#4720 SEPSIS, AKI AND MORTALITY. SEARCHING FOR NEW MARKERS: OUR EXPERIENCE WITH ENDOGENOUS OUABAIN

Abstract

Abstract Background and Aims Sepsis and septic shock are quite common events in the hospital setting. The classification of these events has changed a lot over the years, to ensure better sensitivity in recognizing a situation that, if not managed properly and quickly, leads to the death of the patient. In our study we focused on the search for predictors of acute kidney injury and mortality during the evolution of this pathology, with particular attention to the role of the Endogenous Ouabain hormone. Method We enrolled 177 patients diagnosed with sepsis or septic shock, under an ordinary hospital stay. We standardized patients according to the latest classification criteria (Sepsis-III), we focused our attention specifically on SOFA score and the relationship with acute kidney injury and mortality, including its relationship with other laboratory parameters, especially lactates. In a subgroup of patients was also dosed the level of Endogenous Ouabain (EO - hormone produced by the adrenal glands but which has an important impact on renal hemodynamics), through a venous sampling in 3 different times (at the beginning of the septic state, 24 and 48 hours later). Subsequently the variation of EO and the correlation with laboratory parameters was investigated in this period, to assess its impact on the development of kidney damage and mortality. Results The 70.1% of septic patients in our study develop AKI and, of this percentage, 75% in a severe form (stage 2-3 KDIGO). Both the presence and severity of AKI are unable to predict mortality in our sample (p-value 0.13). The presence of an impaired hemodynamics status (expressed ad MAP < 70 mmHg) has a strong impact in the severe stages of AKI but not in the mild form (p-value 0.006; ExpB 1.81 vs p-value 0.105; ExpB 1.46). The other elements related to the development of AKI were found to be the high levels of white blood cells, respiratory distress and the SOFA value at the presentation, while we found no correlation with CRP and lactate levels. Lactate levels well correlate with SOFA (p-value <0.0001 and Pearson's index 0.407) and mortality, particularly when the initial values are > 2mg/dL (p < 0.0001; ExpB 5.31, IC95% [2.07-13.57]). In the subgroup of patients in which EO was dosed, there was a strong correlation of the basal levels of this hormone with mortality even after correction for lactate levels and SOFA (p-value 0.009) but not with the development of AKI. However, patients in AKI stage-3 show persistently higher levels of EO both at 24 and 48 h (p = 0.015). Conclusion The presence of high levels of lactates at the onset is the most important predictor of mortality, followed by EO levels at presentation and the SOFA value. Elevation of Endogenous Ouabain levels is indicative of an acute state of stress but is not a parameter influenced by the SOFA score, nor by the general condition of patient. It seems non directly related with the development of AKI, tissue hypoperfusion or activation of the inflammatory response but is associated with an inability to rapidly recover renal function. The EO could be very useful in predicting mortality in patients with sepsis and septic shock as it seems to be an earlier, more specific, and sensitive than the other laboratory parameters used so far.