Onconephrology: Update in Anticancer Drug-Related Nephrotoxicity

Abstract

The relation that connects cancer and renal damage is bidirectional and this renal damage worsens quality of life and increases morbidity in high-complexity patients such as patients with cancer and kidney injury. Strikingly, in the last decade, the treatment of advanced cancer has clearly advanced in terms of new therapeutic strategies with the ability to transform the advanced metastatic cancer in a chronic condition. In this new era of cancer therapies, cancer treatment including conventional chemotherapy, targeted cancer agents and immunotherapies among others are significantly associated with kidney injury. Renal toxicity that is currently seen in onconephrology departments is in part related to the new therapies such as immunotherapy, and to the prolonged survival achieved at the expense of increasing therapy lines, and a combination of different drugs. In this review, we will discuss in a practical way, nephrotoxicity caused by the main oncospecific treatments such as classical chemotherapy agents, targeted therapies, and immunotherapy. In addition, strategies for prevention and management recommendations in patients with malignancies and kidney disease will also be addressed.

Pseudo-AKI associated with targeted anti-cancer agents—the truth is in the eye of the filtration marker

“…There are no data on interactions of vemurafenib with renal creatinine transporters. Acute tubular necrosis and acute tubulointerstitial nephritis have been described in patients treated with BRAF inhibitors [ 1 , 2 , 4 ].…”

“…Ironically, in a certain way, they have also been revolutionizing the nephrology practice. Nephrologists are increasingly confronted and challenged with the diagnosis and management of the ever-growing list of renal toxicities associated with targeted agents, which contributes to the emergence of the onco-nephrology subspecialty [ 1–4 ]. Because of their potential to cause bona fide kidney injury and as many of these targeted agents are dosed according to kidney function, renal surveillance by regular estimation of kidney function during treatment is critically important, despite absence of clear guidelines on which filtration markers to use optimally, and when [ 5–7 ].…”

“…Because of their potential to cause bona fide kidney injury and as many of these targeted agents are dosed according to kidney function, renal surveillance by regular estimation of kidney function during treatment is critically important, despite absence of clear guidelines on which filtration markers to use optimally, and when [ 5–7 ]. Targeted agents can broadly be divided in two classes: inhibitory monoclonal antibodies and small molecular, mostly receptor tyrosine kinase, inhibitors [ 1 ]. Targeted key members of immune evasive, tumour-promoting or proto-oncogenic molecular pathways include PD1/PDL1, VEGF, ALK, MET, HER2, CDK4/6, PARP, BCR-ABL and BRAF.…”

“…Targeted key members of immune evasive, tumour-promoting or proto-oncogenic molecular pathways include PD1/PDL1, VEGF, ALK, MET, HER2, CDK4/6, PARP, BCR-ABL and BRAF. The renal toxicities of especially VEGF and PD1/PDL1 have been thoroughly characterized in literature, while data on newer targeted agents such as ALK, MET, CDK4/6 and PARP are lacking [ 1 ].…”

“…It is well established that targeted agents can be both associated with pseudo-AKI and true AKI (see Table 1 ). Additionally, targeted agents have been associated with various electrolyte disorders and/or renal cyst formation, but these will not be further discussed [ 1–3 ].…”