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Kidney Week

Abstract: SA-PO1272

Hyperthermic Intraperitoneal Chemotherapy Associated with Acute Interstitial Nephritis

Session Information

Category: Onconephrology

  • 1600 Onconephrology

Authors

  • Al Masry, Ahmad, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
  • Sampangirama, Neel Anil, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
  • Rungta, Manav, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
  • Tchakarov, Amanda, The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
  • Fournier, Keith F., The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
  • Abudayyeh, Ala, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
  • Mamlouk, Omar, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
Background

Acute kidney injury (AKI) in Hyperthermic intraperitoneal chemotherapy (HIPEC) is a common complication with a reported incidence of 24%. While AKI is primarily attributed to direct nephrotoxicity such as cisplatin induced acute tubular necrosis, other reported etiologies include pre-renal, as a result of hypoperfusion. In HIPEC, there is no reported data on acute interstitial nephritis. Our study reports two cases of biopsy proven AIN, suggesting that AIN is an under-identified cause of AKI.

Methods

We conducted a retrospective study of patients undergoing HIPEC surgery at MD Anderson Cancer Center from 2016 to 2025 to evaluate incidence of AKI, etiology, and kidney and cancer outcomes. AKI was defined using the Kidney Disease Outcome Quality Initiative (KDIGO) criteria. Multiple preoperative and intraoperative variables were collected with the aim of evaluating the independent predictors of AKI after HIPEC.

Results

Of 220 patients, 84 were found to have AKI (34%). Amongst the 84 patients only two cases underwent a kidney biopsy that revealed AIN. The first case consisted of a 50 year-old-male with history of epithelioid mesothelioma s/p exploratory celiotomy and HIPEC with cisplatin. The patient's baseline serum creatinine (Scr) was 1.0 mg/dL. The patient had AKI post-op with peak creatinine of 4.5 mg/dL on day 4. On the day of the surgery, the patient was administered pantoprazole and ertapenem. He was treated with prednisone, and after a 3 month follow-up, his SCr improved to ~1.7mg/dl . The second case is a 62-year-old male with history of peritoneal mesothelioma s/p HIPEC with Cisplatin. His baseline SCr is 0.9mg/dL. By day 5 Post-operation, his SCr trended up peaking at 7.0mg/dL. Notably, he received celecoxib, pantoprazole, and ertapenem on day of surgery. Additionally, the patient was started on prednisone and his Cr improving to 2.5mg/dL and didn’t require dialysis.

Conclusion

To our knowledge, this is the first study to identify AIN as a significant cause of AKI in patients undergoing HIPEC. This novel finding carries substantial clinical implications. While the exact pathophysiology remains complex, we propose that AIN in this setting may result from an idiosyncratic reaction to cisplatin or a synergistic effect of concomitant medications. Furthermore, the hyperthermic environment may exacerbate this response by stimulating the immune system through the release of heat shock proteins.