Establishment of acute kidney injury mouse model by 0.75% adenine ingestion

Acute kidney injury (AKI) has a profound impact on the morbidity and mortality of patients. Tubular obstruction is an important mechanism of AKI development because many molecules will cause tubular obstruction, leading to AKI; however, few AKI animal models by tubular obstruction have been established. The aim of this study was to establish AKI model mice due to tubular obstruction.

C57BL/6 male mice, aged 10 weeks, 20-30 g body weight, were ingested 0.75% adenine compound food. The mice were sacrificed from day 1 to 5 for blood, urine, and histological analysis.

All mice (50/50 mice) developed AKI and had died by day 6 of uremia after ingesting 0.75% adenine. Histological examination of the kidneys of AKI mice showed that dilatation of the tubular lumen in the medullary papilla resulted from the occupation by adenine casts followed by atrophy, scattering, and flattening of the epithelial cells of tubules. The urine neutrophil gelatinase-associated lipocalin (NGAL) level significantly increased in AKI mice on day 1 after ingesting 0.75% adenine.

We established a very simple and reproducible AKI mouse model due to tubular obstruction by ingesting 0.75% adenine.