Kidney Week 2025 Annual Meeting-Onconephrology in the Mainstream: Bedside Application of Recent Advances

Video Transcription

Video Summary

The session opens with moderators introducing a four-talk onconephrology program and presenting Dr. Siskind’s work on treatment-related acute kidney injury (AKI), especially cisplatin. She emphasizes that AKI and chronic kidney disease (CKD) exist on a spectrum, and cancer patients face higher AKI risk. Cisplatin remains highly effective but dose-limited by nephrotoxicity; repeated low-dose mouse models better mimic clinical exposure and show progressive GFR decline, inflammation, failed repair, and interstitial fibrosis.<br /><br />Siskind’s lab adds a key missing element—cancer—into cisplatin kidney injury models. Lung cancer–bearing mice show greater susceptibility to cisplatin AKI/CKD. Surprisingly, tumors alone (without cisplatin) reduce GFR and cause kidney inflammation and fibrosis across multiple cancer models, driven largely by macrophage populations. Depleting macrophages reduces injury markers and fibrosis. Importantly, nephroprotective agents (e.g., SGLT2 inhibitors) that work in non-cancer models fail or worsen fibrosis in cancer-bearing mice, suggesting protective strategies must be tested in tumor models.<br /><br />Dr. Khalla reviews molecular targeted therapy–associated AKI, focusing on VEGF pathway inhibitors causing hypertension, proteinuria, and thrombotic microangiopathy (TMA). She presents a bevacizumab-associated renal TMA case managed with drug holding and complement inhibition (eculizumab). She also summarizes toxicities of other targeted agents, immune checkpoint inhibitor (ICI) AKI (mostly AIN), guideline-based evaluation, steroids, and emerging data supporting infliximab for steroid-refractory ICI-AIN. She highlights “pseudo-AKI” from drugs blocking creatinine secretion, recommending cystatin C to clarify true GFR.<br /><br />Dr. Kuchila explains how inaccurate GFR assessment affects cisplatin eligibility, carboplatin dosing, and trial access. Evidence and an ASON position statement support using CKD-EPI equations—especially combined creatinine+cystatin C—and measured GFR when decisions hinge on accuracy, while avoiding Cockcroft–Gault.<br /><br />Dr. Tuckman provides a hematologist’s view of monoclonal gammopathy of renal significance (MGRS): kidney biopsy is crucial when monoclonal proteins are low-level and causality is uncertain; therapy is “clone-directed” (plasma cell vs B-cell). He contrasts highly nephrotoxic “cyanide-like” paraproteins with less toxic “ethanol-like” ones.

Asset Subtitle

Moderator(s): Abinet Aklilu, Sandra Herrmann

Presentation(s):

Understanding the Cross-Talk Between Remote Organ Cancer and Kidney Injury - Leah Siskind
Molecular Targeted Cancer Therapies and AKI: Recognition and Management - Jaya Kala
GFR Assessment in Patients with Cancer - Abhijat Kitchlu
Monoclonal Gammopathy of Renal Significance: A Hematologist's Perspective - Sascha Tuchman

Meta Tag

Date 11/7/2025

Pathway 1 Onconephrology

Pathway 2 AKI and Critical Care

Session ID 507316

Keywords

onconephrology

acute kidney injury

chronic kidney disease

cisplatin nephrotoxicity

glomerular filtration rate

interstitial fibrosis

tumor-bearing mouse models

macrophage-mediated renal injury

SGLT2 inhibitors

VEGF pathway inhibitors

bevacizumab

thrombotic microangiopathy

immune checkpoint inhibitor nephritis

CKD-EPI creatinine cystatin C

monoclonal gammopathy of renal significance