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Egyptian Liver Journal
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The urine albumin creatinine ratio is one of the predictors of acute kidney injury in hepatitis C-related cirrhotic hepatic encephalopathy

Egyptian Liver Journal volume 12, Article number: 62 (2022) Cite this article

Abstract

Background/objective

Hepatic encephalopathy (HE) is a main manifestation of acute decompensation in liver cirrhosis. Recently, systemic inflammation was proposed as a key mechanism in the development of acute kidney injury (AKI) in cirrhotic patients. The urine albumin creatinine ratio (UACR) is considered a marker of systemic inflammation in a variety of clinical settings. Here, we aimed to evaluate the role of the urine albumin creatinine ratio in the early prediction of AKI in HE.

Patients and methods

Sixty-seven consecutive patients presented with cirrhotic HE, and 59 age- and sex-matched cirrhotic patients with no history of HE served as controls. HE was defined and graded by the West Haven criteria. The severity of liver cirrhosis was evaluated by the Child-Turcotte-Pugh (CTP) score, and model for end-stage liver disease (MELD) score. The incidence of AKI that developed during hospital admission and the in-hospital mortality rate was estimated among HE patients. In addition, predictors of AKI were analyzed.

Results

The mean age of HE patients was 58.09±12.26 years; 36 (53.7%) were males, and 31 (46.3%) were females. Among HE patients, 16 (23.9%) developed AKI during hospital admission. The in-hospital mortality rate among HE patients was 22 (32.8%), the in-hospital mortality among HE-AKI patients was 81.3% (n=13/16), and UACR levels > 91.5 mg/g identified HE-AKI with 81.25% sensitivity (AUC = 0.85, P ≤ 0.001).

Conclusions

Patients with cirrhotic HE are at high risk of AKI. HE-AKI patients had a high rate of in-hospital mortality. Estimation of UACR at hospital admission is suggested for the early detection of patients with HE-AKI.

Introduction

Cirrhosis is the leading cause of liver-related death worldwide. In 2017, cirrhosis caused more than 1.32 million deaths globally [1]. Egypt has a high liver cirrhosis burden [2]. Indeed, it was reported that Egypt had the highest age-standardized death rate due to cirrhosis from 1990 to 2017 [1]. Overt hepatic encephalopathy (OHE) occurs in 30–40% of patients with cirrhosis during the natural course of their disease [3]. Once depicted, the course of decompensated cirrhosis is characterized by repeated episodes of HE. The in-hospital mortality rate of patients with HE ranges from 33 to 75% [4,5,6]. This high in-hospital mortality rate is largely dependent on the grade of HE and associated comorbidities. Acute kidney injury (AKI) is a common comorbidity in patients with decompensated cirrhosis, occurring in 20% of hospitalized patients and resulting in high mortality [7].

The prediction of AKI and early therapeutic intervention in decompensated cirrhosis can decrease in-hospital mortality. Accurate assessment of renal function by serum creatinine is difficult in patients with cirrhosis, due to an enlarged volume of fluid distribution, low protein intake, and decreased creatinine production secondary to muscle atrophy. Alternative urinary markers (e.g., cystatin C, neutrophil gelatinase-associated lipocalin (NGAL) and urinary IL-18) are not widely available [8]. A urine albumin creatinine ratio (UACR) ≥30 mg/g is associated with more severe liver disease and a lower glomerular filtration rate (GFR) in patients with decompensated cirrhosis [9]. It was reported that albuminuria predicted AKI in liver cirrhosis [7] and mortality in HE [10].

The occurrence of albuminuria in patients with HE-related AKI (HE-AKI) may be explained by the associated systemic inflammation. The relationship between microalbuminuria and inflammation has been reported in a variety of clinical settings [11]. On the other hand, recent large-scale European observational studies have shown that systemic inflammation is a hallmark of kidney injury in cirrhotic patients. Indeed, systemic inflammation induces nitric oxide-mediated accentuation of the preexisting splanchnic vasodilation, resulting in the overactivation of the endogenous vasoconstrictor systems, which elicits intense vasoconstriction and hypoperfusion in certain vascular beds, in particular the renal circulation, and subsequently acute kidney injury (AKI) [12].

Data on the prediction of HE-AKI are limited. Here, we attempted to evaluate the role of the UACR in the early prediction of AKI among hospitalized cirrhotic HE patients.

Patients and methods

This prospective case-control study included 126 cirrhotic patients. Sixty-seven (53.2%) consecutive patients presented with hepatic encephalopathy (HE), and 59 (46.8%) age- and sex-matched cirrhotic patients had no history of HE and served as controls. All included patients were admitted to the Department of Internal Medicine, El Hussein University Hospital, Cairo, Egypt, during the period from September 2019 to September 2020. Patients with severe cardiopulmonary disease, history of renal disease, previous liver transplantation, nephrotoxic drugs, and nonsteroidal anti-inflammatory drug (NSAID) use in the last 4 weeks or diabetes mellitus were excluded.

Cirrhosis was diagnosed by liver biopsy, endoscopic signs of portal hypertension, radiological evidence of liver nodularity, or clinical evidence of hepatic decompensation (including ascites, HE, and acute variceal bleeding) in patients with chronic liver disease. Overt ascites was diagnosed by clinical examination and confirmed by ultrasonography. Patients with fibrosis-4 (Fib-4) scores ≥ 3.5 in the absence of liver decompensation and liver biopsy were categorized as compensated liver cirrhosis [13]. HE was defined and graded by the West Haven criteria. The severity of liver cirrhosis was evaluated by the -Turcotte-Pugh (CTP) score and the model for end-stage liver disease (MELD) score. Serum creatinine was measured for all included patients on he first day of hospital admission (considered the baseline serum creatinine) and daily durin the hospital stay to detect patients who developed AKI.

Acute kidney injury (AKI) was defined as an acute increase in serum creatinine (S. Cr) 0.3 mg/dl or more above the baseline serum creatinine in less than 48 h [14]. Diagnosis of hepatorenal syndrome-AKI was based on the criteria previously reported [15]. Prerenal AKI was defined as elevated serum creatinine 0.3 mg/dl or more above the baseline serum creatinine, with a subsequent decrease in S. Cr to ≤1.5 mg/dl within 48 h of treatment with diuretic withdrawal and intravenous hydration [15]. Acute elevation in serum creatinine 0.3 mg/dL or more above the baseline serum creatinine, not responding with 48 h of volume resuscitation and not meeting the criteria for HRS [15] were categorized as intrinsic AKI.

To assess the value of the urine albumin creatinine ratio (UACR) in the prediction of AKI in HE patients, UACR was measured for all included patients (n=126) on the first day of hospital admission.

Detection of UACR

A solid-phase fluorescence immunoassay was used to measure urinary albumin, with a sensitivity level of 0.05 mg/dl. The coefficient of variation for urinary albumin measurement varied from 4.8 to 16.1%. Urine creatinine was measured with the Jaffé rate reaction (Beckman Astra, Brea, CA), and the coefficient of variation ranged from 1.5 to 7.7% (National Center for Health Statistics, 1996).

Statistical analysis

All data were analyzed using the Statistical Package for the Social Sciences, version 20.0 (SPSS Inc., Chicago, Illinois, USA). Quantitative variables that were normally distributed were expressed as the mean values ± standard deviation (SD), and non-normally distributed were expressed as the median values with interquartile range (IQR). Categorical data are expressed as the frequencies and percentages. An independent samples t test was used when comparing two means (for normally distributed data), the Mann-Whitney U test was used when comparing two medians of non normally distributed data, the chi-square test was used when comparing categorical data, and multivariate logistic regression analysis was used to identify the independent factors significantly associated with AKI. The area under a receiver operating characteristic curve (AUROC) was used to detect the cut-off point, sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV). A P value < 0.05 was considered significant.

Results

Among 126 patients with liver cirrhosis, the mean age was 57.9 ± 12.8 years, including 75 (59.5%) men and 51 (40.5%) women. HCV (114 patients, 90.5%) was the most common aetiology of liver cirrhosis. Twenty-three (18.3%), 55 (43.7%), and 48 (38%) patients had child classes A, B, and C, respectively. The mean MELD score was 15.01± 5.8, the median (IQR) UACR was 51.5 (88.6) mg/g, and the hospital stay was ≤ 7 days in the majority of patients (n=106; 84.1%). The incidence of AKI in the included cirrhotic patients who developed AKI during hospital admission was 18.3% (n=23). In addition, the in-hospital mortality rate among the included cirrhotic patients was 17.5% (n=22) (Table 1).

Table 1 Baseline characteristics of the included cirrhotic patients
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Characteristics of cirrhotic-HE patients

Among the 67 patients with cirrhotic HE, the mean age was 58.09±12.26 years; 36 (53.7%) were males and 31 (46.3%) were females. Patients with HE had significantly lower levels of serum albumin (2.35±0.58 g/dl). In addition, they had significantly higher levels of serum bilirubin (3.68±3.86 mg/dl) and international normalized ratio (INR) (1.87±0.64). Although HE patients had normal mean serum creatinine levels (1.0±0.45 mg/dl) at baseline, they were significantly higher than cirrhotic patients without HE (0.87±0.18 mg/dl). However, the mean estimated glomerular filtration rate (eGFR) (77.76±26.91 mL/min/1.73 m2) was significantly lower among cirrhotic HE patients. The mean MELD (17.21± 5.54) and child’s (9.65±1.70) scores were significantly higher among HE patients. There was no significant difference among cirrhotic patients with and without HE regarding UACR levels at hospital admission (Table 2). The incidence of AKI among cirrhotic patients with and without HE was 23.9% and 11.86%, respectively. The in-hospital mortality rate among cirrhotic HE patients was 32.8 %; however, no mortality was detected among cirrhotic patients without HE (Table 2).

Table 2 Baseline characteristics of patients with no-HE versus those with HE
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Hepatic encephalopathy-associated AKI

Among 67 patients with HE, 16 (23.9%) developed AKI during hospital admission. The median (IQR) age for AKI patients was 60.5 (9) years, including 12 (75%) males and 4 (25%) females. Patients with HE-AKI had significantly increased serum bilirubin, higher Child-Turcotte-Pugh (CTP) scores, elevated basal serum creatinine, increased UACR, increased length of hospital stay, and higher in-hospital mortality rates (Table 3). The median (IQR) serum bilirubin, CTP score, admission serum creatinine, and UACR were 4.6 (3.9) mg/dl, 11 (1.75), 1.15 (0.38) mg/dl, and 249 (256.6) mg/g, respectively. All HE patients with AKI had child’s class C liver cirrhosis. Seven (43.8%) HE patients with AKI had hospital stays of more than 7 days, and the in-hospital mortality rate among HE patients with AKI was 81.3% (n=13) (Table 3).

Table 3 Baseline characteristics of patients with HE without AKI versus those with AKI
Full size table

Predictors of AKI in HE patients

Increased serum total bilirubin, elevated basal serum creatinine, elevated UACR, higher CTP score, and increased length of hospital stay were identified as independent risk factors for HE-AKI by multivariate analysis (Table 4).

Table 4 Multi-variate logistic regression analysis for factors predictive of HE-AKI
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ROC curve analysis

Prolonged length of hospital stay identified HE-AKI at a cut-off level of > 5.5 days, with 75% sensitivity, 82.4% specificity, 81% PPV, and 76.7% NPV (AUC = 0.83, P ≤ 0.001). Total serum bilirubin identified HE-AKI at a cut-off level of > 3.1 mg/dl, with 68.75% sensitivity, 66.7% specificity, 67.4% PPV, and 68.1% NPV (AUC = 0.73, P ≤ 0.005). Basal serum creatinine identified HE-AKI at a cut-off level of > 1.05 mg/dl, with 62.5% sensitivity, 66.7% specificity, 65.2% PPV, and 64% NPV (AUC = 0.74, P = 0.005). UACR levels > 91.5 mg/g, identified HE-AKI with 81.25% sensitivity, 82.4% specificity, 82.2% PPV, and 81.5% NPV (AUC = 0.85, P ≤ 0.001). The CTP score could be used to discriminate between HE-AKI and HE patients without AKI at a cut-off level of > 11.5, with 35.3% sensitivity, 90% specificity, 77.9% PPV, and 58.2% NPV (AUC = 0.78, P ≤ 0.001) (Table 5 and Fig. 1).

Table 5 Diagnostic performance of factors predictive of HE-AKI
Full size table
Fig. 1
figure 1

Area under the receiver operating characteristic curve for predictors of HE-AKI

Full size image

Discussion

In the current study, we found that cirrhotic patients with HE had a higher incidence of AKI. Moreover, the occurrence of AKI in HE markedly increased in-hospital mortality. Increased serum total bilirubin, elevated serum creatinine, elevated UACR, higher CTP score at admission, and increased length of hospital stay predicted the development of AKI in hospitalized cirrhotic patients with HE.

Data on the incidence of HE-AKI are limited. In the current study, patients with HE had a 2-fold increase in AKI incidence compared with cirrhotic patients without HE. Based on a single study, renal function impairment (RFI) was an important prognostic factor for mortality in cirrhotic HE. Interestingly, the impact of HRS and acute renal failure (ARF) on the long-term mortality of cirrhotic HE was more deleterious than that of chronic kidney disease and end-stage kidney disease [16].

Among chronic liver disease-related hospitalizations, the crude in-hospital mortality rate is 7.4% [17]. The concurrent cirrhosis-related complications are associated with increasing in-hospital mortality rates [17]. For instance, HRS was associated with higher odds of in-hospital mortality in cirrhotic HE [17]. Based on these results, a higher in-hospital mortality rate was detected among cirrhotic HE-AKI patients in the current study. This impact of AKI on HE patients may be attributed to poor clearance of bloodstream ammonia that increases the susceptibility to brain edema in cirrhotic HE [18]. Taken together, these data suggest early diagnosis and intervention to avoid the grave outcome of AKI on cirrhotic HE.

A urine albumin/creatinine ratio ≥30 mg/g is associated with more severe liver disease, lower GFR, and worse liver transplantation-free survival in patients with decompensated cirrhosis [9]. Indeed, it was reported that albuminuria is associated with AKI in cirrhotic patients [7]. Considering this result, we first showed that UACR levels > 91.5 mg/g identified HE-AKI with reasonable sensitivity (81.25% sensitivity; AUC = 0.85, P ≤ 0.001). Elevated UACR is associated with systemic inflammation, and recent large-scale European observational studies have shown that systemic inflammation is a hallmark of kidney injury in cirrhotic patients [19]. Indeed, it was shown that patients with HRS-AKI have marked systemic inflammation with an altered cytokine profile compared to patients with decompensated cirrhosis without AKI. Interestingly, the intensity of the inflammatory response is correlated with a lack of resolution of AKI and mortality [20]. Taken togethe, these data lent support to the speculation that the higher UACR levels in HE-AKI may reflect greater systemic inflammation.

In pooled analysis, the MELD score and CTP stage class C were associated with an elevated risk of developing AKI, in cirrhotic patients [21,22,23,24]. Although renal function is an important component of the MELD score, and the basal MELD score was significantly higher among HE patients, it could not predict HE-AKI in our cohort. Based on our results, the severity of liver disease in HE may be underestimated by the MELD score [25, 26]. In contrast to the MELD score, HE is a component of the CTP scoring system. Indeed, HE is one of the most important complications of liver cirrhosis, and it has been related to a worse prognosis [26]. This relationship was recently confirmed in patients with acute-on-chronic liver failure [27]. Interestingly, CTP independently predicted HE-AKI in our study. Taken together, these data suggest that CTP reflects the severity of underlying liver disease in HE patients, more so than the MELD score and hence predicts HE-AKI more accurately.

Admitted cirrhotic patients with higher baseline S. Cr are at higher risk for in-hospital development of AKI and are more likely to have AKI progression with reduced survival [28]. Higher S. Cr is independently associated with AKI development [7, 29]. Interestingly, serum creatinine at admission identified HE-AKI at a cut-off level (> 1.05 mg/dl) below the upper limit of the normal laboratory reference range. It was reported that the risk for persistent kidney injury is elevated in cirrhotic patients with basal creatinine within the normal reference range (0.70 mg/dL) [30]. These data support the need for a lower clinical threshold to initiate monitoring of renal function and implementation of kidney-protective strategies in cirrhotic patients.

The limitation of our study may be related to the relatively small number of patients, and patients with AKI were not categorized according to different AKI stages.

Conclusions

Patients with cirrhotic HE are at high risk of AKI and increased in-hospital mortality. UACR estimation at hospital admission is suggested for the early prediction of HE-AKI.

Availability of data and materials

All authors have access to the entirety of the data underlying this manuscript. Access to the data can be granted at any time upon reasonable request.

References

  1. Fleming KM, Aithal GP, Card TR, West J (2012) All-cause mortality in people with cirrhosis compared with the general population: a population-based cohort study. Liver Int. 32:79–84

    Article  PubMed  Google Scholar 

  2. Elbahrawy A, Ibrahim MK, Eliwa A, Alboraie M, Madian A, Aly HH (2021) Current situation of viral hepatitis in Egypt. Microbiol Immunol. https://doi.org/10.1111/1348-0421.12916 Epub ahead of print. PMID: 33990999

  3. American Association for the Study of Liver Diseases, European Association for the Study of the Liver. Hepatic encephalopathy in chronic liver disease (2014) practice guideline by the European Association for the Study of the Liver and the American Association for the Study of Liver Diseases. J Hepatol. 2014(61):642–659

    Google Scholar 

  4. Raphael KC, Matuja SS, Shen NT, Liwa AC, Jaka H (2016) Hepatic encephalopathy; prevalence, precipitating factors and challenges of management in a resource-limited setting. Journal of Gastrointestinal & Digestive System. 6(3):441

    Article  Google Scholar 

  5. Udayakumar N, Subramaniam K, Umashankar L, Verghese J, Jayanthi V (2007) Predictors of mortality in hepatic encephalopathy in acute and chronic liver disease: a preliminary observation. Journal of Clinical Gastroenterology. 41(10):922–926

    Article  CAS  PubMed  Google Scholar 

  6. Sasidharan A, Mavali RT (2013) ‘omas V. Outcome and predictors of mortality in severe hepatic encephalopathy. Journal of Clinical and Experimental Hepatology. 3(1S):S41–S42

    Article  Google Scholar 

  7. Belcher JM, Sanyal AJ, Peixoto AJ, Perazella MA, Lim J, Thiessen-Philbrook H et al (2014) Kidney biomarkers and differential diagnosis of patients with cirrhosis and acute kidney injury. Hepatology. 60(2):622–632

    Article  CAS  PubMed  Google Scholar 

  8. Fagundes C, Pepin MN, Guevara M, Barreto R, Casals G, Sola E et al (2012) Urinary neutrophil gelatinase-associated lipocalin as biomarker in the differential diagnosis of impairment of kidney function in cirrhosis. Journal of Hepatology. 57:267–273

    Article  CAS  PubMed  Google Scholar 

  9. Cholongitas E, Goulis I, Ioannidou M, Soulaidopoulos S, Chalevas P, Akriviadis E. Urine albumin-to-creatinine ratio is associated with the severity of liver disease, renal function and survival in patients with decompensated cirrhosis. Hepatology International. 201711, 306-14.

  10. Shahba HH, Elbahrawy AM, Helal AE, Alashker AM, Abdallah AM, Hemeda MH et al (2016) Albumin creatinine ratio predicts medical intensive care unit outcome of patients with hepatic encephalopathy. Z Gastroenterol 54(12):1343–1404

    Google Scholar 

  11. Scurt FG, Menne J, Brandt S, Bernhardt A, Mertens PR, Haller H et al (2019) Systemic inflammation precedes microalbuminuria in diabetes. Kidney Int Rep. 4(10):1373–1386

    Article  PubMed  PubMed Central  Google Scholar 

  12. Arroyo V, Angeli P, Moreau R, Jalan R, Clària J, Trebicka J et al (2021) The systemic inflammation hypothesis: towards a new paradigm of acute decompensation and multiorgan failure in cirrhosis. J Hepatol. 74(3):670–685

    Article  CAS  PubMed  Google Scholar 

  13. Sterling RL, Lissen E, Clumeck N, Sola R, Correa MC, Montaner J et al (2006) Investigators development of a simple noninvasive index to predict significant fibrosis in patients with HIV/HCV coinfection. Hepatology. 43:1317–1325

    Article  CAS  PubMed  Google Scholar 

  14. Wong F, O’Leary JG, Reddy KR, Patton H, Kamath P, Fallon MB et al (2013) New consensus definition of acute kidney injury accurately predicts 30-day mortality in patients with cirrhosis and infection. Gastroenterology 145:1280–1288

    Article  PubMed  Google Scholar 

  15. Angeli P, Rodríguez E, Piano S, Ariza X, Morando F, Sola E et al (2015) Acute kidney injury and acute-on-chronic liver failure classifications in prognosis assessment of patients with acute decompensation of cirrhosis. Gut 64:1616–1622

    Article  PubMed  Google Scholar 

  16. Hung TH, Tseng CW, Tseng KC, Hsieh YH, Tsai CC, Tsai CC (2014) Effect of renal function impairment on the mortality of cirrhotic patients with hepatic encephalopathy: a population-based 3-year follow-up study. Medicine (Baltimore). 93(14):e79

    Article  PubMed  PubMed Central  Google Scholar 

  17. Hirode G, Vittinghoff E, Wong RJ (2019) Increasing burden of hepatic encephalopathy among hospitalized adults: an analysis of the 2010–2014 national inpatient sample. Dig Dis Sci. 64(6):1448–1457

    Article  CAS  PubMed  Google Scholar 

  18. Guevara M, Baccaro ME, Rios J, Matin-Llahi M, Uriz J, delArbol LR et al (2010) Risk factors for hepatic encephalopathy in patients with cirrhosis and refractory ascites: relevance of serum sodium concentration. Liver Int. 30:1137–1142

    Article  CAS  PubMed  Google Scholar 

  19. Arroyo V, Angeli P, Moreau R, Jalan R, Clària J, Trebicka J et al (2021 Mar) Investigators from the EASL-CLIF Consortium, Grifols Chair and European Foundation for the Study of Chronic Liver Failure (EF-Clif). The systemic inflammation hypothesis: towards a new paradigm of acute decompensation and multiorgan failure in cirrhosis. J Hepatol. 74(3):670–685

    Article  CAS  PubMed  Google Scholar 

  20. Solé C, Solà E, Huelin P, Carol M, Moreira R, Cereijo U et al (2019) Characterization of inflammatory response in hepatorenal syndrome: relationship with kidney outcome and survival. Liver Int. 39(7):1246–1255

    Article  PubMed  PubMed Central  Google Scholar 

  21. Tariq R, Hadi Y, Chahal K, Reddy S, Salameh H, Singal AK (2020) Incidence, mortality and predictors of acute kidney injury in patients with cirrhosis: a systematic review and meta-analysis. J Clin Transl Hepatol. 8(2):135–142

    Article  PubMed  PubMed Central  Google Scholar 

  22. Singal AK, Jackson B, Pereira GB, Russ KB, Fitzmorris PS, Kakati D et al (2018) Biomarkers of renal injury in cirrhosis: association with acute kidney injury and recovery after liver transplantation. Nephron 138:1–12

    Article  CAS  PubMed  Google Scholar 

  23. Romano TG, Schmidtbauer I, Silva FM, Pompilio CE, D’Albuquerque LA, Macedo E (2013) Role of MELD score and serum creatinine as prognostic tools for the development of acute kidney injury after liver transplantation. PLoS One 8:e64089

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  24. Barreto AG, Daher EF, Silva Junior GB, Garcia JH, Magalhães CB, Lima JM et al (2015) Risk factors for acute kidney injury and 30-day mortality after liver transplantation. Ann Hepatol 14:688–694

    Article  CAS  PubMed  Google Scholar 

  25. Bajaj JS, Saeian K (2005) MELD score does not discriminate against patients with hepatic encephalopathy. Dig Dis Sci. 50:753–756

    Article  PubMed  Google Scholar 

  26. Yoo HY, Edwin D, Thuluvath PJ (2003) Relationship of the model for end- stage liver disease (MELD) scale to hepatic encephalopathy, as defined by electroencephalography and neuropsychometric testing, and ascites. Am J Gastroenterol. 98:1395–1399

    Article  PubMed  Google Scholar 

  27. Lucidi C, Corradini SG, Abraldes JG, Merli M, Tandon P, Ferri F et al (2016) Hepatic encephalopathy expands the predictivity of model for end-stage liver disease in liver transplant setting: evidence by means of 2 independent cohorts. Liver Transpl. 22:1333–1342

    Article  PubMed  Google Scholar 

  28. Wong F, O’Leary JG, Reddy KR, Garcia-Tsao G, Fallon MB, Biggins SW et al (2017) Acute kidney injury in cirrhosis: baseline serum creatinine predicts patient outcomes. Am J Gastroenterol. 112:1103–1110

    Article  CAS  PubMed  Google Scholar 

  29. Wong F, Reddy RK, O’Leary JG, Tandon P, Biggins SW, Garcia-Tsao G et al (2019) Impact of chronic kidney disease on outcomes in cirrhosis. Liver Transpl. 25:870–880

    Article  PubMed  Google Scholar 

  30. Cullaro G, Park M, Lai JC (2018) “Normal” creatinine levels predict persistent kidney injury and waitlist mortality in outpatients with cirrhosis. Hepatology. 68(5):1953–1960

    Article  CAS  PubMed  Google Scholar 

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Authors and Affiliations

  1. Department of Internal Medicine, Al-Azhar University, Cairo, Egypt

    Hossam Shahbah, Osman Mohamed Osman, Sadek Mostafa, Abdelgawad Saied Mohamed, Ahmed Alashkar, Mohammed Salah Hussein, Ahmed Eliwa, Ashraf Elbahrawy & Hafez Abdelhafeez

  2. Department of Clinical Pathology, Al-Azhar University, Cairo, Egypt

    Mohamed Saad-Eldeen Radwan

  3. Department of Gastroenterology and Tropical Medicine, Sohag University, Sohag, Egypt

    Alshimaa Alaboudy

  4. Allergy and Immunology Center, Al-Azhar University, Cairo, Egypt

    Hafez Abdelhafeez

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Contributions

A. Elbahrawy and S. Mostafa designed the work, HS and OMO collected the data , A. Mohamed , MSH, A. Alashkar, A. Alaboudy and A. Eliwa did technical support and discussion , M.S-E.R did the laboratory work , and HH supervised the work. The author(s) read and approved the final manuscript.

Corresponding author

Correspondence to Sadek Mostafa.

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The protocol for the research project has been approved by medical ethics committee of Al-Azhar Faculty of Medicine, and it conforms to the provisions of the Declaration of Helsinki. Informed consent was obtained from patients or their next of kin for being included in the study.

Competing interests

Hossam Shahbah, Osman Mohamed Osman,Sadek Mostafa, Abdelgawad Saied Mohamed, Ahmed Alashkar, Mohamed Saad-Eldeen Radwan, Mohammed Salah Hussein, Alshimaa Alaboudy, Ahmed Eliwa, Ashraf Elbahrawy Hafez Abdelhafeez declare that they have no conflict of interest.

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Shahbah, H., Osman, O.M., Mostafa, S. et al. The urine albumin creatinine ratio is one of the predictors of acute kidney injury in hepatitis C-related cirrhotic hepatic encephalopathy. Egypt Liver Journal 12, 62 (2022). https://doi.org/10.1186/s43066-022-00227-7

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