Acute kidney injury is a frequent and life-threatening complication of critical illness. Prevention of this condition is crucial. Two randomized single center trials in critically ill patients have shown a decrease in acute kidney injury by tight glycaemic control, an effect that appears most pronounced in surgical patients. Subsequent randomized trials did not confirm this renoprotective effect. This apparent contradiction is likely explained by methodological differences between studies, including different patient populations, insufficient patient numbers, comparison with a different control group, use of inaccurate blood glucose analyzers, and differences in the degree of reaching the target blood glucose level. The optimal glycaemic target for renoprotection in critical illness remains to be defined. Possible mechanisms underlying the renoprotective effect of tight glycaemic control are prevention of glucose overload and toxicity and the associated mitochondrial damage, an anti-inflammatory or anti-apoptotic effect, prevention of endothelial dysfunction, and an improvement of the lipid profile.