Understanding urine output in critically ill patients

Acute renal failure or acute kidney injury (AKI) is defined by an acute decline of glomerular filtration rate (GFR). Occurrence of AKI is associated with substantial in-hospital mortality, exceeding 50% when AKI is part of a multiple organ failure syndrome [1,2]. Therefore, early recognition of AKI, better understanding of its pathogenesis, and development of preventing strategies appear to be potential areas of improvement of patient's prognosis. The decrease of glomerular filtration rate and urine output in response to a decrease of renal blood flow is classically referred as pre-renal azotemia, which can evolve into structural damage if renal hypoperfusion persists. In this line, urine output often is used as a marker of AKI but also to guide fluid resuscitation in critically ill patients. However, both the contribution of renal hypoperfusion to AKI and the genuine definition of pre-renal and intra-renal azotemia have been challenged by several authors [3-5]. The recent international consensus conference on acute renal failure therefore recommended the term "acute kidney insufficiency" rather than "acute kidney injury" in the light of paucity of evidence of a relation between tissue damage and organ failure in human AKI [6]. The purpose of this review is to discuss the mechanism of diuresis regulation and the interpretation of urine output in critically ill patients in the light of clinical and physiological studies.There is accumulating evidence that critically ill patients developing AKI have an increase relative risk of death. Occurrence of AKI is a marker of severity of the underlying acute illness but also appears as an independent factor associated with mortality in unselected critically ill patients [7], in sepsis [8], pneumonia [9], or cardiac surgery [10]. The mechanistic pathways of such an association remain elusive, with intrication of inflammation, metabolism, and apoptotic phenomena. Remote organs damage has been suggested in several experimental st