Abstract
Urinary sodium (NaU) is one of the oldest parameters used in the evaluation of azotemia and oliguria. Over the past years, however, it has progressively been considered as obsolete and useless, especially in sepsis. It is common sense that NaU frequently does not correlate well with global renal blood flow. If intrarenal microcirculatory changes are more important in acute kidney injury (AKI) than changes in global renal blood flow, we speculate that decreases in NaU may be viewed as a possible marker of microcirculatory impairment in the kidneys. Recent findings by our group (some not yet published) in which sodium retentive capacity is preserved until advanced stages of AKI and the observation of decreases in NaU preceding increases in creatinine bring us to conclude that the new paradigm of abolishing NaU consideration from daily approaches to managing patients at risk for AKI must be reevaluated.