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. 2016 Nov 16;2016:3763250. doi: 10.1155/2016/3763250

Table 3.

Rat and mouse models of CI-AKI.

Injury type (besides RCM injection) Species Advantage Disadvantage Ref.
Inhibition of vasodilators Pronounced medullary hypoxia Multiple insults
Indomethacin (+salt depletion ± UNX) Rat Complex, clin. relevant CPN for all rat models [6569]
Indomethacin + L-NAME Rat Medullary hypoxia
Indomethacin + L-NAME Mouse pathomechanistic High drug dose needed [70, 71]
Water deprivation (dehydration) Dehydration amplifies injury Hydration state affects CI-AKI progression
Dehydration (24 h) Rat [72, 73]
Dehydration (72 h) Mouse, Rat [35, 74, 75]
Dehydration (24 h) + eNOS deficiency (KO) Mouse [76]
Dehydration (24 h) + Indomethacin + furosemide Rat [34]
Dehydration (24 h) + glycerol rhabdomyolysis Rat [36, 7780]
Surgical kidney injury models Reliable models Microsurgery experience
Acute kidney injury (AKI) Short duration Species differences
Ischemia-reperfusion Mouse [81]
Chronic kidney disease (CKD) Clinical relevance Chronic protocol
Diabetes (streptozotocin: STZ) Rat [82, 83]
5/6 nephrectomies + dehydration (48 h) Rat [84, 85]
Long term cholesterol feeding Rat [86]

clin.: clinically, UNX: Uninephrectomy, CPN: chronic progressive nephropathy, and eNOS: endothelial nitrogen monoxide synthase.