Assessment of NGAL, eGFR, and tubular injury markers for early detection of chemotherapy-induced nephrotoxicity in pediatric oncology patients

Introduction : Acute kidney injury is a common complication in children with oncological diseases. Its etiology is multifactorial, with key risk factors including drug-induced nephrotoxicity, tumor lysis syndrome, and infection—including sepsis during periods of aplasia. The classical diagnostic criteria for AKI rely on monitoring serum creatinine levels and detecting oliguria. In the context of drug-induced nephrotoxicity, the predominant pathophysiological mechanism is tubular injury, which is typically non-oliguric and may not cause changes in serum creatinine, even in cases of severe damage. Materials and methods : We studied 40 children undergoing 116 chemotherapy cycles with nephrotoxic agents at the Pediatric Hematology-Oncology Department, St. George University Hospital. Urinary NGAL, estimated GFR (eGFR) using the Schwartz, Schwartz-adjusted, and Brandt formulas, and tubular markers—fractional excretion of phosphate (FeP) and tubular maximum reabsorption of phosphate per GFR (Tmp/GFR)—were measured before and 12 hours after each cycle. Results : Urinary NGAL increased significantly after later chemotherapy cycles but remained within reference ranges and failed to detect two KDIGO-defined AKI episodes. The classical Schwartz formula identified only two AKI cases, while adjusted formulas revealed decreased eGFR in 36% of patients and a reduction in hyperfiltration prevalence from 50% to 28%. Tubular markers (FeP, Tmp/GFR) showed consistent and significant changes across all cycles. Conclusion : NGAL is not a reliable early biomarker for chemotherapy-related AKI in children. Adjusted eGFR formulas and tubular injury markers provide greater sensitivity and should be incorporated into monitoring protocols to enable earlier detection and reduce the risk of chronic kidney damage.