Cisplatin re-challenge following recovery from carboplatin-induced, biopsy-proven acute tubular necrosis in a 57-year-old patient with squamous-transformed non-small cell lung cancer: a case report

Introduction

There have been remarkable advances in the systemic treatment of advanced non-small cell lung cancer (NSCLC) in recent years, highlighted by the development of novel therapeutic strategies such as molecularly targeted agents and immune checkpoint inhibitors. Nevertheless, platinum-based cytotoxic chemotherapeutic agents remain integral to improving survival outcomes. In the management of NSCLC, combination regimens incorporating cisplatin with immunotherapy have already been established as the standard of care, as demonstrated in pivotal clinical trials (1-5).

Despite these advances, acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) remains inevitable. Among the reported resistance mechanisms, histologic transformation represents an uncommon but clinically important phenomenon. Although small cell transformation has been more extensively described, transformation to squamous cell carcinoma has also been reported but appears to be exceedingly rare, and its underlying biological mechanisms remain incompletely understood (6). After histologic transformation, treatment options are often limited. Established targeted therapies are generally lacking in this setting, and the efficacy of later-line non-platinum regimens may be modest. Therefore, platinum-based chemotherapy may remain one of the few clinically meaningful systemic treatment options for selected patients. In such situations, the continued clinical relevance of cisplatin reflects a real-world need to balance potential therapeutic benefit against treatment-related risks.

However, cisplatin carries a substantial risk of acute kidney injury (AKI), most commonly manifesting as acute tubular necrosis (ATN), which occurs in a significant proportion of treated patients (7). In contrast, carboplatin is generally considered less nephrotoxic, and biopsy-proven carboplatin-associated ATN appears to be exceedingly rare, with limited available evidence. When ATN is histologically confirmed, clinicians often hesitate to readminister platinum agents because of concerns regarding recurrent renal injury. Furthermore, most existing studies define AKI based solely on serum creatinine criteria without histological confirmation, making the extent of tubular damage and the safety of the re-challenge difficult to interpret. Consequently, evidence regarding the feasibility of cisplatin re-challenge after recovery from biopsy-proven ATN remains extremely limited.

This situation creates a critical therapeutic dilemma: effective treatment options may be scarce; however, the use of potentially beneficial platinum-based chemotherapy is constrained by prior severe renal toxicity. Here, we report a case of EGFR-mutant NSCLC with squamous transformation in which cisplatin-based therapy was reconsidered after recovery from carboplatin-induced, biopsy-proven ATN. Rather than establishing general safety, this case illustrates a clinically relevant framework for risk assessment and multidisciplinary management in situations where treatment options are limited. The overall clinical course and radiographic findings are summarized in Figure 1. We present this case in accordance with the CARE reporting checklist (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0097/rc).

Figure 1 A patient with EGFR-mutated non-small cell lung carcinoma. (A) Chest radiograph showing a nodule in the right upper lobe (red arrow). (B) Chest CT image showing the right upper lobe nodule (red arrow). (C) Chest CT image showing left axillary lymphadenopathy (red arrow). (D) Contrast-enhanced magnetic resonance image showing left posterior cervical lymphadenopathy (red arrow). (E,F) Contrast-enhanced magnetic resonance image showing brain metastases (red arrows). (G) Chest CT image showing enlargement of the right upper lobe nodule during disease progression after osimertinib treatment (red arrow). (H) Chest CT showing mediastinal lymph node enlargement during disease progression after osimertinib treatment (red arrow). (I,J) Contrast-enhanced MRI showing the progression of brain metastases (red arrows). CT, computed tomography; EGFR, epidermal growth factor receptor; MRI, magnetic resonance imaging.

Case presentation

Initial diagnosis and first-line therapy

A 57-year-old Japanese man with a history of smoking two packs of cigarettes daily from the age of 20 to 53 years was referred to our hospital with symptoms of exertional dyspnea. Chest radiography and computed tomography (CT) revealed an irregular nodule in the right lung (Figure 1A,1B) and left axillary lymphadenopathy (Figure 1C). Contrast-enhanced magnetic resonance imaging (MRI) of the brain revealed left posterior cervical lymphadenopathy and multiple brain metastases (Figure 1D-1F). Radiographic and pathological evaluations confirmed the diagnosis of lung adenocarcinoma (cT3N3M1c, cStage IVB). Genetic testing identified an EGFR exon 21 L858R mutation, which led to the initiation of oral targeted therapy with osimertinib. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. This report was approved by the Institutional Review Board of Nagasaki University Hospital (No. 25102313, approved on Oct, 23, 2025). Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Histological transformation and second-line therapy

After 30 months of osimertinib treatment, chest CT revealed enlargement of the right upper lobe and mediastinal lymph nodes (Figure 1G,1H). A re-biopsy showed histological transformation to squamous cell carcinoma, prompting second-line treatment with carboplatin [510 mg (flat dose)], nab-paclitaxel (100 mg/m²), and pembrolizumab [200 mg (flat dose)] at standard doses, in accordance with the treatment algorithm for tumors with low expression of programmed death-ligand 1 (PD-L1; 20%).

ATN event and biopsy results

During the first cycle, the patient developed rapidly progressive renal impairment (Table 1), and a renal biopsy was performed after the first cycle of carboplatin-based chemoimmunotherapy, following the onset of AKI. Renal biopsy specimens stained with hematoxylin and eosin at ×100 magnification and Masson’s trichrome at ×400 magnification. The findings excluded glomerulonephritis and tubulointerstitial nephritis but revealed tubular epithelial swelling and vacuolar degeneration with concomitant loss of microvilli, which is consistent with carboplatin-induced ATN rather than an immune-related adverse event (Figure 2). Consequently, the treatment regimen was changed to pembrolizumab monotherapy.

Figure 2 Renal biopsy findings at the time of carboplatin-induced ATN. Representative renal biopsy specimens stained with (A) hematoxylin and eosin staining at 100× magnification and (B) Masson’s trichrome staining at 400× magnification. These demonstrate the loss of microvilli, necrotic and sloughed tubular epithelial cells, and granular casts within the tubular lumen. Tubular epithelial cell swelling was also observed. ATN, acute tubular necrosis.

Renal recovery

Renal function normalized within 1 month. However, 3 months later, contrast-enhanced brain MRI revealed progression of brain metastases (Figure 1I,1J), necessitating further systemic treatment modification following stereotactic radiosurgery-mediated local control of brain metastases with 20 Gy in a single fraction to two lesions.

Cisplatin re-challenge and monitoring protocols

This patient had brain metastases; however, they were asymptomatic, and he maintained an Eastern Cooperative Oncology Group Performance Status score of 0 with an otherwise good general condition. Given the limited therapeutic options and recovery of renal function with an estimated glomerular filtration rate (eGFR) of 67.40 mL/min/1.73 m² and creatinine clearance of 83.60 mL/min/1.73 m², cisplatin re-challenge was initiated approximately 120 days after the onset of biopsy-confirmed ATN. The regimen consisted of a combination of cisplatin (80 mg/m²), gemcitabine (1,250 mg/m²), and necitumumab [1,200 mg (flat dose)], which we referred to as the CGN regimen, and was initiated following nephrology consultation and intensive monitoring (Table 1). The standard starting dose of cisplatin was selected because renal function had recovered above the predefined eligibility threshold, the patient maintained an Eastern Cooperative Oncology Group performance status of 0, and treatment was initiated under close nephrology supervision with planned dose modification if clinically necessary. Baseline hypomagnesemia prompted daily magnesium sulfate supplementation (10 mEq/day) along with intensive hydration for 4 days. Body weight and urine output were closely monitored, with a target urine output of ≥0.5 mL/kg/h to ensure adequate renal perfusion during cisplatin administration (Figure 3). From day 6, the patient developed severe chemotherapy-induced nausea and anorexia, with oral intake decreasing to approximately 30% of the baseline. During this period, systolic blood pressure decreased from a baseline in the 130 mmHg range to 90–110 mmHg. In addition, body weight decreased from 65.1 kg to 62.6 kg, suggesting volume depletion. On day 7, the patient developed AKI meeting the criteria for Kidney Disease: Improving Global Outcomes (KDIGO) stage 1 (Table 1), which subsequently progressed to a maximum of stage 2. Supportive management, including intravenous hydration, electrolyte replacement, and careful fluid balance adjustment, was initiated promptly. Renal function subsequently improved following these interventions, and the clinical course was considered most consistent with dehydration-associated pre-renal AKI. However, because a repeat renal biopsy was not performed, recurrent tubular injury could not be completely excluded.

Figure 3 Time course of the case. (A) The case in the lines of treatment. (B) Changes in renal function and urine output during treatment with cisplatin, gemcitabine, and necitumumab, along with the clinical interventions implemented to preserve renal function. FR, furosemide.

Outcome

Radiologic evaluation according to RECIST version 1.1 demonstrated stable disease as the best overall response. The progression-free survival from the initiation of cisplatin-based therapy was 2.8 months.

Although the patient met the criteria for continuation of combination therapy, the regimen was de-escalated to necitumumab maintenance from the second cycle onward due to gastrointestinal toxicity and patient preference. Renal function remained stable after recovery from the AKI, and no further episodes of severe renal impairment were observed during follow-up.

Discussion

Cisplatin is a platinum-based cytotoxic chemotherapeutic agent that exerts antitumor effects primarily through the formation of DNA crosslinks, thereby inhibiting DNA replication and transcription (8). It remains a key component of standard regimens for several solid tumors, including lung cancer.

ATN is the most common histopathological subtype of intrinsic AKI. The characteristic histological features include tubular epithelial cell swelling, necrosis, detachment from the basement membrane, and intraluminal cast formation (9). These structural alterations disrupt tubular reabsorption and concentration capacity, resulting in a decreased glomerular filtration rate, electrolyte imbalances, and either oliguric or non-oliguric AKI. Mechanistically, ATN can result from diverse insults, including hemodynamic disturbances, inflammation, oxidative stress, and exposure to nephrotoxic agents. Among drug-induced etiologies, cisplatin-associated ATN is particularly relevant in oncology because cisplatin exerts direct tubular toxicity through DNA damage, mitochondrial dysfunction, and the induction of reactive oxygen species (10).

In this case, the diagnosis of ATN was confirmed histologically following the administration of a carboplatin-containing chemotherapy regimen, which demonstrated typical tubular injury findings consistent with ATN. Although immune checkpoint inhibitor-related renal adverse events were considered, their predominant pathological manifestation was acute interstitial nephritis characterized by lymphocyte-rich interstitial infiltration (11), which was not observed in this case. Moreover, nab-paclitaxel carries a low risk of inducing renal impairment, and its safety in patients with pre-existing renal dysfunction has been documented (12). Therefore, carboplatin was identified as the causative agent in this case.

Although cisplatin-induced AKI typically resolves within approximately 2–4 weeks (13), evidence of renal recovery after ATN and the safety of cisplatin re-challenge following normalization of renal function remains limited. Therefore, this case should not be interpreted as demonstrating the general safety of cisplatin re-administration after structural renal recovery. Rather, it illustrates how cisplatin-based therapy may be cautiously reconsidered in highly selected patients when therapeutic options are limited, and the potential antitumor benefit is judged to outweigh the renal risk.

In all major guidelines, including those from the Japanese Lung Cancer Society, the European Society for Medical Oncology, and the National Comprehensive Cancer Network, CGN remains recommended solely as a first-line regimen for advanced squamous NSCLC.

However, evidence supporting its use beyond the first-line setting is limited.

Therefore, no guideline-based recommendation exists for its use in second-line or later therapy, where single-agent regimens such as docetaxel remain the standard of care (1-3). Nevertheless, Murata et al. and Kinoshita et al. have reported promising outcomes with CGN administered as second- or later-line treatment, suggesting that although not endorsed by current guidelines, CGN may represent a feasible therapeutic option for selected patients who remain platinum-sensitive and maintain a good performance status (14,15). Considering the patient’s prior renal injury, the use of a less nephrotoxic platinum agent, such as nedaplatin, could have been considered as an alternative. However, among these combinations, CGN has demonstrated promising antitumor activity, specifically in squamous histology, and we regarded it as a potentially meaningful choice for achieving a survival benefit in this patient. Although carboplatin and nedaplatin carry a lower risk of nephrotoxicity, cisplatin is the only platinum agent approved for use in this regimen; therefore, CGN was ultimately selected as the most appropriate option for this patient, who had a good performance status and limited alternative systemic therapies. However, it should be noted that the evidence supporting the use of CGN beyond the first-line setting is limited to retrospective analyses, and these findings may be subject to selection bias, which limits their generalizability.

Reported risk factors for cisplatin-induced nephrotoxicity include older age, female sex, high-dose cisplatin administration (≥80 mg), poor performance status, and concomitant use of other nephrotoxic drugs (16-18). In the present case, cisplatin was administered at a standard dose, and none of these additional risk factors were present; thus, the decision to proceed was considered clinically appropriate.

An important safety issue in this case was baseline hypomagnesemia. Serum magnesium was critically low at 1.0 mg/dL before cisplatin initiation, making magnesium management a central component of renal risk mitigation rather than a minor supportive measure. Hypomagnesemia is a recognized risk factor for cisplatin-induced nephrotoxicity (17,19), and prophylactic intravenous magnesium supplementation has been associated with a reduced risk of cisplatin-associated AKI (19). This issue is especially relevant because necitumumab is known to induce hypomagnesemia at a high frequency, reportedly in up to 31% of treated patients (20,21). Therefore, in the present case, the combination of baseline hypomagnesemia, concurrent necitumumab exposure, and cisplatin treatment represented a clinically important interaction that required proactive magnesium supplementation and close biochemical monitoring throughout therapy.

Adequate hydration is another essential strategy for preventing cisplatin nephrotoxicity (22). Recent literature has supported short hydration protocols for many patients receiving cisplatin-based chemotherapy (10,22). However, our patient differed from typical candidates for standard short hydration because he had several high-risk features, including prior biopsy-proven ATN, marked baseline hypomagnesemia, concurrent necitumumab exposure, and a high likelihood of reduced oral intake due to treatment-related gastrointestinal toxicity. For these reasons, we selected intensive hydration and prolonged monitoring rather than the conventional short hydration approach. We believe that this intensified strategy was clinically reasonable in the context of the patient’s cumulative renal risk.

However, the transient recurrence of AKI underscores the need to consider cisplatin dose reduction. Although hypomagnesemia may also have been present during the episode of renal impairment that developed during second-line chemotherapy, serum magnesium levels were not measured at that time and, therefore, remain unknown.

Another clinical concern with this regimen is the occurrence of treatment-emergent gastrointestinal adverse events. In a randomized multicenter phase III trial of cisplatin, gemcitabine, and necitumumab, severe gastrointestinal toxicities were common (20). Moreover, previous reports of necitumumab monotherapy have shown that nausea (33%) and vomiting (20%) occur with a relatively high frequency (21), conferring a significant risk of dehydration-induced AKI. In addition, dehydration resulting from cisplatin-induced gastrointestinal toxicity can readily precipitate pre-renal AKI (23). The second AKI episode during cisplatin re-challenge was clinically most consistent with dehydration-associated pre-renal injury rather than definite recurrent ATN. This interpretation was supported by a marked reduction in oral intake to approximately 30% of baseline, a decline in systolic blood pressure from the 130 mmHg range to 90–110 mmHg, and body weight loss from 65.1 to 62.6 kg, together with subsequent improvement after intravenous hydration and electrolyte replacement. Simultaneously, because a repeat renal biopsy was not performed, recurrent tubular injury could not be completely excluded. Accordingly, this event should be interpreted with caution, and our case should not be considered evidence that re-challenge after biopsy-proven ATN is uniformly safe.

Although end-stage renal disease requiring dialysis after cisplatin therapy is rare, many patients develop mild-to-moderate chronic renal impairment in the long term (24). In our case, renal function showed partial recovery within a short time frame; however, prior studies suggested that renal injury may persist or progress over time, even after apparent recovery, reflecting the potential for cumulative and subclinical tubular damage (24). Renal function remained stable during follow-up, and the patient was monitored for 3 months after cisplatin re-challenge. Accordingly, we have planned a continued longitudinal follow-up to evaluate the patient’s renal outcomes. In the context of advanced lung cancer, long-term renal outcomes may be difficult to fully assess due to the underlying disease prognosis; nevertheless, continued monitoring of renal function remains clinically important for as long as feasible. Taken together, this case does not establish general safety, but instead provides a clinically relevant framework for multidisciplinary risk assessment, magnesium-focused supportive care, and individualized hydration management when cisplatin must be reconsidered despite prior platinum-associated renal injury. Despite these findings, this study has several limitations. First, serum magnesium levels at the time of the initial carboplatin-induced ATN were not available because of incomplete documentation, limiting the ability to fully assess its contribution to the initial renal injury. Second, a repeat renal biopsy was not performed during the second AKI episode; therefore, recurrent tubular injury could not be completely excluded. Third, patient-reported outcomes were not systematically collected, and pharmacogenetic factors potentially influencing cisplatin susceptibility were not evaluated. These limitations highlight the need for cautious interpretation and further investigation. Further accumulation of similar cases and systematic data collection are important to better define the safety and clinical applicability of cisplatin re-challenge after platinum-associated ATN. In addition, the need for intensive multidisciplinary management, including close nephrology involvement, may have implications for resource utilization and cost, which was not formally evaluated in this report.

Conclusions

This case suggests that cisplatin re-challenge should be cautiously considered after recovery from biopsy-proven ATN, provided that strict renal management protocols are implemented and close multidisciplinary supervision is maintained. Clinicians should incorporate routine magnesium supplementation, proactive hydration strategies, and frequent monitoring of serum creatinine levels, electrolyte levels, and urine output. Dose reduction of cisplatin should be considered early when gastrointestinal toxicity or volume depletion is anticipated. Although long-term renal function preservation remains unknown and findings cannot be generalized beyond individual conditions, this case underscores that previous platinum-associated renal injury does not automatically preclude future cisplatin use and that a structured nephrology-supported approach may broaden treatment opportunities for selected patients with previously treated NSCLC.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0097/rc

Peer Review File: Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0097/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0097/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. This report was approved by the Institutional Review Board of Nagasaki University Hospital (No. 25102313, approved on Oct, 23, 2025). Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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