Introduction to AKI Animal Models

Acute kidney injury (AKI) animal models are a class of classic disease models designed to mimic the rapid decline in renal function that occurs over a short period, and they are widely used in studies of the mechanisms underlying kidney injury and in the development of nephroprotective therapeutics. These models typically exhibit pathological features such as elevated serum creatinine (Scr) and blood urea nitrogen (BUN), tubular epithelial cell damage and necrosis, and infiltration of inflammatory cells. Common modeling approaches include ischemia-reperfusion injury (IRI) models, cisplatin‑induced models, gentamicin‑induced models, lipopolysaccharide (LPS)‑induced models, and rhabdomyolysis‑induced models. Such models effectively recapitulate the pathophysiological processes of acute kidney injury triggered by clinical factors like ischemia, drug toxicity, infection, and inflammation.

Service Advantages of Aniphe BioLab’s AKI Animal Model Platform

Leveraging its extensive experience in establishing well‑validated renal disease models and a standardized experimental platform, Aniphe BioLab offers a range of AKI animal model services, providing customers with a stable and reliable in vivo pharmacological evaluation platform.

	A rich model framework It supports multiple AKI models, including renal ischemia-reperfusion (IRI) and lipopolysaccharide (LPS)-induced injury.
	Modeling is stable and reliable. Standardized operating procedures, high model success rate, and excellent phenotypic consistency in renal dysfunction.
	Comprehensive evaluation metrics It encompasses serum biochemistry (Scr, BUN), urinary parameters, histopathology, and molecular biology assays.
	Extensive experimental experience Different animal species and modeling protocols can be selected according to the research objectives, thereby meeting the needs of mechanistic studies and efficacy evaluations.
	End-to-end quality management Strictly adhere to SOPs and the QA management system to ensure that experimental data are authentic, traceable, and reproducible.

Modeling cycle	1–2 weeks
Laboratory animals	C57BL/6 or BALB/c mice
Positive drug	N-acetylcysteine (antioxidant), erythropoietin (anti-apoptotic/proliferative), an α‑melanocyte‑stimulating hormone analog (anti-inflammatory), and others; the diuretic furosemide is frequently used as a control intervention.
Application areas	The pathophysiological mechanisms of ischemic AKI—including oxidative stress, inflammation, apoptosis, and autophagy—along with the protective effects of ischemic preconditioning, and the pharmacological screening of novel nephroprotective agents.

Construction of an AKI animal model

An acute kidney injury (AKI) model was established using the ischemia–reperfusion injury (IRI) method. After anesthetizing the experimental animals, bilateral kidneys were exposed through an abdominal or lumbar incision. Non‑invasive vascular clamps were then applied to simultaneously occlude both renal arteries for 30–60 minutes, inducing acute renal ischemia. During clamping, the kidneys gradually changed in color from reddish‑brown to dark purple, indicating successful ischemia; subsequently, the clamps were released to restore renal blood flow, and the renal coloration returned to normal. Within 24–72 hours after reperfusion, significant increases in serum creatinine (Scr) and blood urea nitrogen (BUN), along with typical pathological changes such as tubular epithelial cell necrosis, cast formation, and inflammatory cell infiltration, could be observed. This model is well‑established and highly reproducible, accurately mimicking the pathophysiological process of AKI induced by renal ischemia–reperfusion, and is widely used in studies investigating the mechanisms of AKI and evaluating renoprotective agents.