An aqueous extract of Phyllanthus urinaria L (PU) protected mice against acute kidney injury (AKI) caused by cisplatin, a widely used chemotherapy drug whose dose-limiting kidney toxicity affects nearly 30% of recipients. The preclinical findings, reported in Pediatric Discovery in 2025, suggest that PU may shield renal tubular epithelial cells through multiple pathways, though the authors stress that clinical validation is still needed.
The study matters because acute kidney injury is common in hospitalized patients and rises sharply in intensive care, yet treatment options remain largely supportive. Drug-induced kidney injury accounts for a substantial share of cases, and cisplatin is a leading culprit: it accumulates in renal tubular epithelial cells and triggers inflammation, apoptosis, and oxidative stress. Current management relies heavily on renal replacement therapy because effective preventive medicines are lacking, creating an urgent need for nephroprotective strategies.
Researchers at the Children's Hospital of Chongqing Medical University and affiliated laboratories in Chongqing, China, tested a PU aqueous extract in 24 male C57BL/6 mice with cisplatin-induced AKI. The experiment used three groups: control, cisplatin, and cisplatin plus PU. Mice received a single intraperitoneal injection of cisplatin at 20 mg/kg; the treatment group also received PU at 250 mg/kg by oral gavage on days 0–2, and kidney and blood samples were collected on day 4. All mice survived. The team combined biochemical assays, histology, quantitative polymerase chain reaction, Western blot, and immunofluorescence to assess renal function, tissue damage, inflammatory cytokine expression, apoptosis-related proteins, and antioxidant pathways.
Cisplatin raised blood urea nitrogen and serum creatinine and disrupted tubular architecture, with inflammatory cell infiltration and increased neutrophil gelatinase-associated lipocalin. PU significantly attenuated these changes. It suppressed messenger RNA levels of Il1b, Il6, and Tnf, which encode interleukin-1β, interleukin-6, and tumor necrosis factor-α. PU also lowered Bcl-2-associated X protein and cleaved caspase-3 while raising B-cell leukemia/lymphoma 2, indicating less apoptosis. Additionally, PU reduced malondialdehyde, increased superoxide dismutase activity, and restored nuclear factor erythroid 2-related factor 2 and NAD(P)H:quinone oxidoreductase 1 expression, supporting stronger antioxidant defense. Histology showed more organized tubules in the PU group than in cisplatin-only mice.
The authors said the study provides a multi-pathway rationale for PU in cisplatin-induced AKI, rather than a single-target effect. They described the findings as a foundation for translational work, not a clinical recommendation, and emphasized that the mouse data are encouraging but early. Next steps should define active compounds, optimize dosing, and test safety and efficacy in clinically relevant models before any patient use is considered. For patients receiving cisplatin, a nephroprotective adjunct could widen therapeutic options and reduce treatment interruptions, but key questions remain: identifying the constituents responsible, confirming target engagement in human cells or organoids, determining whether PU interferes with cisplatin's anticancer activity, and evaluating safety, dosing, and drug interactions. Such work, detailed in the study with DOI 10.1002/pdi3.70000, would need to balance kidney protection with unchanged tumor killing. If those questions are addressed, PU could become a candidate for further development as a supportive therapy for cisplatin-associated kidney injury.
