Acute kidney injury (AKI) is a frequent complication of the
systemic inflammatory response syndrome (SIRS), which is triggered by many conditions in the intensive care unit, including different types of circulatory
shock. One under-recognized characteristic of the SIRS-induced AKI is its avidity for
sodium retention, with progressive decreases in urinary
sodium concentration (NaU) and its fractional excretion (FENa). This phenomenon occurs in parallel with increases in serum
creatinine, being only transitorily mitigated by
diuretic use. In the present case, we report a situation of two consecutive shocks: the first
shock is hemorrhagic in origin and then the second
shock is a septic one in the same patient. The SIRS and AKI triggered by the first
shock were not completely solved when the second
shock occurred. This could be viewed as a persistent avid
sodium-retaining state, which may be appreciated even during
renal replacement therapy (in the absence of complete
anuria) and that usually solves only after complete AKI and SIRS resolution. We suggest that decreases in NaU and FENa are major characteristics of SIRS-induced AKI, irrespective of the primary cause, and may serve as additional monitoring tools in its development and resolution.