Background: To compare the predictors In-hospital mortality of patients with septic Acute Kidney Injury (S-AKI) and non-septic AKI (NS-AKI). Methods: a cohort study of critically ill patients with AKI admitted to the emergency room at a tertiary hospital from January to June 2019. The primary outcome was hospital mortality. Results: There were 116 patients who met the inclusion criteria. Compared with NS-AKI, patients with S-AKI had significantly lower mean MAP, median eGFR, and urine output. (UO). S-AKI had higher mortality and vasopressor requirements and had a lower renal recovery than NS-AKI (63.2% vs 31.4%, p=0.001; 30.8% vs 13.7%, p=0.031, and 36.9% vs 60.8%, p=0.011, respectively). AKI stage 3 and vasopressor requirements were dependent risk factors for both S-AKI and NS-AKI mortality. Meanwhile, SOFA score > 7 and the need for dialysis are dependent and independent risk factors for mortality in S-AKI. Worsening and/or persistence in UO, serum urea and creatinine levels at 48 h after admission were predictors of mortality in S-AKI and NS-AKI. Improvement in UO in surviving patients was more pronounced in S-AKI than in NS-AKI (50% vs 17.1%, p=0.007). The surviving S-AKI patients had a longer hospital stay than surviving NS-AKI [8 (6-14.5) vs 5 (4 – 8), p=0.004]. S-AKI have higher mortality and vasopressor requirements and have lower renal recovery than NS-AKI. Conclusion: S-AKI have higher mortality and vasopressor requirements and a lower renal recovery than NS-AKI. Independent predictors of mortality in S-AKI were high SOFA scores and the need for dialysis.

Hepatic encephalopathy (HE) is brain dysfunction manifested as a broad spectrum of neuropsychiatric abnormalities caused by hepatic insufficiency or portosystemic shunting due to portal hypertension. Portal hypertension in liver cirrhosis also causes ascites, as the most common clinical manifestation. Further, immune dysfunction, one of which is decreased total lymphocyte count (TLC), happens at liver cirrhosis, which triggers the systemic inflammatory response. This systemic inflammatory response plays a role in HE. Objective of this study is to know the correlation between ascites and TLC with occurence of HE in liver cirrhosis patient. This study was conducted by retrospective cohort design in Saiful Anwar Hospital. Determination of sample amount at this study used total sampling method. Hepatic encephalopathy diagnosis was based on West Haven Criteria. Ascites was determined by physical examination and/or abdominal ultasonography. Total lymphocyte count data was taken from medical record, with complete blood count examination used XS-800i hematology analyzer machine. Data were analyzed using a logistic regression test, with p&lt;0.05 was considered significant and Confidence Interval (CI) 95%. Seventy-eight liver cirrhosis patients were observed using a retrospective cohort method regarding the HE occurrence, and physical examination for ascites and laboratory examination were performed. The statistical analysis result of the correlation between ascites and HE is significant with an odds ratio of 5.108 and CI of 1.36-19.25. On the other hand, TLC has no significant correlation with the occurrence of HE. Based on this analysis result, it is concluded that ascites has a correlation with HE, but TLC does not.<p> </p>

Background: To compare the predictors In-hospital mortality of patients with septic Acute Kidney Injury (S-AKI) and non-septic AKI (NS-AKI). Methods: a cohort study of critically ill patients with AKI admitted to the emergency room at a tertiary hospital from January to June 2019. The primary outcome was hospital mortality. Results: There were 116 patients who met the inclusion criteria. Compared with NS-AKI, patients with S-AKI had significantly lower mean MAP, median eGFR, and urine output. (UO). S-AKI had higher mortality and vasopressor requirements and had a lower renal recovery than NS-AKI (63.2% vs 31.4%, p=0.001; 30.8% vs 13.7%, p=0.031, and 36.9% vs 60.8%, p=0.011, respectively). AKI stage 3 and vasopressor requirements were dependent risk factors for both S-AKI and NS-AKI mortality. Meanwhile, SOFA score > 7 and the need for dialysis are dependent and independent risk factors for mortality in S-AKI. Worsening and/or persistence in UO, serum urea and creatinine levels at 48 h after admission were predictors of mortality in S-AKI and NS-AKI. Improvement in UO in surviving patients was more pronounced in S-AKI than in NS-AKI (50% vs 17.1%, p=0.007). The surviving S-AKI patients had a longer hospital stay than surviving NS-AKI [8 (6-14.5) vs 5 (4 – 8), p=0.004]. S-AKI have higher mortality and vasopressor requirements and have lower renal recovery than NS-AKI. Conclusion: S-AKI have higher mortality and vasopressor requirements and a lower renal recovery than NS-AKI. Independent predictors of mortality in S-AKI were high SOFA scores and the need for dialysis.