The meaning of transient azotemia

Acute kidney injury (AKI) is common in hospitalized patients and its associated mortality is high. The causes of AKI are commonly divided into 3 groups: pre-renal, intra-renal, and post-renal. According to this paradigm, pre-renal azotemia (PRA) represents a separate entity characterized by a rapidly reversible increase in serum creatinine and urea concentration. This rapid reversibility is believed to reflect a functional reduction in glomerular filtration rate as opposed to established structural kidney injury, which leads to acute tubular necrosis (ATN). This PRA vs. ATN paradigm is well established in the medical and renal literature and widely discussed in textbooks. However, there is no consensus definition for PRA or ATN. The typical description for PRA in the literature is 'reversible increase in serum creatinine and urea concentrations', 'characterized by intact renal parenchymal function but renal hypoperfusion'. Therefore, although the term PRA implies that it is defined histopathologically, it also contains a functional aspect (transient azotemia, TA). Early recognition of PRA or ATN is considered important because PRA can be reversed with fluid resuscitation, but such treatment causes edema in lungs as well as other tissues and therefore can be harmful in ATN. However, evidence suggests that PRA cannot be diagnosed prospectively and is clinically the same as TA, that urinary analysis and biochemistries cannot distinguish PRA and ATN in septic AKI, and that ATN is histologically uncommon in septic AKI. Recent observational studies also found that TA cannot be distinguished from ATN epidemiologically and that the existence of TA is related to high hospital mortality. These findings suggest the need for specific and focused investigations directed at identifying effective treatments to decrease the incidence of TA in hospitalized patients.