Can we identify prerenal physiology and does it matter?

The classic concept of 'prerenal azotemia' is an entity not well diagnosed in the clinic as it is mainly the time evolution that confirms the absence of renal injury. However, this entity seems to be associated with a worse prognosis compared to patients with normal kidney function. In intensive care unit (ICU) patients, this entity results from the interaction with outside factors, renal hypoxia and cellular infiltration by immune cells. The mechanism of such an entity may result from perfusion abnormalities, but more importantly from an oxygenation deficit. This syndrome can be seen as the first step in a continuum from adapted renal function to the occurrence of renal injury. Early renal hemodynamics might be important for predicting the occurrence of AKI. However, the paradigm of renal ischemia as a major mechanism is associated with microcirculation alteration and immune cell infiltration in the generation of AKI. Because creatinine elevation is delayed from renal injury, early detection might help in deciding on the therapeutic strategy. To achieve such a goal, the development of biomarkers for renal injury might be helpful. Some molecules such as NGAL, kidney injury molecule-1, interleukin-18 and cystatin have been proposed and validated as predictors of renal injury in clinical contexts. Although controversial results have been published, most of the results demonstrate a normal level in the presence of prerenal azotemia compared to AKI, limiting their interest for prediction. Importantly, clusters of proteome in urine might improve the sensitivity and specificity to predict AKI in presence of prerenal azotemia.