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Review
. 2017 Feb 16;2(4):504-514.
doi: 10.1016/j.ekir.2017.02.008. eCollection 2017 Jul.

Anticancer Drug-Induced Acute Kidney Injury

Hassan Izzedine  1 , Mark A Perazella  2
Affiliations
Review

Anticancer Drug-Induced Acute Kidney Injury

Hassan Izzedine et al. Kidney Int Rep. .

Abstract

Acute kidney injury (AKI) is a growing problem with untoward economic and medical consequences. Anticancer drug toxicity remains an important and increasing cause of AKI. Importantly, drug-induced AKI affects all nephron segments-vasculature, glomerulus, tubules, and interstitium. Recent studies have increased insight into the subcellular mechanisms of drug-induced AKI that include direct cellular toxicity and immune-mediated effects. Identification of patients with high-risk cancer before drug exposure may allow prevention or at least a reduction in the development and severity of nephrotoxicity. Recognition of drug-induced AKI and rapid discontinuation (or dose reduction) of the offending agents, when appropriate, are critical to maximizing kidney function recovery. Preventive measures require understanding patient and drug-related risk factors coupled with correcting risk factors, assessing baseline kidney function before initiation of therapy, adjusting the drug dosage and avoiding use of nephrotoxic drug combinations.

Keywords: acute interstitial nephritis; acute kidney injury; acute tubular necrosis; drug nephrotoxicity; glomerulopathy; onco-nephrology; thrombotic microangiopathy.

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Figures

Figure 1
Figure 1
Proximal tubular cell with various basolateral transporters and apical efflux transporters. MATE, multidrug and toxic compound extrusion; MRP, multidrug resistant protein transporter; OAT, organic anion transporter; OCT, organic cation transporter; P-gp, p-glycoprotein; PEPT, peptide transporter; SGLT2, sodium glucose cotransporter-2.
Figure 2
Figure 2
Histology demonstrating focal segmental necrotizing glomerulonephritis.
Figure 3
Figure 3
Histology demonstrating acute tubular injury. Note the tubular vacuoles, apical blebbing, tubular cell dropout, and proteinaceous casts.
Figure 4
Figure 4
Histology demonstrating acute interstitial nephritis. Note the interstitial inflammatory infiltrate composed of lymphocytes, plasma cells, and eosinophils.
See this image and copyright information in PMC

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