Acute Kidney Injury in Patients with Liver Disease

Abstract

AKI is commonly encountered in patients with decompensated cirrhosis, and it is associated with unfavorable outcomes. Among factors specific to cirrhosis, hepatorenal syndrome type 1, also referred to as hepatorenal syndrome-AKI, is the most salient and unique etiology. Patients with cirrhosis are vulnerable to traditional causes of AKI, such as prerenal azotemia, acute tubular injury, and acute interstitial nephritis. In addition, other less common etiologies of AKI specifically related to chronic liver disease should be considered, including abdominal compartment syndrome, cardiorenal processes linked to cirrhotic cardiomyopathy and portopulmonary hypertension, and cholemic nephropathy. Furthermore, certain types of GN can cause AKI in cirrhosis, such as IgA nephropathy or viral hepatitis related. Therefore, a comprehensive diagnostic approach is needed to evaluate patients with cirrhosis presenting with AKI. Management should be tailored to the specific underlying etiology. Albumin-based volume resuscitation is recommended in prerenal AKI. Acute tubular injury and acute interstitial nephritis are managed with supportive care, withdrawal of the offending agent, and, potentially, corticosteroids in acute interstitial nephritis. Short of liver transplantation, vasoconstrictor therapy is the primary treatment for hepatorenal syndrome type 1. Timing of initiation of vasoconstrictors, the rise in mean arterial pressure, and the degree of cholestasis are among the factors that determine vasoconstrictor responsiveness. Large-volume paracentesis and diuretics are indicated to relieve intra-abdominal hypertension and renal vein congestion. Direct-acting antivirals with or without immunosuppression are used to treat hepatitis B/C–associated GN. In summary, AKI in cirrhosis requires careful consideration of multiple potentially pathogenic factors and the implementation of targeted therapeutic interventions.

Detection of potential drug-drug interactions for risk of acute kidney injury: a population-based case-control study using interpretable machine-learning models

“…The demographic information was composed of age, sex, and three hospitals (Itabashi, Hikarigaoka, and Surugadai; dummy variables). The medical history was composed of hypertension, diabetes, heart failure, anemia, sepsis, chronic kidney disease (stage ≤2), and chronic liver disease, which are known risk factors for AKI (ICD-10 codes are shown in Supplementary Table S1B ) ( Poston and Koyner, 2019 ; Ostermann et al, 2020 ; Yu et al, 2020 ; Cullaro et al, 2022 ). A diagnosis was regarded as “present” if there was a diagnosis before baseline.…”

Identification of novel prognostic targets in acute kidney injury using bioinformatics and next generation sequencing data analysis

“…PAH is a reported prevalence of 5.0–7.5% of hospitalized patients and in 50–60% of critically ill patients [3]. There are substantial causative factors of AKI, like cardiovascular events [4], older adults [5], mechanical ventilator [6], nephrotoxic agents [7], vasopressors [8], hypertension [9], hypercholesterolemia [10], liver disease [11], hypoalbuminemia [12], sepsis [13], renal ischemia [14], diabetes mellitus [15], obesity [16], anemia [17] and chronic kidney disease [18]. Studies have revealed that the progression of AKI is related to genetic factors [19].…”

“…Clin Chem Lab Med. 2020;58(11):1819-1827. doi:10.1515/cclm-2019-0292 284. Tzveova R, Naydenova G, Yaneva T, Dimitrov G, Vandeva S, Matrozova Y, Pendicheva-Duhlenska D, Popov I, Beltheva O, Naydenov C, et al Gender-Specific Effect of CYP2C8*3 on the Risk of Essential Hypertension in Bulgarian Patients.…”

Acute Kidney Injury Induces Oxidative Stress and Hepatic Lipid Accumulation through AMPK Signaling Pathway

“…Over the past decade, there has been extensive research into the mechanisms of distant organ dysfunction caused by AKI, in which the most studied organ was the lung, followed by the heart, brain, liver, and gut [ 4 , 5 , 6 ]. AKI patients with a complication of liver dysfunction had poor clinical outcomes [ 7 , 8 ]. Several clinical studies reported that AKI patients with hepatic dysfunction had alterations in protein synthesis, inflammatory responses, and abnormal metabolism of lipids, proteins, and drugs [ 5 , 9 ].…”