Urine output (UO) is a major clinical sign, available at the bedside for all patients, all over the world. Currently, oliguria is defined according to the KDIGO guidelines as a UO < 0.5 mL/kg/h over 6 h. The threshold was originally selected by expert consensus and has since been associated with adverse outcomes, although the optimal cut-off remains uncertain, and its bedside relevance is regularly challenged by clinicians. Observational studies have suggested that transient or mild oliguria may not consistently be associated with adverse outcomes. Indeed, mild oliguria may capture episodes of physiological water retention rather than pathological kidney injury with structural damage. However, oliguria remains one of the main triggers for fluid or diuretic administration in intensive care units.

Improving the understanding of oliguria at the bedside and its influence on clinical decisions requires a thorough knowledge of the physiological mechanisms underlying urine formation and the pathophysiology of oliguria. In this review, we describe the process of urine formation and explain the different physiological and pathological mechanisms leading to oliguria. We further discuss how pathological and physiological oliguria can be differentiated at the bedside, highlighting the role of clinical tools, biomarkers and imaging techniques. Finally, we examine how this distinction may inform clinical decision making and guide interventions.