Herein we demonstrate the suppression of LPS- and TNFα-induced inflammatory mediator production by resident kidney cells by nicotinic agonists, enhanced renal proteasome activity during LPS-AKI, and the attenuation of renal injury in LPS-induced AKI following treatment with nicotinic agonists (which suppressed both ATP-dependent and ATP-independent proteasome activity). Here, TNF is linked to acute kidney injury.