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The association between mean arterial pressure and acute kidney injury reversal among decompensated cirrhosis patients.
Hepatology : Official Journal of the American Association for the Study of Liver Diseases 2024 March 28
BACKGROUND: This study informs how mean arterial pressure (MAP) impacts AKI recovery among all patients hospitalized with cirrhosis, regardless of etiology.
METHODS: We identified incident AKI episodes among subjects in our cohort of decompensated cirrhosis patients. AKI was defined as a ≥50% increase in creatinine (sCr) from an outpatient baseline (≥7 days prior) that required hospitalization. Linear mixed-effects models were completed to determine the impact between AKI recovery, MAP, and time. To determine the impact of MAP on AKI reversal, we completed time-dependent Cox-regression models with time beginning at the time of peak sCr and ending at death, discharge, or AKI reversal, among those hospitalized with AKI and those with Persistent AKI (≥48 hours).
RESULTS: We identified 702 hospitalized cirrhosis patients with AKI. We found those with AKI reversal had, on average, higher MAP (2.1 mmHg, p<0.05) and a greater increase in MAP over time (0.1 mmHg per hour, p<0.001). Among all 702 hospitalized patients with AKI and adjusted for confounders, each 5 mmHg increase in MAP was associated with 1.07x the hazard of AKI reversal (p<0.01). Similarly, among those with persistent AKI after adjusting for confounders, each 5 mmHg increase in MAP was associated with 1.19x greater likelihood of AKI reversal (p<0.001). Discussion: Our data demonstrate that MAP significantly increases the likelihood of AKI recovery regardless of severity or injury or AKI phenotype. We believe these data highlight the importance of MAP as a clinical tool to promote kidney function recovery among cirrhosis patients hospitalized with AKI.
METHODS: We identified incident AKI episodes among subjects in our cohort of decompensated cirrhosis patients. AKI was defined as a ≥50% increase in creatinine (sCr) from an outpatient baseline (≥7 days prior) that required hospitalization. Linear mixed-effects models were completed to determine the impact between AKI recovery, MAP, and time. To determine the impact of MAP on AKI reversal, we completed time-dependent Cox-regression models with time beginning at the time of peak sCr and ending at death, discharge, or AKI reversal, among those hospitalized with AKI and those with Persistent AKI (≥48 hours).
RESULTS: We identified 702 hospitalized cirrhosis patients with AKI. We found those with AKI reversal had, on average, higher MAP (2.1 mmHg, p<0.05) and a greater increase in MAP over time (0.1 mmHg per hour, p<0.001). Among all 702 hospitalized patients with AKI and adjusted for confounders, each 5 mmHg increase in MAP was associated with 1.07x the hazard of AKI reversal (p<0.01). Similarly, among those with persistent AKI after adjusting for confounders, each 5 mmHg increase in MAP was associated with 1.19x greater likelihood of AKI reversal (p<0.001). Discussion: Our data demonstrate that MAP significantly increases the likelihood of AKI recovery regardless of severity or injury or AKI phenotype. We believe these data highlight the importance of MAP as a clinical tool to promote kidney function recovery among cirrhosis patients hospitalized with AKI.
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