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      Nephrotoxicity of recent anti-cancer agents

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          Abstract

          Cancer patients may develop a variety of kidney lesions that impair not only their immediate survival but also limit the adequate treatment of the underlying malignant process. This review summarizes the nephrotoxic potential of some of the most recently developed anti-cancer drugs, focusing on those interfering with the vascular endothelial growth factor and epidermal growth factor receptor pathways and mammalian target of rapamycin inhibitors. Thrombotic microangiopathy (haemolytic-uraemic syndrome), proteinuria, hypertension and magnesium depletion are the most common side effects. Also the risk for developing acute kidney injury in patients with advanced prostate cancer undergoing androgen deprivation therapy is discussed.

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          A randomized trial of bevacizumab, an anti-vascular endothelial growth factor antibody, for metastatic renal cancer.

          James Yang, Leah A. Haworth, Richard Sherry … (2003)
          Mutations in the tumor-suppressor gene VHL cause oversecretion of vascular endothelial growth factor by clear-cell renal carcinomas. We conducted a clinical trial to evaluate bevacizumab, a neutralizing antibody against vascular endothelial growth factor, in patients with metastatic renal-cell carcinoma. A randomized, double-blind, phase 2 trial was conducted comparing placebo with bevacizumab at doses of 3 and 10 mg per kilogram of body weight, given every two weeks; the time to progression of disease and the response rate were primary end points. Crossover from placebo to antibody treatment was allowed, and survival was a secondary end point. Minimal toxic effects were seen, with hypertension and asymptomatic proteinuria predominating. The trial was stopped after the interim analysis met the criteria for early stopping. With 116 patients randomly assigned to treatment groups (40 to placebo, 37 to low-dose antibody, and 39 to high-dose antibody), there was a significant prolongation of the time to progression of disease in the high-dose--antibody group as compared with the placebo group (hazard ratio, 2.55; P 0.20 for all comparisons). Bevacizumab can significantly prolong the time to progression of disease in patients with metastatic renal-cell cancer. Copyright 2003 Massachusetts Medical Society
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            Mutations of the VHL tumour suppressor gene in renal carcinoma.

            J R Gnarra, K Tory, Y. Weng … (1994)
            Multiple, bilateral renal carcinomas are a frequent occurrence in von Hippel-Lindau (VHL) disease. To elucidate the aetiological role of the VHL gene in human kidney tumorigenesis, localized and advanced tumours from 110 patients with sporadic renal carcinoma were analysed for VHL mutations and loss of heterozygosity (LOH). VHL mutations were identified in 57% of clear cell renal carcinomas analysed and LOH was observed in 98% of those samples. Moreover, VHL was mutated and lost in a renal tumour from a patient with familial renal carcinoma carrying the constitutional translocation, t(3;8)(p14;q24). The identification of VHL mutations in a majority of localized and advanced sporadic renal carcinomas and in a second form of hereditary renal carcinoma indicates that the VHL gene plays a critical part in the origin of this malignancy.
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              ErbB receptors and signaling pathways in cancer.

              Nancy E. Hynes, Gwen MacDonald (2009)
              The ErbB receptor tyrosine kinases play important roles in normal physiology and in cancer. Epidermal growth factor receptor (EGFR) and ErbB2 in particular are mutated in many epithelial tumors, and clinical studies suggest that they play roles in cancer development and progression. These receptors have been intensely studied, not only to understand the mechanisms underlying their oncogenic potential, but also to exploit them as therapeutic targets. ErbB receptors activate a multiplicity of intracellular pathways via their ability to interact with numerous signal transducers. Furthermore, there are now many ErbB-targeted inhibitors used in the clinic. In this review we will concentrate on breast tumors with ERBB2 gene amplification/receptor overexpression and non-small cell lung cancer (NSCLC) with activating EGFR mutations. We will discuss data showing the important role that the PI3K/Akt pathway plays, not only in cancer development, but also in response to targeted therapies. Finally, mechanisms contributing to resistance to ErbB-targeted therapeutics will also be discussed.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Kidney J
                Journal ID (iso-abbrev): Clin Kidney J
                Journal ID (publisher-id): ckj
                Journal ID (hwp): ndtplus
                Title: Clinical Kidney Journal
                Publisher: Oxford University Press
                ISSN (Print): 2048-8505
                ISSN (Electronic): 2048-8513
                Publication date (Print): February 2014
                Publication date (Electronic): 26 November 2013
                Publication date PMC-release: 26 November 2013
                Volume: 7
                Issue: 1
                Pages: 11-22
                Affiliations
                University Hospital , 185, De Pintelaan, Gent 9000, Belgium
                Author notes
                Correspondence and offprint requests to: N. Lameire; E-mail: norbert.lameire@ 123456ugent.be
                Article
                Publisher ID: sft135
                DOI: 10.1093/ckj/sft135
                PMC ID: 4389154
                PubMed ID: 25859345
                SO-VID: 244cf325-13f6-4d1d-8e22-b403a350195e
                Copyright © © The Author 2013. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For permissions, please email: journals.permissions@oup.com.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                Date received : 8 October 2013
                Date accepted : 8 October 2013
                Categories
                Subject: Original Contributions
                Subject: in-Depth Review

                ScienceOpen disciplines: Nephrology
                Keywords: anti-angiogenesis drugs and cancer,anti-cancer drugs and nephrotoxicity,androgen deprivation therapy and aki
                Data availability:
                ScienceOpen disciplines: Nephrology
                Keywords: anti-angiogenesis drugs and cancer, anti-cancer drugs and nephrotoxicity, androgen deprivation therapy and aki

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