Evidence map›Paper›PMID 41987381›Full record

ArticleThe Journal of veterinary medical science2026

Cisplatin-induced acute kidney injury in lupus-prone NZB/W F1 mice: a potential experimental model of acute kidney injury superimposed on chronic kidney disease.

Eun Wha Choi

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In one paragraph

Article in The Journal of veterinary medical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

1 author.

Eun Wha ChoiDepartment of Veterinary Clinical Pathology, College of Veterinary Medicine & Institute of Veterinary Science, Kangwon National University, Chuncheon, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease frequently complicated by immune complex-mediated glomerulonephritis that can progress to chronic kidney disease (CKD). Acute kidney injury (AKI) superimposed on CKD (AKI on CKD) is associated with a markedly poor prognosis; however, experimental models that accurately reflect this condition in SLE are limited. This study aimed to establish and characterize an AKI on CKD model using SLE-prone mice with pre-existing immune complex-mediated glomerulonephritis. Female NZB/W F1 mice with established glomerulonephritis at 32 weeks of age were administered cisplatin (10 mg/kg, intraperitoneally) to induce AKI. Blood urea nitrogen (BUN), serum neutrophil gelatinase-associated lipocalin (NGAL), urinary NGAL, and the urinary NGAL-to-creatinine ratio were evaluated as clinicopathological indicators of renal injury. Following cisplatin administration, BUN and serum NGAL concentrations increased significantly. Urinary NGAL concentrations and the urinary NGAL-to-creatinine ratio were also significantly elevated on days 1-4 after AKI induction compared with baseline, whereas urinary protein concentration, urinary creatinine concentration, and the urinary protein-to-creatinine ratio showed no significant changes. NGAL is synthesized by macrophages, glial cells, and epithelial cells under inflammatory conditions and is an established biomarker of tubular injury in AKI. The observed increases in BUN and NGAL parameters confirm successful induction of AKI in SLE mice with pre-existing CKD. This cisplatin-induced AKI model in NZB/W F1 mice may serve as a useful AKI on CKD model for investigating disease mechanisms and developing therapeutic strategies for AKI in patients with SLE and CKD.

Indexed as

Acute Kidney InjuryCisplatinDisease Models, AnimalLupus Erythematosus, SystemicRenal Insufficiency, ChronicAnimalsBlood Urea NitrogenCreatinineFemaleLipocalin-2MiceMice, Inbred NZBCisplatinCreatinineLcn2 protein, mouseLipocalin-2acute kidney injury on chronic kidney diseaselupus nephritisneutrophil gelatinase–associated lipocalin(NZB×NZW) F1 micesystemic lupus erythematosus

Identifiers

PMID41987381
PMCPMC13279907

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.