Acute hyperglycaemia, systemic and intra-renal inflammation and RAS activation were independently triggered by induction of anaesthesia. Each confounder aggravated the impacts of the others, bringing about concomitant deterioration of renal function. Increased insulin secretion attenuated but did not abolish hyperglycaemia. Systemic inflammation was counterforced by anti-inflammatory cytokines, whereas intra-renal inflammation persisted, so that AKI progressed unopposed.