Acute kidney injury (AKI) is a major complication of critical illness [1] occurring in 30 to 40 % of all critically ill patients and in its sev ere form requires renal replacement therapy (RRT), in approximately 5 % of patients [2]. AKI has been s hown to be an independent predictor for mortality [3] and is associated with invasive therapy and substantial costs [4].Despite its impor tance, the pathoph ysiology of AKI is still poorly understood. AKI is most commonly associated with systemic diseases, such as septic shock, major surgery and cardiogenic shock [1], but a specifi c mechanism causing AKI to develop in specifi c patients can rarely be determined. Since the early description of an "acute uremia syndrome" in crush injury victims during World War II [5,6] and its association with histopathological fi ndings similar to those found in experimental renal artery ligation, ischemia or some form of alteration in renal blood fl ow has been thought to play a pivotal role in the pathogenesis of AKI. Th is paradigm that essentially all AKI in critically ill patients is the result of some form or degree of ischemia remains of continuing conceptual dominanc e to this day [7]. Despite such dominance, there are only very limited data supporting this concept. In a recent systematic review, Prowle et al. [8] highlighted the extraordinary fact that renal blood fl ow measurement, irrespective of the technique used, has only been reported in 46 critically ill patients (fi ve studies) within the last sixty years. Th us, our knowledge, understanding, and theoretical constructs regarding global renal perfu sion in critically ill patients with RRT-treated AKI (an estimated 5 % of all ICU admissions for a total of approximately a quarter of a million such patients each year in developed countries alone) is, like an inverted pyramid, based on extremely weak evidence.Furthermore, given the complex and heterogeneous nature of the renal vasculature, evaluating the fl ow in the main renal arteries (macrocirculation) might not provide suffi cient information to adequately understand perfusion alterations in complex diseases, such as septic or cardio genic shock. Indeed, some pathophysiological processes may be associated with increased global renal blood fl ow [9,10] despite loss of f un ction. In such instances, there is experimental evidence that, at least in sepsis, this phenomenon may be caused by intra-renal shunting [11]. Hence, correlation between macroscopic renal blood fl ow and function is far from linear. Th erefore, techniques allowing the study of microcircu latory parameters, such as cortico-med ullary perfusion ratio and regional tissue oxygenation measurement, and assessment of their relative change over time may be more valuable in increasing our understanding of the pathophysiology of AKI.In this state-of-the art review, we discuss the value, challenges, limitations, safety and feasibility of diff erent techniques for the measurement of kidney perfusion in critically ill patients. Th e advantages of each technique wi...