Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Sep 21;2(1):108-123.
doi: 10.1016/j.ekir.2016.09.055. eCollection 2017 Jan.

Adverse Renal Effects of Novel Molecular Oncologic Targeted Therapies: A Narrative Review

Kenar D Jhaveri  1 , Rimda Wanchoo  1 , Vipulbhai Sakhiya  1 , Daniel W Ross  1 , Steven Fishbane  1
Affiliations
Review

Adverse Renal Effects of Novel Molecular Oncologic Targeted Therapies: A Narrative Review

Kenar D Jhaveri et al. Kidney Int Rep. .

Abstract

Novel targeted anti-cancer therapies have resulted in improvement in patient survival compared to standard chemotherapy. Renal toxicities of targeted agents are increasingly being recognized. The incidence, severity, and pattern of renal toxicities may vary according to the respective target of the drug. Here we review the adverse renal effects associated with a selection of currently approved targeted cancer therapies, directed to EGFR, HER2, BRAF, MEK, ALK, PD1/PDL1, CTLA-4, and novel agents targeted to VEGF/R and TKIs. In summary, electrolyte disorders, renal impairment and hypertension are the most commonly reported events. Of the novel targeted agents, ipilumumab and cetuximab have the most nephrotoxic events reported. The early diagnosis and prompt recognition of these renal adverse events are essential for the general nephrologist taking care of these patients.

Keywords: AKI; chemotherapy; hypokalemia; hyponatremia; nephrotoxicity; onconephrology; renal failure; targeted therapy.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Summary of renal adverse events noted with targeted therapies. ALK, anaplastic lymphoma kinase; BCR-ABL, breakpoint cluster region–abelson; CTLA, cytotoxic T lymphocyte antigen−4; EGFR, epidermal growth factor receptor; HER-2, human epidermal growth factor−2; PD, programmed cell death; TKI, tyrosine kinase inhibitors; VEGF, vascular endothelial growth factor.
Figure 2
Figure 2
Simplistic view of various tyrosine kinases available for treatment of cancer. There are 2 types of tyrosine kinases: cellular and receptor tyrosine kinases. Receptor tyrosine kinase inhibitors (TKIs) are designed to target the epidermal growth factor (EGFR), platelet-derived growth factor (PDGFR), and vascular endothelial growth factor receptor (VEGFR) tyrosine kinase families. These could target single receptors such as EGFR (gefitinib) or could be multikinase or multitarget TKIs and target many receptors such as sunitinib, which targets VEGFR,, , PDGFR, kit, Flt3, and RET. The figure represents the predominant receptor involved as the target.
See this image and copyright information in PMC

References

    1. National Cancer Institute. Targeted therapy. Available at: http://www.cancer.gov/about-cancer/treatment/types/targeted-therapies. Accessed January 1, 2016.
    1. Jhaveri K.D., Sakhiya V.B., Wanchoo R. Renal effects of novel anti cancer targeted therapies: a review of the FDA Adverse Event Reporting System. Kidney Int. 2016;90:705–707. - PubMed
    1. Folkman J. Tumor angiogenesis: therapeutic implications. N Engl J Med. 1971;285:1182–1186. - PubMed
    1. Gurevich F., Perazella M.A. Renal effects of anti-angiogenesis therapy: update for the internist. Am J Med. 2009;122:322–328. - PubMed
    1. Eremina V., Jefferson J.A., Kowalewska J. VEGF inhibition and renal thrombotic microangiopathy. N Engl J Med. 2008;358:1129–1136. - PMC - PubMed