Early recognition of acute kidney injury (AKI) is critical to prevent its associated complications as well as its progression to long term adverse outcomes like chronic kidney disease. A growing body of evidence from both laboratory and clinical studies suggests that inflammation is a key factor contributing to the progression of AKI regardless of the initiating event. Biomarkers of inflammation are therefore of interest in the evaluation of AKI pathogenesis and prognosis. There is evidence that the renin angiotensin aldosterone system is activated in AKI, which leads to an increase in angiotensin II (Ang II) formation within the kidney. Ang II activates pro-inflammatory and pro-fibrotic pathways that likely contribute to the progression of AKI. Angiotensinogen is the parent polypeptide from which angiotensin peptides are formed and its stability in urine makes it a more convenient marker of renin angiotensin system activity than direct measurement of Ang II in urine specimens, which would provide more direct information. The potential utility of urinary angiotensinogen as a biomarker of AKI is discussed in light of emerging data showing a strong predictive value of AKI progression, particularly in the setting of decompensated heart failure. The prognostic significance of urinary angiotensinogen as an AKI biomarker strongly suggests a role for renin–angiotensin system activation in modulating the severity of AKI and its outcomes.