Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

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	[65–69]
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, 77–80]
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.