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Multicenter Study
. 2024 Sep;60(6):778-786.
doi: 10.1111/apt.18159. Epub 2024 Jul 15.

Outcomes of patients with alcohol-associated hepatitis and acute kidney injury - Results from the HRS Harmony Consortium

Ann T Ma  1 , Andrew S Allegretti  2 , Giuseppe Cullaro  3 , Tianqui Ouyang  2 , Sumeet K Asrani  4 , Raymond T Chung  5 , Eric M Przybyszewski  5 , Robert M Wilechansky  5 , Jevon E Robinson  2 , Pratima Sharma  6 , Douglas A Simonetto  7 , Prasun Jalal  8 , Eric S Orman  9 , Hani M Wadei  10 , Shelsea A St Hillien  2 , Danielle Saly  2 , Nneka N Ufere  5 , Leigh Anne Dageforde  11 , Kevin R Regner  12 , Justin M Belcher  13   14 , Kavish R Patidar  8   15 ; from the HRS Harmony Consortium
Affiliations
Multicenter Study

Outcomes of patients with alcohol-associated hepatitis and acute kidney injury - Results from the HRS Harmony Consortium

Ann T Ma et al. Aliment Pharmacol Ther. 2024 Sep.

Abstract

Background & aims: The development of acute kidney injury (AKI) in the setting of alcohol-associated hepatitis (AH) portends a poor prognosis. Whether the presence of AH itself drives worse outcomes in patients with cirrhosis and AKI is unknown.

Methods: Retrospective cohort study of 11 hospital networks of consecutive adult patients admitted in 2019 with cirrhosis and AKI. AKI phenotypes, clinical course, and outcomes were compared between AH and non-AH groups.

Results: A total of 2062 patients were included, of which 303 (15%) had AH, as defined by National Institute on Alcohol Abuse and Alcoholism (NIAAA) criteria. Patients with AH, compared to those without, were younger and had higher Model for End-stage Liver Disease-Sodium (MELD-Na) scores on admission. AKI phenotypes significantly differed between groups (p < 0.001) with acute tubular necrosis occurring more frequently in patients with AH. Patients with AH reached more severe peak AKI stage, required more renal replacement therapy, and had higher 90-day cumulative incidence of death (45% [95% CI: 39%-51%] vs. 38% [95% CI: 35%-40%], p = 0.026). Using no AH as reference, the unadjusted sHR for 90-day mortality was higher for AH (sHR: 1.24 [95% CI: 1.03-1.50], p = 0.024), but was not significant when adjusting for MELD-Na, age and sex. However, in patients with hepatorenal syndrome, AH was an independent predictor of 90-day mortality (sHR: 1.82 [95% CI: 1.16-2.86], p = 0.009).

Conclusions: Hospitalised patients with cirrhosis and AKI presenting with AH had higher 90-day mortality than those without AH, but this may have been driven by higher MELD-Na rather than AH itself. However, in patients with hepatorenal syndrome, AH was an independent predictor of mortality.

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Conflict of interest statement

CONFLICT OF INTEREST STATEMENT

ASA reports consultant fees from Mallinckrodt Pharmaceuticals and Ocelot Bio. GC reports consulting fees from Ocelot Bio and Retro Biosciences. ESO reports consultant fees from Biovie. HMW reports consultant fees from Mallinckrodt Pharmaceuticals. KRR reports consultant fees from Mallinckrodt Pharmaceuticals. JMB reports consultant fees from Mallinckrodt Pharmaceuticals. The other authors have no conflict of interest to declare.

Figures

FIGURE 1
FIGURE 1
Distribution of AKI phenotype, by severity of alcohol-associated hepatitis. p value by Pearson’s Chi-squared test. AH, alcohol-associated hepatitis; ATN, acute tubular necrosis; AKI, acute kidney injury; HRS, hepatorenal syndrome.
FIGURE 2
FIGURE 2
AKI response rate* in the different AKI phenotypes, by alcohol-associated hepatitis status, in (A) prerenal AKI, (B) hepatorenal syndrome, and (C) acute tubular necrosis. *Includes both full and partial response, defined respectively as a decrease in serum creatinine to within 0.3 mg/dL of baseline creatinine during the admission, and as downstaging in at least one AKI stage (example from AKI stage 3 to stage 2), but with a serum creatinine >0.3 mg/dL from baseline. p value by Pearson’s Chi-squared test. AH, alcohol-associated hepatitis, AKI, acute kidney injury; ATN, acute tubular necrosis; HRS, hepatorenal syndrome.
FIGURE 3
FIGURE 3
Cumulative incidence of death by alcohol-associated hepatitis status. AH, alcohol-associated hepatitis. Statistical significance p = 0.026 by Grey’s test.
FIGURE 4
FIGURE 4
Cumulative incidence of death in patients with hepatorenal syndrome, by alcohol-associated hepatitis status. AH, alcohol-associated hepatitis. Statistical significance p = 0.008 by Grey’s test.
See this image and copyright information in PMC

References

    1. Crabb DW, Im GY, Szabo G, Mellinger JL, Lucey MR. Diagnosis and treatment of alcohol-associated liver diseases: 2019 practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2020;71:306–33. - PubMed
    1. Singal AK, Arsalan A, Dunn W, Arab JP, Wong RJ, Kuo YF, et al. Alcohol-associated liver disease in the United States is associated with severe forms of disease among young, females and Hispanics. Aliment Pharmacol Ther. 2021;54:451–61. - PubMed
    1. Arab JP, Díaz LA, Baeza N, Idalsoaga F, Fuentes-López E, Arnold J, et al. Identification of optimal therapeutic window for steroid use in severe alcohol-associated hepatitis: a worldwide study. J Hepatol. 2021;75:1026–33. - PMC - PubMed
    1. Thursz MR, Richardson P, Allison M, Austin A, Bowers M, Day CP, et al. Prednisolone or pentoxifylline for alcoholic hepatitis. N Engl J Med. 2015;372:1619–28. - PubMed
    1. Altamirano J, Fagundes C, Dominguez M, García E, Michelena J, Cárdenas A, et al. Acute kidney injury is an early predictor of mortality for patients with alcoholic hepatitis. Clin Gastroenterol Hepatol. 2012;10:65–71.e3. 10.1016/J.CGH.2011.09.011 - DOI - PubMed

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