Dynamics of serum anion gaps with in-hospital mortality: Analysis of the multi-open databases.

BACKGROUND: Few studies have investigated the relationship between the anion gap, including the corrected anion gap, and patient mortality in intensive care units (ICUs) without restricting the analysis to specific diseases or medical specialties. Our primary objective was to investigate the association between the anion gap and ICU mortality using multiple open-access databases. METHODS: We identified 4229 subjects from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database, whose entries were from between 2008 and 2019. For each patient, the anion gap and corrected anion gap were calculated, and the study sample was divided into tertile groups (T) according to these levels. The association between the anion gap and in-hospital mortality was assessed using hazard ratios (HRs) and 95% confidence intervals (CIs) derived from a multivariable-adjusted Cox proportional hazards model. Besides MIMIC-IV, we also incorporated study samples from two other databases (MIMIC-III and electronic ICU) to calculate summary HRs using a random-effects meta-analysis. RESULTS: Within MIMIC-IV, 1015 patients (24%) died during an average follow-up period of 15.5 days. The fully adjusted HRs and 95% CIs for T2 and T3, relative to T1, were 1.31 (95% CI 1.08-1.58) and 1.54 (95% CI 1.24-1.90), respectively. When grouped by corrected anion gap, the results remained statistically significant. In the meta-analysis, the summary HRs and 95% CIs for T2 and T3 were 1.24 (95% CI 1.08-1.43) and 1.55 (95% CI 1.33-1.82), respectively. CONCLUSIONS: Both the anion gap and corrected anion gap were associated with in-hospital mortality regardless of specific diseases or medical specialties.

Relationship between albumin-corrected anion gap and non-alcoholic fatty liver disease varied in different waist circumference groups: a cross-sectional study.

OBJECTIVES: To investigate the association of albumin-corrected anion gap (ACAG) with non-alcoholic fatty liver disease (NAFLD) and clinically significant fibrosis (CSF) defined by vibration-controlled transient elastography measurements. METHODS: This cross-sectional study including 4531 participants was conducted using the data from the NHANES database of cycles 2017-2018. The outcomes were set as NAFLD vs. non-NAFLD and NAFLD with CSF vs. NAFLD without CSF. The generalized additive model and restricted cubic spline analyses were used to assess the nonlinear relationship. The generalized linear models, logistic regression models, sensitivity analysis, P trend test, subgroup analysis, and mediation analysis were employed to analyze the association. Finally, an ACAG-based model was constructed and evaluated. RESULTS: A higher ACAG level was an independent risk factor for NAFLD (P < 0.05), but not for CSF (P > 0.05). The sensitivity analysis and P trend test results substantiated the significantly positive relationship between ACAG and NAFLD (P < 0.05). Interestingly, the obvious connection between ACAG and NAFLD varied in different waist circumference groups and played a central role in the central obesity group. In addition, alanine aminotransferase and waist circumference were the mediators in their relationship. Moreover, the ACAG-based model performed well in predicting NAFLD. CONCLUSIONS: ACAG level is independently associated with NAFLD but not CSF. ACAG might be a novel and reliable biomarker for predicting NAFLD clinically especially in the central obesity population.

State of knowledge on ammonia handling by the kidney.

The disposal of ammonia, the main proton buffer in the urine, is important for acid-base homeostasis. Renal ammonia excretion is the predominant contributor to renal net acid excretion, both under basal condition and in response to acidosis. New insights into the mechanisms of renal ammonia production and transport have been gained in the past decades. Ammonia is the only urinary solute known to be produced in the kidney and selectively transported through the different parts of the nephron. Both molecular forms of total ammonia, NH3 and NH4+, are transported by specific proteins. Proximal tubular ammoniagenesis and the activity of these transport processes determine the eventual fate of total ammonia produced and excreted by the kidney. In this review, we summarized the state of the art of ammonia handling by the kidney and highlighted the newest processes described in the last decade.

Effects of Alterations in Acid-Base Effects on Insulin Signaling.

Insulin tightly regulates glucose levels within a narrow range through its action on muscle, adipose tissue and the liver. The activation of insulin receptors activates multiple intracellular pathways with different functions. Another tightly regulated complex system in the body is acid-base balance. Metabolic acidosis, defined as a blood pH < 7.35 and serum bicarbonate < 22 mmol/L, has clear pathophysiologic consequences including an effect on insulin action. With the ongoing intake of typical acid-producing Western diets and the age-related decline in renal function, there is an increase in acid levels within the range considered to be normal. This modest increase in acidosis is referred to as "acid stress" and it may have some pathophysiological consequences. In this article, we discuss the effects of acid stress on insulin actions in different tissues.

Venous blood gases and electrolyte values of captive red foot tortoise (Chelonoidis carbonarius).

Blood gas analysis reflects the exchange of oxygen and carbon dioxide in the lungs. This test provides important information, since the relationship between these gases has a direct impact on the acid-basic balance in the body. Given the significance of blood gas analysis in Brazilian reptiles, this study set out to establish temperature-corrected and uncorrected reference intervals for venous blood gas measurements in Chelonoidis carbonarius, and to compare values between females and males. In this study, 19 animals were used, 8 males and 11 females. Blood samples were collected from the dorsal coccygeal vein, and the analyses were performed immediately after blood sample collection. The following parameters were measured: pH, PO2, HCO3-, TCO2, BEecf, Na, K, ICa, and Glu, and were compared between females and males. Additionally, pH, pCO2, and pO2 values were compared with and without temperature correction. Oxygen saturation and Na levels were significantly higher (p<0.05) in males. Furthermore, it was possible to infer that the lower the body temperature relative to the environmental temperature, the larger the difference in pH following temperature correction.

Association Between Serum Anion Gap and Mortality in Critically Ill Patients with COPD in ICU: Data from the MIMIC IV Database.

Background: Serum anion gap (AG) has been proven to be associated with prognosis in critically ill patients. However, few studies have investigated the association between AG and all-cause mortality in critically ill patients with chronic obstructive pulmonary disease (COPD). Objective: We hypothesized that the initial AG level would predict the mortality risk in critically ill patients with COPD. Methods: This retrospective cohort study was based on the Medical Information Mart for Intensive Care (MIMIC) IV database. We extracted demographics, vital signs, laboratory tests, comorbidity, and scoring systems from the first 24 hours after patient ICU admission. Multivariable logistic regression analysis models were used to explore the association between serum AG levels and mortality. Interaction and stratified analyses were conducted including age, gender and comorbidity. Results: A total of 5531 critically ill patients with COPD were enrolled, composed of 53.6% male and 46.4% female with a median age of 73 years. The all-cause mortality of these patients during ICU hospitalization was 13.7%. The risk of all-cause mortality increased as the AG level increased in the univariate logistic regression analysis (OR=1.13, 95% CI: 1.11-1.15, p<0.01). After adjusting for all the covariates in multivariate logistic regression analysis, the odds ratio was 1.06 (95% CI: 1.04-1.09, p<0.01). Compared with the lowest AG group Q1 (≤11mmol/L), the adjusted OR value for AG and mortality in Q2 (12-13mmol/L) was 0.89 (95% CI: 0.63-1.25, p=0.502), Q3 (14-15mmol/L) was 0.95 (95% CI: 0.68-1.34, p=0.788), and Q4 (≥16mmol/L) was 1.49 (95% CI: 1.10-2.02, p=0.009) respectively. In addition, the results of the subgroup and stratified analyses were robust. Conclusion: AG is positively related to all-cause mortality in critically ill patients with COPD.

Association between albumin-corrected anion gap and in-hospital mortality of intensive care patients with trauma: A retrospective study based on MIMIC-â ¢ and â £ databases.

BACKGROUND: To investigate the correlation between albumin-corrected anion gap(ACAG) within the first 24 hours of admission and in-hospital mortality in trauma patients in intensive care unit(ICU). MATERIALS AND METHODS: We utilized the MIMIC-Ⅲ and MIMIC-Ⅳ databases to examine trauma patients admitted to the ICU. The relationship between ACAG and in-hospital mortality in trauma patients was analyzed using Receiver Operating Characteristic(ROC) curve, Kaplan-Meier (K-M) survival curve, and Cox regression model. Propensity score matching (PSM) and subgroup analysis were conducted to enhance stability and reliability of the findings. Mortality at 30-day and 90-day served as secondary outcomes. RESULTS: The study enrolled a total of 1038 patients. The AUC for ACAG (0.701, 95%CI: 0.652-0.749) was notably higher than that for anion gap and albumin. The Log-rank test revealed that the optimal cut-off point of ACAG for predicting in-hospital mortality was determined to be 20.375mmol/L. The multivariate Cox regression analysis demonstrated an independent association between high ACAG level and a higher risk of in-hospital mortality (HR = 3.128, 95% CI: 1.615-6.059). After PSM analysis, a matched cohort consisting of 291 subjects was obtained. We found no signifcant interaction in most stratas. Finally, The in-hospital, 30-day, and 90-day survival rates in the high ACAG group exhibited a statistically decrease compared to those in the low ACAG group both pre- and post-matching. CONCLUSION: The elevated level of ACAG was found to be independently associated with increased in-hospital mortality among trauma patients in the ICU.

Association Between Albumin-Corrected Anion Gap and In-Hospital Mortality and Sepsis-Associated Acute Kidney Injury.

BACKGROUND This study aimed to investigate the association between albumin-corrected anion gap (ACAG) and in-hospital mortality in sepsis-associated acute kidney injury (S-AKI). MATERIAL AND METHODS We conducted this retrospective study based on data from the Medical Information Mart for Intensive Care IV database, and assessed the prognostic capabilities of ACAG in comparison with albumin (ALB) and anion gap (AG) to predict in-hospital mortality of patients with S-AKI. Binomial logistic regression analysis was performed to identify whether ACAG was an independent risk factor for in-hospital mortality for the patients, and receiver operating characteristic (ROC) curves were plotted to clarify its efficacy in predicting in-hospital mortality. We also performed a decision curve analysis (DCA) to determine whether there were net clinical benefits for patients when ACAG was used to predict in-hospital mortality. RESULTS Binary logistic regression analysis showed that ACAG was an independent risk factor for in-hospital mortality in patients with S-AKI, with an area under the ROC (AUC) curve of 0.675 (moderate predictive value) for the prediction of in-hospital mortality, higher than that of ALB or AG alone, with the highest Youden's index (0.2675). The DCA substantiated the superiority of ACAG in net clinical benefits at various threshold probability, enhancing its clinical applicability. CONCLUSIONS The research emphasizes the potential of ACAG as a valuable predictive tool for in-hospital mortality in S-AKI patients, which is better than albumin and AG, encouraging its consideration in clinical practice.

Flagellar pH homeostasis mediated by Na+/H+ exchangers regulates human sperm functions through coupling with CatSper and KSper activation.

STUDY QUESTION: Whether and how do Na+/H+ exchangers (NHEs) regulate the physiological functions of human sperm? SUMMARY ANSWER: NHE-mediated flagellar intracellular pH (pHi) homeostasis facilitates the activation of the pH-sensitive, sperm-specific Ca2+ channel (CatSper) and the sperm-specific K+ channel (KSper), which subsequently modulate sperm motility, hyperactivation, flagellar tyrosine phosphorylation, and the progesterone (P4)-induced acrosome reaction. WHAT IS KNOWN ALREADY: Sperm pHi alkalization is an essential prerequisite for the acquisition of sperm-fertilizing capacity. Different sperm functions are strictly controlled by particular pHi regulatory mechanisms. NHEs are suggested to modulate sperm H+ efflux. STUDY DESIGN, SIZE, DURATION: This was a laboratory study that used samples from >50 sperm donors over a period of 1 year. To evaluate NHE action on human sperm function, 5-(N,N-dimethyl)-amiloride (DMA), a highly selective inhibitor of NHEs, was utilized. All experiments were repeated at least five times using different individual sperm samples or cells. PARTICIPANTS/MATERIALS, SETTING, METHODS: By utilizing the pH fluorescent indicator pHrodo Red-AM, we detected alterations in single-cell pHi value in human sperm. The currents of CatSper and KSper in human sperm were recorded by the whole-cell patch-clamp technique. Changes in population and single-cell Ca2+ concentrations ([Ca2+]i) of human sperm loaded with Fluo 4-AM were measured. Membrane potential (Vm) and population pHi were quantitatively examined by a multimode plate reader after sperm were loaded with 3,3'-dipropylthiadicarbocyanine iodide and 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein, acetoxymethyl ester, respectively. Sperm motility parameters were assessed by a computer-assisted semen analysis system. Tyrosine phosphorylation was determined by immunofluorescence, and sperm acrosome reaction was evaluated by Pisum sativum agglutinin-FITC staining. MAIN RESULTS AND THE ROLE OF CHANCE: DMA-induced NHEs inhibition severely acidified the human sperm flagellar pHi from 7.20 ± 0.04 to 6.38 ± 0.12 (mean ± SEM), while the effect of DMA on acrosomal pHi was less obvious (from 5.90 ± 0.13 to 5.57 ± 0.12, mean ± SEM). The whole-cell patch-clamp recordings revealed that NHE inhibition remarkably suppressed alkalization-induced activation of CatSper and KSper. As a consequence, impairment of [Ca2+]i homeostasis and Vm maintenance were detected in the presence of DMA. During the capacitation process, pre-treatment with DMA for 2 h potently decreased sperm pHi, which in turn decreased sperm motility and kinetic parameters. Sperm capacitation-associated functions, including hyperactivation, tyrosine phosphorylation, and P4-induced acrosome reaction, were also compromised by NHE inhibition. LARGE SCALE DATA: N/A. LIMITATIONS, REASONS FOR CAUTION: This was an in vitro study. Caution should be taken when extrapolating these results to in vivo applications. WIDER IMPLICATIONS OF THE FINDINGS: This study revealed that NHEs are important physiological regulators for human CatSper and KSper, which are indispensable for human sperm fertility, suggesting that malfunction of NHEs could be an underlying mechanism for the pathogenesis of male infertility. FUNDING/COMPETING INTEREST(S): This work was supported by the National Natural Science Foundation of China (32271167 and 81871202 to X.Z.), Jiangsu Innovation and Entrepreneurship Talent Plan (JSSCRC20211543 to X.Z.), the Social Development Project of Jiangsu Province (No. BE2022765 to X.Z.), the Society and livelihood Project of Nantong City (No. MS22022087 to X.Z.), and the Natural Science Foundation of Jiangsu Province (BK20220608 to H.K.). The authors have no competing interests to declare.

Quantifying pH-induced changes in plasma strong ion difference during experimental acidosis: clinical implications for base excess interpretation.

It is commonly assumed that changes in plasma strong ion difference (SID) result in equal changes in whole blood base excess (BE). However, at varying pH, albumin ionic-binding and transerythrocyte shifts alter the SID of plasma without affecting that of whole blood (SIDwb), i.e., the BE. We hypothesize that, during acidosis, 1) an expected plasma SID (SIDexp) reflecting electrolytes redistribution can be predicted from albumin and hemoglobin's charges, and 2) only deviations in SID from SIDexp reflect changes in SIDwb, and therefore, BE. We equilibrated whole blood of 18 healthy subjects (albumin = 4.8 ± 0.2 g/dL, hemoglobin = 14.2 ± 0.9 g/dL), 18 septic patients with hypoalbuminemia and anemia (albumin = 3.1 ± 0.5 g/dL, hemoglobin = 10.4 ± 0.8 g/dL), and 10 healthy subjects after in vitro-induced isolated anemia (albumin = 5.0 ± 0.2 g/dL, hemoglobin = 7.0 ± 0.9 g/dL) with varying CO2 concentrations (2-20%). Plasma SID increased by 12.7 ± 2.1, 9.3 ± 1.7, and 7.8 ± 1.6 mEq/L, respectively (P < 0.01) and its agreement (bias[limits of agreement]) with SIDexp was strong: 0.5[-1.9; 2.8], 0.9[-0.9; 2.6], and 0.3[-1.4; 2.1] mEq/L, respectively. Separately, we added 7.5 or 15 mEq/L of lactic or hydrochloric acid to whole blood of 10 healthy subjects obtaining BE of -6.6 ± 1.7, -13.4 ± 2.2, -6.8 ± 1.8, and -13.6 ± 2.1 mEq/L, respectively. The agreement between ΔBE and ΔSID was weak (2.6[-1.1; 6.3] mEq/L), worsening with varying CO2 (2-20%): 6.3[-2.7; 15.2] mEq/L. Conversely, ΔSIDwb (the deviation of SID from SIDexp) agreed strongly with ΔBE at both constant and varying CO2: -0.1[-2.0; 1.7], and -0.5[-2.4; 1.5] mEq/L, respectively. We conclude that BE reflects only changes in plasma SID that are not expected from electrolytes redistribution, the latter being predictable from albumin and hemoglobin's charges.NEW & NOTEWORTHY This paper challenges the assumed equivalence between changes in plasma strong ion difference (SID) and whole blood base excess (BE) during in vitro acidosis. We highlight that redistribution of strong ions, in the form of albumin ionic-binding and transerythrocyte shifts, alters SID without affecting BE. We demonstrate that these expected SID alterations are predictable from albumin and hemoglobin's charges, or from the noncarbonic whole blood buffer value, allowing a better interpretation of SID and BE during in vitro acidosis.

Correlation between urine anion gap and urine ammonia-creatinine ratio in healthy cats and cats with kidney disease.

BACKGROUND: Ammonium excretion decreases as kidney function decreases in several species, including cats, and may have predictive or prognostic value in patients with chronic kidney disease (CKD). Urine ammonia measurement is not readily available in clinical practice, and urine anion gap (UAG) has been proposed as a surrogate test. OBJECTIVES: Evaluate the correlation between urine ammonia-to-creatinine ratio (UACR) and UAG in healthy cats and those with CKD and determine if a significant difference exists between UAG of healthy cats and cats with CKD. ANIMALS: Urine samples collected from healthy client-owned cats (n = 59) and those with stable CKD (n = 17). METHODS: Urine electrolyte concentrations were measured using a commercial chemistry analyzer and UAG was calculated as ([sodium] + [potassium]) - [chloride]. Urine ammonia and creatinine concentrations had been measured previously using commercially available enzymatic assays and used to calculate UACR. Spearman's rank correlation coefficient between UAG and UACR was calculated for both groups. The UAG values of healthy cats and cats with CKD were assessed using the Mann-Whitney test (P < .05). RESULTS: The UAG was inversely correlated with UACR in healthy cats (P < .002, r0 = -0.40) but not in cats with CKD (P = .55; r0 = -0.15). A significant difference was found between UAG in healthy cats and those with CKD (P < .001). CONCLUSIONS AND CLINICAL IMPORTANCE: The UAG calculation cannot be used as a substitute for UACR in cats. The clinical relevance of UAG differences between healthy cats and those with CKD remains unknown.

Association between serum anion gap and risk of in-hospital mortality in patients with acute heart failure.

A high serum anion gap (AG) at the time of patient admission can lead to the deterioration or even death; data are lacking for patients who suffer acute heart failure (AHF). The present study aimed at exploring the impact of serum AG (SAG) levels on the in-hospital mortality in AHF patients. The study conducted retrospective analysis on the data from the medical information mart for intensive care (MIMIC-IV) database in severe AHF cases. Serum AG, age, sex, concomitant diseases and laboratory tests were collected from patients at admission. Multivariate Cox proportional hazard regression model together with Kaplan Meier (K-M) survival curve served for analyzing the relationship of serum AG with the hospital all-cause mortality (ACM). In addition, subgroup analysis assisted in assessing the concordance. Data from 2774 AHF patients were collected in the study. The hospital ACM rate was 9.2% (254/2774). After correcting potential confounders, multivariate analysis compared the high serum AG level (≥ 16 mmol/L) and the low serum AG level (< 16 mmol/L) (hazard ratio (HR): 1.89 [95% CI 1.42-2.51]). In a similar way, K-M survival curve indicated that hospital survival was lower in patients with high serum, suggesting that high serum AG level could lead to poor AHF prognosis. In patients with AHF, high serum AG level could increase the hospital ACM.

Pathophysiology of Diet-Induced Acid Stress.

Diets can influence the body's acid-base status because specific food components yield acids, bases, or neither when metabolized. Animal-sourced foods yield acids and plant-sourced food, particularly fruits and vegetables, generally yield bases when metabolized. Modern diets proportionately contain more animal-sourced than plant-sourced foods, are, thereby, generally net acid-producing, and so constitute an ongoing acid challenge. Acid accumulation severe enough to reduce serum bicarbonate concentration, i.e., manifesting as chronic metabolic acidosis, the most extreme end of the continuum of "acid stress", harms bones and muscles and appears to enhance the progression of chronic kidney disease (CKD). Progressive acid accumulation that does not achieve the threshold amount necessary to cause chronic metabolic acidosis also appears to have deleterious effects. Specifically, identifiable acid retention without reduced serum bicarbonate concentration, which, in this review, we will call "covert acidosis", appears to cause kidney injury and exacerbate CKD progression. Furthermore, the chronic engagement of mechanisms to mitigate the ongoing acid challenge of modern diets also appears to threaten health, including kidney health. This review describes the full continuum of "acid stress" to which modern diets contribute and the mechanisms by which acid stress challenges health. Ongoing research will develop clinically useful tools to identify stages of acid stress earlier than metabolic acidosis and determine if dietary acid reduction lowers or eliminates the threats to health that these diets appear to cause.

The Role of the Endocrine System in the Regulation of Acid-Base Balance by the Kidney and the Progression of Chronic Kidney Disease.

Systemic acid-base status is primarily determined by the interplay of net acid production (NEAP) arising from metabolism of ingested food stuffs, buffering of NEAP in tissues, generation of bicarbonate by the kidney, and capture of any bicarbonate filtered by the kidney. In chronic kidney disease (CKD), acid retention may occur when dietary acid production is not balanced by bicarbonate generation by the diseased kidney. Hormones including aldosterone, angiotensin II, endothelin, PTH, glucocorticoids, insulin, thyroid hormone, and growth hormone can affect acid-base balance in different ways. The levels of some hormones such as aldosterone, angiotensin II and endothelin are increased with acid accumulation and contribute to an adaptive increase in renal acid excretion and bicarbonate generation. However, the persistent elevated levels of these hormones can damage the kidney and accelerate progression of CKD. Measures to slow the progression of CKD have included administration of medications which inhibit the production or action of deleterious hormones. However, since metabolic acidosis accompanying CKD stimulates the secretion of several of these hormones, treatment of CKD should also include administration of base to correct the metabolic acidosis.

Dietary acid load in health and disease.

Maintaining an appropriate acid-base equilibrium is crucial for human health. A primary influencer of this equilibrium is diet, as foods are metabolized into non-volatile acids or bases. Dietary acid load (DAL) is a measure of the acid load derived from diet, taking into account both the potential renal acid load (PRAL) from food components like protein, potassium, phosphorus, calcium, and magnesium, and the organic acids from foods, which are metabolized to bicarbonate and thus have an alkalinizing effect. Current Western diets are characterized by a high DAL, due to large amounts of animal protein and processed foods. A chronic low-grade metabolic acidosis can occur following a Western diet and is associated with increased morbidity and mortality. Nutritional advice focusing on DAL, rather than macronutrients, is gaining rapid attention as it provides a more holistic approach to managing health. However, current evidence for the role of DAL is mainly associative, and underlying mechanisms are poorly understood. This review focusses on the role of DAL in multiple conditions such as obesity, cardiovascular health, impaired kidney function, and cancer.

The correlation between albumin-corrected anion gap and prognosis in patients with acute myocardial infarction.

AIMS: Acute myocardial infarction (AMI) is a cardiovascular disease with high morbidity and mortality. We collected patients with AMI from the Medical Information Mart for Intensive Care IV (v2.0) database and explored the association between serum albumin-corrected anion gap (ACAG) level and mortality in patients with AMI. METHODS AND RESULTS: Data of adult patients with AMI were collected. According to the 360 day prognosis, patients were divided into survival and non-survival groups. Based on the ACAG level, patients were then divided into normal and high ACAG groups. Cox hazard proportional models and restricted cubic splines (RCSs) were used to investigate the correlation between ACAG and mortality. Kaplan-Meier curves were created to compare the cumulative survival rates between the high and normal ACAG groups. The receiver operating characteristic (ROC) curve was used to analyse the predictive value of ACAG for the prognosis of patients with AMI. Sensitivity and subgroup analyses were conducted to revalidate the results. Finally, 1783 patients were included. Elevated ACAG (>20 mmol/L) was significantly associated with 30 and 360 day mortality (P < 0.001). Adjusted for multiple confounding factors, the Cox proportional hazard analysis showed that elevated ACAG (>20 mmol/L) was an independent risk factor of increased all-cause mortality in patients with AMI (hazard ratio 1.423, 95% confidence interval 1.206-1.678, P < 0.001). RCS analysis further showed that there was a non-linear trend relationship between ACAG and the risk of all-cause mortality at 30 and 360 days (χ2 = 10.750, P = 0.013; χ2 = 13.960, P = 0.003). Kaplan-Meier survival curves showed that the 30 and 360 day cumulative survival rates of patients with AMI were significantly lower (log-rank test, χ2 = 98.880, P < 0.001; χ2 = 105.440, P < 0.001) in the high ACAG group. ROC curve analysis showed that the area under the curve (AUC) of ACAG was 0.651, while the AUC of anion gap (AG) was 0.609, indicating that ACAG had a higher predictive value for 360 day mortality than AG. When combined with Sequential Organ Failure Assessment score, the predictive performance of ACAG for 360 day mortality was better, with an AUC of 0.699. Sensitivity and subgroup analyses were conducted suggesting the stability of our results. CONCLUSIONS: Elevated serum ACAG (≥20 mmol/L) is an independent risk factor for short-term and long-term mortality in critically ill patients with AMI, and it may assist clinicians and nurses identifying high-risk patients.

Blood glucose monitoring in critically ill adult patients: type of sample and method of analysis. Systematic review and meta-analysis.

INTRODUCTION: The clinical guideline for the management of sepsis, recommends using arterial blood samples for glycaemic control. A multicentre study in 86 Spanish intensive care units (ICU) revealed that 85.4% of ICUs used capillary puncture. OBJECTIVE: To analyse the reliability of glycaemia by comparing different blood samples (arterial, venous, capillary) and instruments (glucometers, gasometers, central laboratory). Secondarily, to estimate the effect of confounding variables and the performance of measuring instruments as determined by different quality standards. METHODOLOGY: Systematic review and meta-analysis with search in PubMed, CINAHL and Embase databases in September-2021 and September-2022, with no time or language limits. Grey literature sources: DART-Europe, OpenGrey and Google Scholar. Results summarised by qualitative (description of results, study characteristics) and quantitative (meta-analysis to assess standardised mean difference) synthesis. Methodological quality of articles assessed with Quality Assessment of Diagnostic Accuracy Studies-2 (QUADAS-2). PROTOCOL: https://osf.io/ DOI 10.17605/OSF.IO/T8KYP. RESULTS: A total of 32 articles and 5451 patients were included. No discrepancies were obtained between arterial glucometer vs laboratory samples [bias (95%CI): 0.01 (-0.12 to 0.14) mg/dL]. In contrast, arterial samples with a gasometer did significantly overestimate [bias (95%CI): 0.12 (0.01 to 0.24) mg/dL]. The same trend is seen in capillaries with a glucometer, although not significantly [bias (95%CI): 0.07 (--0.02 to 0.15) mg/dL]. There is discrepancy between studies on the effect of haematocrit and acid-base balance. The greatest consensus is on the poor agreement of glucometer with capillary vs laboratory samples in the presence of shock and vasopressor support, renal failure or during vitamin C treatment. CONCLUSIONS: The evidence to date recommends the use of arterial blood with a blood glucose meter for better reliability of glycaemic analysis and less effect of possible confounding variables, frequently present in the critically ill adult patient.