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Anticancer drug-induced nephrotoxicity: biopsy-proven patterns and outcomes across chemotherapy, targeted therapy,
Jing Tian1, Jingying Lian2, Yuanyuan Xia1
1National Clinical Research Center for Kidney Diseases, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Abstract:
Biopsy-confirmed anticancer drug-induced kidney injury is underreported. This study aimed to characterize its clinicopathological features and outcomes. We retrospectively analyzed 52 patients with biopsy-proven anticancer drug-induced nephrotoxicity (2005-2024). Patients were classified into chemotherapy drugs (CTD, n = 25), molecularly targeted therapies (MTT, n = 22), and immune checkpoint inhibitors (ICI, n = 5; PD-1 inhibitors). The CTD group (e.g. cisplatin, capecitabine, gemcitabine) caused frequent acute kidney injury (AKI, 80%), with acute tubulointerstitial nephritis (ATIN, 32%). Notable glomerular lesions in the CTD group included thrombotic microangiopathy (TMA, 12%), minimal change disease (8%), and focal segmental glomerulosclerosis (8%). The MTT group (e.g. bevacizumab, lenvatinib, sorafenib) had higher proteinuria (0.4 vs. 3.1 vs. 0.7 g/24h; p < 0.05) and TMA incidence (86%). MTT-induced TMA produced distinct subtypes: anti-VEGF(R) therapy (n = 11) caused glomerular capillary ballooning (100%); non-VEGFR-TKIs (n = 4) were associated with segmental glomerulopathy; combined anti-VEGF/VEGFR-TKI (n = 4) resulted in more extensive and severe TMA (>75% of glomeruli). ICI therapy (nivolumab, camrelizumab, sintilimab) led to early AKI, mainly ATIN (80%), with glomerular IgA deposition (80%) and low serum C3 (60%). After a median follow-up of 23.0 months, MTT showed faster AKI recovery than CTD (0.5 vs. 8.0 months; p = 0.002). Anticancer drugs induce distinct nephrotoxic patterns. CTD causes direct cytotoxicity and high irreversible injury risk. MTT drives functional TMA, and new-onset hypertension with proteinuria should raise concern for anti-VEGF-related TMA. ICI triggers immune dysregulation with humoral disturbances, and AKI with low serum C3 can be a safety signal for clinical monitoring.
Insights
Anticancer drugs cause kidney injury through distinct mechanisms. Chemotherapy drugs lead to direct damage, while targeted therapies and immune inhibitors trigger unique kidney pathologies requiring specific monitoring.
Area of Science:
- Nephrology
- Oncology
- Pathology
Background:
- Anticancer drug-induced kidney injury (ADIK) is an underreported complication.
- Understanding the clinicopathological features of ADIK is crucial for patient management.
Purpose of the Study:
- To characterize the clinicopathological features and outcomes of biopsy-proven ADIK.
- To differentiate the nephrotoxic patterns induced by chemotherapy drugs (CTD), molecularly targeted therapies (MTT), and immune checkpoint inhibitors (ICI).
Main Methods:
- Retrospective analysis of 52 patients with biopsy-proven ADIK from 2005-2024.
- Classification of patients based on drug type: CTD (n=25), MTT (n=22), and ICI (n=5).
- Evaluation of clinicopathological findings, including kidney biopsy results and patient outcomes.
Main Results:
- CTD frequently caused acute kidney injury (AKI) and acute tubulointerstitial nephritis (ATIN), with risks of thrombotic microangiopathy (TMA) and other glomerular lesions.
- MTT was associated with higher proteinuria and a high incidence of TMA, with distinct subtypes related to anti-VEGF(R) therapy and VEGFR-TKIs.
- ICI therapy primarily led to early AKI, ATIN, glomerular IgA deposition, and low serum C3 levels.
- MTT showed faster AKI recovery compared to CTD.
Conclusions:
- Anticancer drugs induce specific nephrotoxic patterns, necessitating tailored clinical monitoring.
- CTD can cause direct cytotoxicity and irreversible injury.
- MTT-induced TMA requires vigilance for new-onset hypertension and proteinuria, especially with anti-VEGF therapy.
- ICI-related AKI with low C3 may serve as a safety signal for monitoring immune-related adverse events.
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