Creatinine-lactate score predicts mortality in non-acetaminophen-induced acute liver failure in patients listed for liver transplantation

Figueira, Estela Regina Ramos; Rocha-Filho, Joel Avancini; Lanchotte, Cinthia; Nacif, Lucas Souto; Haddad, Luciana Bertocco de Paiva; Assalin, Adriana Rochetto; Shinkado, Yumi Ricucci; Vintimilla, Agustín; Galvão, Flávio Henrique Ferreira; D’Albuquerque, Luiz Augusto Carneiro

doi:10.1186/s12876-021-01830-5

Cited by 4 publications

(4 citation statements)

References 43 publications

(68 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Martín et al [ 3 ] reported an AUC of 0.867 for 2-day mortality. Figueira et al [ 24 ] developed a score for use in patients listed for liver transplantation (including lactate and creatinine), with an AUC of 0.835 to detect in-hospital mortality. By the same way, pCO 2 has been used in several scores.…”

Section: Discussionmentioning

confidence: 99%

Derivation and validation of a blood biomarker score for 2-day mortality prediction from prehospital care: a multicenter, cohort, EMS-based study

et al. 2023

View full text Add to dashboard Cite

Identifying potentially life-threatening diseases is a key challenge for emergency medical services. This study aims at examining the role of different prehospital biomarkers from point-of-care testing to derive and validate a score to detect 2-day in-hospital mortality. We conducted a prospective, observational, prehospital, ongoing, and derivation—validation study in three Spanish provinces, in adults evacuated by ambulance and admitted to the emergency department. A total of 23 ambulance-based biomarkers were collected from each patient. A biomarker score based on logistic regression was fitted to predict 2-day mortality from an optimum subset of variables from prehospital blood analysis, obtained through an automated feature selection stage. 2806 cases were analyzed, with a median age of 68 (interquartile range 51–81), 42.3% of women, and a 2-day mortality rate of 5.5% (154 non-survivors). The blood biomarker score was constituted by the partial pressure of carbon dioxide, lactate, and creatinine. The score fitted with logistic regression using these biomarkers reached a high performance to predict 2-day mortality, with an AUC of 0.933 (95% CI 0.841–0.973). The following risk levels for 2-day mortality were identified from the score: low risk (score < 1), where only 8.2% of non-survivors were assigned to; medium risk (1 ≤ score < 4); and high risk (score ≥ 4), where the 2-day mortality rate was 57.6%. The novel blood biomarker score provides an excellent association with 2-day in-hospital mortality, as well as real-time feedback on the metabolic-respiratory patient status. Thus, this score can help in the decision-making process at critical moments in life-threatening situations.

show abstract

Section: Discussionmentioning

confidence: 99%

Derivation and validation of a blood biomarker score for 2-day mortality prediction from prehospital care: a multicenter, cohort, EMS-based study

et al. 2023

View full text Add to dashboard Cite

show abstract

“…However, low serum concentrations of creatinine were observed in severe hepatic failure patients like fulminant hepatitis ( Takabatake et al, 1988 ). Some reports showed that the creatinine-lactate score could predict the mortality of acute liver failure in patients listed for liver transplantation ( Figueira et al, 2021 ). While the role of creatinine in drug-induced liver injury is unclear.…”

Section: Discussionmentioning

confidence: 99%

Creatinine accelerates APAP-induced liver damage by increasing oxidative stress through ROS/JNK signaling pathway

Liu

Peng

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

Serum creatinine is an endogenous biomarker to estimate glomerular filtration rate (GFR) and is commonly used to assess renal function in clinical practice. Acetaminophen (APAP), the most available analgesic and antipyretic medication, is recommended as the drug of choice for pain control in patients with renal diseases. However, an overdose of APAP can lead to severe acute liver injury, which is also the most common cause of acute liver failure in western countries. The role of creatinine in APAP-induced liver injury is unclear and should be further explored. Herein, clinical data on patients with drug-induced liver injury revealed that the creatinine concentration between 82-442 μmol/L for female and 98–442 μmol/L for male is positively correlated with alanine aminotransferase (ALT), aspartate aminotransferase (AST). While there was no correlation between creatinine and ALT and AST when creatinine concentration is over 442 μmol/L. In addition, mice were administrated with creatinine intraperitoneally for 1 week before APAP injection to investigated the pathophysiological role of creatinine in APAP-induced acute liver injury. The results showed that creatinine administration aggravated hepatic necrosis and elevated serum lactate dehydrogenase (LDH) and ALT levels in mice upon APAP injection. The mechanism study demonstrated that creatinine could increase the production of reactive oxygen activation (ROS) and the activation of c-Jun N-terminal kinase (JNK). Furthermore, the liver injury was alleviated and the difference between APAP-treated mice and APAP combined with creatinine-treated mice was blunted after using specific ROS and JNK inhibitors. Significantly, creatinine stimulation aggravates APAP-induced cell death in HepaRG cells with the same mechanism. In summary, this study proposed that creatinine is closely related with liver function of drug-induced liver injury and exacerbates APAP-induced hepatocyte death by promoting ROS production and JNK activation, thus providing new insight into the usage of APAP in patients with kidney problems.

show abstract

“…85 The addition of lactate to bilirubin and etiology to create the Bilirubin Lactate and Etiology score, 86 as well as lactate when combined with creatinine may predict mortality better than MELD but has yet to be validated. 87 The Acute Physiology and Chronic Health Evaluation score has also been applied. 88 Another more recent scoring system, the ALF early dynamic model, utilizes changes in ammonia, bilirubin, INR, and stage of encephalopathy over 3 days to predict outcomes more accurately.…”

Section: Prognostic Scoringmentioning

confidence: 99%

Section: Section Iii: Prognostic Scoring and Liver Transplantation Fo...mentioning

confidence: 99%

Management of Acute Liver Failure: Update 2022

2022

View full text Add to dashboard Cite

Abbreviated pathogenesis and clinical course of the acute liver failure syndrome. The pathogenesis and clinical course of the syndrome of acute liver failure (ALF) differs depending upon the etiology of the primary liver injury. In turn, the severity of the liver injury and resulting synthetic failure is often the primary determinant of whether a patient is referred for emergency liver transplantation. Injuries by viral etiologies trigger the innate immune system via pathogen-associated molecular patterns (PAMPs), while toxin-induced (and presumably ischemia-induced) injuries do so via damage-associated molecular patterns (DAMPs). The course of the clinical syndrome further depends upon the relative intensity and composition of cytokine release, resulting in an early proinflammatory phenotype (SIRS) and later compensatory anti-inflammatory response phenotype (CARS). The outcomes of overwhelming immune activation are the systemic (extrahepatic) features of ALF (cardiovascular collapse, cerebral edema, acute kidney injury, respiratory failure, sepsis) which ultimately determine the likelihood of death.Acute liver failure (ALF) continues to carry a high risk of mortality or the need for transplantation despite recent improvements in overall outcomes over the past two decades. Optimal management begins with identifying that liver failure is indeed present and its etiology, since outcomes and the need for transplantation vary widely across the different etiologies. Most causes of ALF can be divided into hyperacute (ischemia and acetaminophen) and subacute types (other etiologies), based on time of evolution of signs and symptoms of liver failure; the former evolve in 3 to 4 days and the latter typically in 2 to 4 weeks. Both involve intense release of cytokines and hepatocellular contents into the circulation with multiorgan effects/consequences.Management involves optimizing fluid balance and cardiovascular support, including the use of continuous renal replacement therapy, vasopressors, and pulmonary ventilation. Early evaluation for liver transplantation is advised particularly for acetaminophen toxicity, which evolves so rapidly that delay is likely to lead to death.Vasopressor support, high-grade hepatic encephalopathy, and unfavorable (subacute) etiologies heighten the need for urgent listing for liver transplantation. Prognostic scores such as Kings Criteria, Model for End-Stage Liver Disease, and the Acute Liver Failure Group prognostic index take these features into account and provide reasonable but imperfect predictive accuracy. Future treatments may include liver support devices and/or agents that improve hepatocyte regeneration.

show abstract

Creatinine-lactate score predicts mortality in non-acetaminophen-induced acute liver failure in patients listed for liver transplantation

Cited by 4 publications

References 43 publications

Derivation and validation of a blood biomarker score for 2-day mortality prediction from prehospital care: a multicenter, cohort, EMS-based study

Derivation and validation of a blood biomarker score for 2-day mortality prediction from prehospital care: a multicenter, cohort, EMS-based study

Creatinine accelerates APAP-induced liver damage by increasing oxidative stress through ROS/JNK signaling pathway

Management of Acute Liver Failure: Update 2022

Contact Info

Product

Resources

About