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Chemotherapy nephrotoxicity, and dose modification in patients with renal insufficiency: Conventional cytotoxic agents

Jaime R Merchan, MD, MMSc
Kenar D Jhaveri, MD
Section Editors
Reed E Drews, MD
Jeffrey S Berns, MD
Deputy Editors
Diane MF Savarese, MD
Albert Q Lam, MD


A variety of renal diseases and electrolyte disorders can result from the drugs that are used to treat malignant disease, including conventional cytotoxic agents and molecularly targeted agents, which take advantage of molecular abnormalities that have been detected in certain types of cancer. All of these drugs can affect the glomerulus, tubules, interstitium, or renal microvasculature, with clinical manifestations that range from an asymptomatic elevation of serum creatinine and electrolyte disorders to acute kidney injury requiring dialysis.

The kidneys are a major elimination pathway for many antineoplastic drugs and their metabolites, and renal impairment can result in delayed drug excretion and metabolism of chemotherapeutic agents, and increased systemic toxicity. Many drugs require dose adjustment when administered in the setting of renal insufficiency (table 1). Minimizing nonrenal systemic toxicity may be a particular problem in patients on chronic hemodialysis, especially when the details of drug elimination and metabolism are not fully known.

The nephrotoxicity of conventional cytotoxic chemotherapy agents, preventive strategies, and recommended dose modifications in patients with renal insufficiency will be reviewed here. Renal toxicities seen with several classes of molecularly targeted and biologic agents, renal toxicity associated with drugs that target the vascular endothelial growth factor pathway, immune-mediated renal toxicity associated with checkpoint inhibitor immunotherapy (ie, ipilimumab, pembrolizumab, nivolumab), an overview of renal diseases associated with various cancers (including paraneoplastic syndromes), and the renal complications of tumor lysis syndrome and hematopoietic cell transplantation are discussed elsewhere. (See "Chemotherapy nephrotoxicity and dose modification in patients with renal insufficiency: Molecularly targeted agents" and "Toxicity of molecularly targeted antiangiogenic agents: Non-cardiovascular effects", section on 'Proteinuria/nephrotic syndrome' and "Toxicities associated with checkpoint inhibitor immunotherapy", section on 'Kidney' and "Overview of kidney disease in the cancer patient" and "Tumor lysis syndrome: Definition, pathogenesis, clinical manifestations, etiology and risk factors" and "Kidney disease following hematopoietic cell transplantation".)


There are two principal pathways for drug excretion by the kidney: glomerular filtration and tubular secretion. Glomerular filtration plays a major role with non-protein-bound small molecules (ie, of a size that can pass through the glomerular capillary wall). Such molecules cannot be filtered if they are protein bound in the circulation; these drugs, if they are renally excreted, enter the urine by secretion in the proximal tubule.

For those drugs in which renal excretion is an important determinant of elimination of the intact drug or an active metabolite, dose adjustment is often required if renal function is impaired. Although the prevalence of an elevated serum creatinine is low in cancer patients (<10 percent), the prevalence of a reduced glomerular filtration rate (GFR) is relatively high (50 to 53 percent in two cohort studies [1,2]).

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Literature review current through: Nov 2017. | This topic last updated: Dec 01, 2017.
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