which underlie cisplatin-induced renal cell death. It has also become apparent that inflammation provoked by injury to renal epithelial cells serves to amplify kidney injury and dysfunction in vivo. This review summarizes recent advances in our understanding of cisplatin nephrotoxicity and discusses how these advances might lead to more effective prevention.

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Kidney injury molecule-1 (KIM-1), a putative epithelial cell adhesion molecule containing a novel immunoglobulin domain, is up-regulated in renal cells after injury.

T Ichimura, J V Bonventre, V Bailly … (1998)

We report the identification of rat and human cDNAs for a type 1 membrane protein that contains a novel six-cysteine immunoglobulin-like domain and a mucin domain; it is named kidney injury molecule-1 (KIM-1). Structurally, KIM-1 is a member of the immunoglobulin gene superfamily most reminiscent of mucosal addressin cell adhesion molecule 1 (MAdCAM-1). Human KIM-1 exhibits homology to a monkey gene, hepatitis A virus cell receptor 1 (HAVcr-1), which was identified recently as a receptor for the hepatitis A virus. KIM-1 mRNA and protein are expressed at a low level in normal kidney but are increased dramatically in postischemic kidney. In situ hybridization and immunohistochemistry revealed that KIM-1 is expressed in proliferating bromodeoxyuridine-positive and dedifferentiated vimentin-positive epithelial cells in regenerating proximal tubules. Structure and expression data suggest that KIM-1 is an epithelial cell adhesion molecule up-regulated in the cells, which are dedifferentiated and undergoing replication. KIM-1 may play an important role in the restoration of the morphological integrity and function to postischemic kidney.

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The mitochondrial p53 pathway.

Angelina V Vaseva, Ute Moll (2009)

p53 is one of the most mutated tumor suppressors in human cancers and as such has been intensively studied for a long time. p53 is a major orchestrator of the cellular response to a broad array of stress types by regulating apoptosis, cell cycle arrest, senescence, DNA repair and genetic stability. For a long time it was thought that these functions of p53 solely rely on its function as a transcription factor, and numerous p53 target genes have been identified [1]. In the last 8 years however, a novel transcription-independent proapoptotic function mediated by the cytoplasmic pool of p53 has been revealed. p53 participates directly in the intrinsic apoptosis pathway by interacting with the multidomain members of the Bcl-2 family to induce mitochondrial outer membrane permeabilization. Our review will discuss these studies, focusing on recent advances in the field.

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Journal

Journal ID (nlm-ta): Int J Mol Sci

Journal ID (iso-abbrev): Int J Mol Sci

Journal ID (publisher-id): ijms

Title: International Journal of Molecular Sciences

Publisher: MDPI

ISSN (Electronic): 1422-0067

Publication date (Electronic): 22 October 2019

Publication date Collection: October 2019

Volume: 20

Issue: 20

Electronic Location Identifier: 5238

Affiliations

[1 ]Department of Internal Medicine, “Grigore T. Popa” University of Medicine and Pharmacy, 700111 Iasi, Romania; tanasedm@ 123456gmail.com (D.M.T.); ciprianrezus@ 123456yahoo.com (C.R.)

[2 ]Internal Medicine Clinic, “Sf. Spiridon” County Clinical Emergency Hospital Iasi, 700115 Iasi, Romania; sminelaaida@ 123456yahoo.com

[3 ]Department of Cardiology, “Grigore T. Popa” University of Medicine and Pharmacy, 700111 Iasi, Romania; radu.smaranda@ 123456gmail.com

[4 ]Cardiology Clinic, “Prof. Dr. George I.M. Georgescu” Institute of Cardiovascular Diseases, 700503 Iasi, Romania

[5 ]Department of Ophthalmology, “Grigore T. Popa” University of Medicine and Pharmacy, 700115 Iasi, Romania; costea10@ 123456yahoo.com

[6 ]2nd Ophthalmology Clinic, “Prof. Dr. Nicolae Oblu” Emergency Clinical Hospital, 700115 Iași, Romania

[7 ]Department of Pathophysiology, Faculty of Medicine, “Grigore T. Popa” University of Medicine and Pharmacy, 700115 Iasi, Romania; mciocoiu2003@ 123456yahoo.com

[8 ]Department of Obstetrics and Gynecology, “Grigore T. Popa” University of Medicine and Pharmacy, 700111 Iasi, Romania; drcarauleanu@ 123456yahoo.com

[9 ]Unit of Diabetes, Nutrition and Metabolic Diseases, “Grigore T. Popa” University of Medicine and Pharmacy, 700115 Iasi, Romania; cmlacatusu@ 123456yahoo.co.uk

[10 ]Clinical Center of Diabetes, Nutrition and Metabolic Diseases, “Sf. Spiridon” County Clinical Emergency Hospital, 700111 Iasi, Romania

[11 ]Department of Physiology, “Grigore T. Popa” University of Medicine and Pharmacy, 700111 Iasi, Romania

Author notes

[* ]Correspondence: dr.evelinagosav@ 123456yahoo.com (E.M.G.); floria_mariana@ 123456yahoo.com (M.F.)

Author information

Evelina Maria Gosav https://orcid.org/0000-0003-1730-9306

Smaranda Radu https://orcid.org/0000-0001-8873-2887

Cristina Mihaela Lacatusu https://orcid.org/0000-0002-9012-5901

Mariana Floria https://orcid.org/0000-0002-9465-1503

Article

Publisher ID: ijms-20-05238

DOI: 10.3390/ijms20205238

PMC ID: 6834366

PubMed ID: 31652595

SO-VID: ed8c68bb-fbec-4e72-af16-e0b6c11bf240

License:

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

The Predictive Role of the Biomarker Kidney Molecule-1 (KIM-1) in Acute Kidney Injury (AKI) Cisplatin-Induced Nephrotoxicity

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Abstract

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Karger: Nephrology

Most cited references 148

Mechanisms of Cisplatin Nephrotoxicity

Kidney injury molecule-1 (KIM-1), a putative epithelial cell adhesion molecule containing a novel immunoglobulin domain, is up-regulated in renal cells after injury.

The mitochondrial p53 pathway.

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