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Sepsis is life-threatening organ dysfunction caused by dysregulated body response to an infection. Mortality rate ranging over 60% for septic shock. AKI is final common pathway of this immune dysregulation leading to systemic inflammation (SI) due to uncontrolled circulating levels of pro-inflammatory mediators and cytokine induced direct organ damage. KRT is often required in SA-AKI and could improve SI removing pathogens and inflammatory factors. Various blood purification techniques have been used: HCO/MCO membranes, hemoperfusion, plasma filtration/adsorption and, anecdotal, Hemo Filtrate Reinfusion Supra (HFR): endogenous reinfusion HDF based on adsorbing resin cartridge that remove cytokines and pro-inflammatory mediators whose full spectrum is not yet know and also myoglobin. Aim of this study is to test HFR on outcome of SA-AKI in critically ill patients (pts).
In a retrospective observational study we evaluated development of AKI requiring KRT in 10 consecutive SA-AKI pts admitted in the ICU of our two hospitals from December 2022 to July 2023. ESKD pts in chronic dialysis are excluded. SA-AKI were treated with daily HFR. Given the laboratory operating standards they were daily assessed: urea, creatinine, C-reactive protein (CRP), procalcitonin (PCT), WBC, platelets (PLT), myoglobin, albumin. Mean arterial pressure (MAP), need for vasopressor, and outcome are also evaluated. The values have been reported as mean ±SD or median and interquartile range. AKI was defined according to KDIGO. Statistical analysis were performed with the Wilcoxon Signed Rank Test
Among the 10 pts 7 had AKI III stage. The mean age was 76 ± 9,4 years, 6 were male. 90% were hypertensive, some with heart disease; 50% with CKD (70% G3-KDIGO, 30% G2) 30% were obese or with diabetes, 40% with COPD. All received mechanical ventilation and several antibiotics, 80% received amines.
They underwent IRRT by HFR-Supra with an average of 7.3 treatments (range 2-16 sessions); Qb= 230 ±18.8 ml/m, TT 228.7 ±27.7m'. UF 404 ± 121ml/h. HFR confirm an expected reduction for urea and creatinin, significant abatement of CRP, PCT and Myoglobin. Albumin remain stable. Neutral is the effect on WBC and PLT. Cardiovascular instability decreased significantly with the treatments allowing the suspension of vasoactive amines, as shown by the significant increase in MAP (Tab. 1). None of those undergoing HFR had poor intradialytic compliance. Three patients did not survive (two had surgical complications and one pulmonary), 5 patients had renal recovery, 2 patients had chronic dialysis.
Conclusions
Our experience with HFR may promote a new strategy to decrease SI and support renal recovery in SA-AKI pts even in the not survived. The adsorbing resin is able to efficacy remove proinflammatory cytokines and many other unknow mediators, that lead to improved MAPs and lower critical illness scores, and allow to eliminate myoglobin too. Indeed there is no study on the use of HFR in SA-AKI and very few experience on his use to hypermyoglobinemia.
Finally HFR is the safe and the cheapest technique for SA-AKI in comparison to the other techniques available (e.g. CRRT, HCO, Cytosorb) by excellent cost-effectiveness-sustainability ratio regarding treatment times and staff-sparing. Larger studies could confirm our evidence but, in the meantime, our cases could help to build a new scientific evidence.