Nephrotoxicity of anticancer treatment

Abstract

Severe adverse systemic drug events occur commonly as a result of treatment of cancer patients. Nephrotoxicity of chemotherapeutic agents remains a significant complication limiting the efficacy of the treatment. A variety of renal disease and electrolyte disorders can result from the drugs that are used to treat malignant disease. The kidneys are a major elimination pathway for many antineoplastic drugs and their metabolites. Tumour lysis syndrome, an emergency in haematooncology, occurs most often after the initiation of cytotoxic therapy in patients with high-grade lymphomas and acute lymphoblastic leukaemia. Chemotherapeutic agents can affect the glomerulus, tubules, interstitium and renal microvasculature, with clinical manifestations that range from asymptomatic elevation of serum creatinine to acute renal failure requiring dialysis. Some factors such as intravascular volume depletion, as well as concomitant use of other drugs or radiographic ionic contrast media, can potentiate or contribute to the nephrotoxicity. Cytotoxic agents can cause nephrotoxicity by a variety of mechanisms. The most nephrotoxic chemotherapeutic drug is cisplatin, which is often associated with acute kidney injury. Many other drugs such as alkylating agents, antimetabolites, vascular endothelial growth factor pathway inhibitors and epidermal growth factor receptor pathway inhibitors may have toxic effects on the kidneys. The aim of this review is to discuss the issue of nephrotoxicity associated with chemotherapy. In routine clinical practice, monitoring of kidney function is mandatory in order to identify nephrotoxicity early, allowing dosage adjustments or withdrawal of the offending drug.

Use of Intravenous Iodinated Contrast Media in Patients with Kidney Disease: Consensus Statements from the American College of Radiology and the National Kidney Foundation

“…This is especially true for patients who have normal eGFR or mild-to-moderate reductions in eGFR because they are not considered at risk, regardless of the drug(s) prescribed (13,15). However, monitoring eGFR in patients receiving nephrotoxic medications (eg, aminoglycosides) or undergoing chemotherapy is important before, during, and after treatment to identify incident nephrotoxicity (eg, AKI or new eGFR ,30 mL/min/1.73 m 2 ) (49).…”

Platycodon grandiflorum Saponins Ameliorate Cisplatin-Induced Acute Nephrotoxicity through the NF-κB-Mediated Inflammation and PI3K/Akt/Apoptosis Signaling Pathways

“…The molecular mechanism underling cisplatin-evoked renal injuries is multifactorial [ 3 ]. Among them, accumulation of cisplatin in straight proximal and distal curved tubules, along with its interference with nuclear DNA and the mitochondrial respiratory chain are regarded as the major causes [ 4 ]. The over-generation of ROS and the decrease in renal antioxidant capacity caused by cisplatin further trigger apoptosis and inflammation in renal tissues [ 5 ].…”

Repurposing Combination Therapy of Voacamine with Vincristine for Down Regulation of HIF-1α/FASN Co-Axis and PHD2 Activation in ER+ Mammary Neoplasia

“…Continuous detoxi cation and excretion of harmful drug molecules specially those which belongs to the anticancer class, can cause harm to these organs and ultimately becomes the reason of nephrotoxicity and hepatotoxicity if dose is not monitored adequately. Most of the anticancer drugs are reported to have varying degree of nephrotoxicity and hepatotoxicity in patients taking them [35]. Nephrotoxicities due to chemotherapy is marked by the necrosis of the proximal convoluted tubule (PCT), distal convoluted tubule (DCT) epithelial cells and injury to the Bowman's capsule, ultimately kidney failure [36].…”