Metabolic Acidosis in Critically Ill Cirrhotic Patients with Acute Kidney Injury

Abstract

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 BE UMA 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 BE UMA , novel markers of acid-base disorders, show promise in predicting mortality rate of CICPs with AKI.

Serum Anion Gap Predicts All-Cause Mortality in Critically Ill Patients with Acute Kidney Injury: Analysis of the MIMIC-III Database

“…AKI is defined as rapid decline in renal function lasting from hours to days, as opposed to chronic kidney disease [27]. Critically ill patients are often exposed to hypoxia and anaerobic tissue conditions, leading to rapid accumulation of pyruvate, which is almost completely converted to lactate [28]. The kidney is known for lactate dehydrogenase dysfunction in the setting of patients with AKI [29], and the renal acid excretion does not fully offset endogenous acid production [30].…”

Association of Plasma Anion Gap with 28-Day Inhospital Mortality and 1-Year Mortality of Patients with Alcohol Use Disorder at ICU Admission: A Retrospective Cohort Study

“…Critically ill patients often suffer from hypoxia and anoxia, which can lead to a rapid accumulation of pyruvate and eventually almost conversion to lactic acid [ 34 ]. The possible reason for metabolic acidosis caused by elevated blood lactic acid level may be that alcohol over consumption in critically ill patients with AUD can increase NADH/NAD ratio and promote pyruvate metabolism into lactic acid.…”

Serum lactate dehydrogenase level is associated with in-hospital mortality in critically Ill patients with acute kidney injury

“…Local and systematic inflammation are involved in both AKI and CKD progression [ 26 ]. Moreover, critically ill patients are always exposed to hypoxia and anaerobic tissue, which results in the rapid accumulation of pyruvate, and pyruvate may be converted into lactate in some circumstances [ 27 ]. However, patients with AKI always suffer from lactate dehydrogenase dysfunction, and they are not able to clear endogenous acid production, which causes high levels of LDH [ 28 , 29 ].…”