The renin-angiotensin-aldosterone system (RAAS) plays a major role in the regulation of blood pressure, renal hemodynamic, myocardial contractility via an enzymatic cascade leading to the synthesis of angiotensin 2. The activation of the RAAS system after acute kidney injury triggers renal inflammation and fibrotic process with long-term damaging consequences. To date, there is still a debate on the benefits of RAAS for the kidney in acute settings. Effects of RAAS antagonists are variable in chronic or acute conditions. The aim of this review is to discuss the renal and systemic effects of the RAAS, and its modulation, in acute situations.