Admission serum sodium and potassium levels predict survival among critically ill patients with acute kidney injury: a cohort study.

BACKGROUND: Patients suffering from acute kidney injury (AKI) were associated with impaired sodium and potassium homeostasis. We aimed to investigate how admission serum sodium and potassium independently and jointly modified adverse clinical outcomes among AKI patients. METHODS: Patient data were extracted from the Multiparameter Intelligent Monitoring in Intensive Care Database III. Participants were categorized into three groups according to admission serum sodium and potassium, and the cut-off values were determined using smooth curve fitting. The primary outcome was 90-day mortality in the intensive care unit (ICU). Cox proportional hazards models were used to evaluate the prognostic effects of admission serum sodium and potassium levels. RESULTS: We included 13,621 ICU patients with AKI (mean age: 65.3 years; males: 55.4%). The middle category of admission serum sodium and potassium levels were 136.0-144.9 mmol/L and 3.7-4.7 mmol/L through fitting smooth curve. In multivariable Cox models, compared with the middle category, patients with hyponatremia or hypernatremia were associated with excess mortality and the HRs and its 95%CIs were 1.38 (1.27, 1.50) and 1.56 (1.36, 1.79), and patients with either hypokalemia or hyperkalemia were associated with excess mortality and the hazard ratios (HRs) and its 95% confidential intervals (95% CIs) were 1.12 (1.02, 1.24) and 1.25 (1.14, 1.36), respectively. Significant interactions were observed between admission serum sodium and potassium levels (P interaction = 0.001), with a higher serum potassium level associated with increased risk of 90-day mortality among patients with hyponatremia, whereas the effects of higher sodium level on prognostic effects of potassium were subtle. CONCLUSIONS: Admission serum sodium and potassium were associated with survival in a U-shaped pattern among patients with AKI, and hyperkalemia predict a worse clinical outcome among patients with hyponatremia.

Prognostic value of platelet-to-lymphocyte ratios among critically ill patients with acute kidney injury.

BACKGROUND: Inflammation plays an important role in the initiation and progression of acute kidney injury (AKI). However, evidence regarding the prognostic effect of the platelet-to-lymphocyte ratio (PLR), a novel systemic inflammation marker, among patients with AKI is scarce. In this study, we investigated the value of the PLR in predicting the outcomes of critically ill patients with AKI. METHODS: Patient data were extracted from the Multiparameter Intelligent Monitoring in Intensive Care Database III version 1.3. PLR cutoff values were determined using smooth curve fitting or quintiles and were used to categorize the subjects into groups. The clinical outcomes were 30-day and 90-day mortality in the intensive care unit (ICU). Cox proportional hazards models were used to evaluate the association between the PLR and survival. RESULTS: A total of 10,859 ICU patients with AKI were enrolled. A total of 2277 thirty-day and 3112 ninety-day deaths occurred. A U-shaped relationship was observed between the PLR and both 90-day and 30-day mortality, with the lowest risk being at values ranging from 90 to 311. The adjusted HR (95% CI) values for 90-day mortality given risk values < 90 and > 311 were 1.25 (1.12-1.39) and 1.19 (1.08-1.31), respectively. Similar trends were observed for 30-day mortality or when quintiles were used to group patients according to the PLR. Statistically significant interactions were found between the PLR and both age and heart rate. Younger patients (aged < 65 years) and those with more rapid heart rates (≥89.4 beats per minute) tended to have poorer prognoses only when the PLR was < 90, whereas older patients (aged ≥ 65 years) and those with slower heart rates (<89.4 beats per minute) had higher risk only when the PLR was > 311 (P < 0.001 for age and P < 0.001 for heart rate). CONCLUSIONS: The preoperative PLR was associated in a U-shaped pattern with survival among patients with AKI. The PLR appears to be a novel, independent prognostic marker of outcomes in critically ill patients with AKI.

Metabolic Acidosis in Critically Ill Cirrhotic Patients with Acute Kidney Injury.

Background and Aims: The metabolic acid-base disorders have a high incidence of acute kidney injury (AKI) in critically ill cirrhotic patients (CICPs). The aims of our study were to ascertain the composition of metabolic acidosis of CICPs with AKI and explore its relationship with hospital mortality. Methods: Three-hundred and eighty consecutive CICPs with AKI were eligible for the cohort study. Demographic, clinical and laboratory parameters were recorded and arterial acid-base state was analyzed by the Stewart and Gilfix methodology. Results: Net metabolic acidosis, lactic acidosis, acidosis owing to unmeasured anions, acidemia, and dilutional acidosis were less frequent in the non-survival group compared to the survival group of CICPs. The presence of acidemia, acidosis owing to unmeasured anions, and lactic acidosis were independently associated with increased risk of intensive care unit 30-day mortality, with hazard ratios of 2.11 (95% confidence interval (CI): 1.43-3.12), 3.38 (95% CI: 2.36-4.84), and 2.16 (95% CI: 1.47-3.35), respectively. After full adjustment for confounders, the relationship between acidosis owing to unmeasured anions with hospital mortality was still significant, with hazard ratio of 2.29 (95% CI: 1.22-4.30). Furthermore, arterial lactate concentration in combination with chronic liver failure-sequential organ failure assessment and BEUMA had the strongest ability to differentiate 30-day mortality (area under the receiver operating characteristic curve: 0.79, 95% CI: 0.74-0.83). Conclusions: CICPs with AKI exhibit a complex metabolic acidosis during intensive care unit admission. Lactic acidosis and BEUMA, novel markers of acid-base disorders, show promise in predicting mortality rate of CICPs with AKI.

Serum lactate level accurately predicts mortality in critically ill patients with cirrhosis with acute kidney injury.

BACKGROUND AND AIM: Serum lactate levels are routinely measured in critically ill patients with cirrhosis, and hyperlactatemia is a common finding, but its prognostic value remains controversial. Our aim was to examine whether serum lactate level could be used as a predictor of outcome in critically ill patients with cirrhosis (CICP) with acute kidney injury (AKI). PATIENTS AND METHODS: In this study, we included 480 consecutive patients with cirrhosis admitted to ICU, complicated with AKI, and were followed up for 365 days. Patients were divided into four groups (Q1-Q4) by serum lactate quartiles: Q1≤1.8 mg/dl, Q2=1.9-2.4 mg/dl, Q3=2.5-4.0 mg/dl, and Q4≥4.1 mg/dl. The hazard ratio (HR) and 95% confidence intervals (CIs) for hospital mortality were calculated across each quartile of serum lactate, using the Q1 as reference, and four models were built to adjust for the HR of mortality. RESULTS: Compared with patients in the survival group, nonsurvivors had higher serum lactate levels. Mortality rate increased progressively as the serum lactate level increased (Q1: 56.06%, Q2: 62.16%, Q3: 72.73% and Q4: 75.86%), and this relationship remained statistically significant after rigorous control of confounding factors in Q2, Q3, and Q4 with HRs of 1.03 (95% CI: 0.73-1.46), 1.40 (95% CI: 1.01-1.95), and 1.84 (95% CI: 1.28-2.64), respectively. CONCLUSION: Our study brings a new perspective to the role of lactate monitoring in CICP with AKI. Elevated serum lactate levels are associated with a higher mortality rate in CICP with AKI. Elevated serum lactate levels should be part of rapid diagnosis and initiation of therapy to improve clinical outcome.

AKI-CLIF-SOFA: a novel prognostic score for critically ill cirrhotic patients with acute kidney injury.

Critically ill cirrhotic patients with acute kidney injury (AKI) are associated with high mortality rates. The aims of this study were to develop a specific prognostic score for critically ill cirrhotic patients with AKI, the acute kidney injury - Chronic Liver Failure - Sequential Organ Failure- Assessment score (AKI-CLIF-SOFA) score. This study focused on 527 cirrhotic patients with AKI admitted to intensive care unit and constructed a new scoring system, the AKI-CLIF-SOFA, which can be used to prognostically assess mortality in these patient population. Parameters included in this model were analysed by cox regression. The area under the receiver operating characteristic curve (auROC) of AKI-CLIF-SOFA scoring system was 0.74 in 30 days, 0.74 in 90 days, 0.72 in 270 days and 0.72 in 365 days. Additionally, this study demonstrated that the new model had more discriminatory power than chronic liver failure- sequential organ failure assessment score (CLIF-SOFA), SOFA, model for end stage liver disease (MELD), kidney disease improving global outcomes (KDIGO) and simplified acute physiology score II (SAPS II) (auROC: 0.72, 0.66, 0.64, 0.62, 0.63 and 0.65 respectively, all P < 0.05) for the prediction of the 365-days mortality. Therefore, AKI-CLIF-SOFA demonstrated a valuable discriminative ability compared with KDIGO, CLIF-SOFA, MELD, SAPS II and SOFA in critically ill cirrhotic patients with AKI.

Remodeling the model for end-stage liver disease for predicting mortality risk in critically ill patients with cirrhosis and acute kidney injury.

Serum creatinine measurement demonstrates a poor specificity and sensitivity for the early diagnosis of acute kidney injury (AKI) in patients with cirrhosis. The existing model for end-stage liver disease (MELD) score reveals multiple pitfalls in critically ill patients with cirrhosis and acute kidney injury (CAKI). The aim of this study was to re-evaluate the role of creatinine values in the existing MELD score and to develop a novel score for CAKI, named the "acute kidney injury-model for end-stage liver disease score" (AKI-MELD score). We extracted 651 CAKI from the Multiparameter Intelligent Monitoring in Intensive Care database. A time-dependent Cox regression analysis was performed for developing remodeled MELD scores (Reweight-MELD score, Del-Cr-MELD score, and AKI-MELD score). The area under the receiver operating characteristic curve provided the discriminative power of scoring models related to outcome. The hazard ratio of creatinine was 1.104 (95% confidence interval [CI], 0.945-1.290; P = 0.211). Reweight-MELD score and Del-Cr-MELD score (decreasing the weight of creatinine) were superior to the original MELD score (all P < 0.001). The new AKI-MELD score consists of bilirubin, the international normalized ratio, and the ratio of creatinine in 48 hours to creatinine at admission. It had competitive discriminative ability for predicting mortality (area under the receiver operating characteristic curve, 0.720 [95% CI, 0.653-0.762] at 30 days, 0.688 [95% CI, 0.630-0.742] at 90 days, and 0.671 [95% CI, 0.612-0.725] at 1 year). Further, AKI-MELD score had significantly higher predictive ability in comparison with MELD score, MELD-Na score, and Updated MELD score (all P < 0.001). Conclusion: The predictive value of creatinine for CAKI should be re-evaluated. AKI-MELD score is a potentially reliable tool to determine the prognosis for mortality of CAKI. (Hepatology Communications 2017;1:748-756).