Search

Introduction and Objectives: : The development of acute kidney injury (AKI) in cirrhotic patients is of multifactorial origin, including urinary tract infection, diuretics, portal hypertension, shock, etc. Another important factor is cholemic nephrosis, it is considered when total bilirubin exceeds 20 mg/dl, this implies that bile pigments damage the distal tubule with deterioration of renal function, increasing morbidity and mortality. This study aimed to evaluate the levels of hyperbilrubinemia in the development of AKI and its association with biomarkers of renal failure. Materials and Patients: : Retrospective and analytical study of a cohort of cirrhotic patients, to evaluate the development of AKI associated with bilirubin levels. Statistical analysis: A binary logistic regression model was performed considering bilirubin (greater than 20), NGAL (greater than 150) and cystatin (greater than 0.95) as associated factors. The significance of the model was considered with an alpha level less than 0.05. Results: 109 patients were included, 45 women 64 men, age 54.67 ± 11.6, Child Pugh A: 2, B: 29, C: 78. The binary logistic model was significant W(1)=11.089, p=0.001. The OR for bilirubin was 4.37 (1.168-16.35, 95% CI P=.027), for NGAL OR 2.7 (1.08-6.71, 95% CI; p=.032), cystatin 0.64 (0.35-11.66, CI 95%; p=0.764) not significant. Conclusions: Hyperbilirubinemia increases the risk of developing AKI by up to 4 times. The useful biomarker for AKI was NGAL.

Introduction and Objectives: Hepatic encephalopathy (HE) is one of the most frequent complications of cirrhosis, minimal hepatic encephalopathy (MHE) is the initial stage and is characterized by the fact that it has no clinical data, its diagnosis is made with neuropsychological tests, the MHE produces a deterioration in the quality of life of patients and an increased risk of accidents. Hence, it is relevant to diagnose. Performing neuropsychological tests requires prolonged time, so validating an MHE count test that is easy, reproducible, and in less time is recommended. The simplified-animal naming test (S-ANT) test is performed by asking the patient to nominate 20 animals in one minute. In the reference cutoff for the non-Mexican population, a score lower than 15 suggests MHE.We aimed to assess the validity of the S-ANT scale as a screening test in patients with cirrhosis without overt HE. Materials and Patients: We present a prospective, descriptive, and analytical study of patients with cirrhosis of different etiology without overt HE who underwent S-ANT, PHES, and Flicker tests. We determine the area under the receiver operator characteristic (AUROC) curve to validate the S-ANT test. MHE was detected if the PHES and Flicker tests were abnormal.We compared the S-ANT scores of both groups with and without MHE with the student's t-test for independent groups. Sensitivity (S) and specificity (SE) were calculated with the AUROC cutoff point for MHE. Results: Detection of MHE was in 12/83 patients (14.5%); 43 (51.83%) women, mean age 52.7 ± 7.5 years, median schooling 8.3 years (range 0-17), the etiology of cirrhosis was: 39 (47.0%) alcohol, 9 (28.9%) primary biliary cirrhosis, 17 (20.5%) metabolic fatty liver, 18 (21.7%) hepatitis C virus According to Child-Pugh: 57 (68.7%) A, 25 (30.1%) B, and 1 (1.2%) C. The mean S-ANT for non-MHE was 19.35±5.4, and for MHE, 14.7±5.6, p=0.024 AUROC was significant .760 (.577- .942, 95%CI); p=0.037 with S=83% and SE=77% cutoff= 17.5 words, which is higher than for other populations. Conclusions: In the Mexican population, S-ANT reliably discriminates against patients with cirrhosis without overt HE with cognitive impairment, confirmed by PHES and Flicker test

Introduction and Objectives: MAFLD is a highly prevalent cause of chronic liver disease, present in 70% of overweight people, 70% of diabetics, and 90% of morbidly obese people. It is the hepatic manifestation of the metabolic syndrome, defined by the presence of central obesity, insulin resistance, hyperlipidemia, hyperglycemia, and hypertension. The development of liver fibrosis is secondary to several factors, steatosis being one of them. To evaluate the correlation of steatosis with hepatic fibrosis in patients with metabolic syndrome using transition elastography. Materials and Patients: Patients older than 18 years who met MALFD criteria were included, transition elastography was performed to calculate CAP and kilopascals, steatosis degree and fibrosis degree were calculated according to the myfibroscan application, for statistical analysis Pearson's bivariate correlations were used between CAP and kilopascal values. The association between the degree of steatosis and fibrosis was performed using the chi-square test. Was considered significant at p < 0.05. Results: 94 patients were included, 20 men (21.3%), 74 women (78.7%), mean age 40.5 ± 10.02, CAP 300.6 ± 63.4, kilopascals 6.4 ± 2.7, steatosis grade S0: 8, S1: 8, S2: 20, S3: 58, degree of fibrosis F0: 58, F1: 14, F2:14, F3: 6, F4:2. The correlation between CAP and kilopascals was moderate and significant RHO=0.343 P =0.001. A significant association was found between the degree of steatosis and that of fibrosis chi-square (12) =25.1, p=0.015. The proportions were 50% (S0:F0), 16% (S1:F3), 50% (S2:F3), 100% (S3:F4). Conclusions: The correlation between steatosis and fibrosis is moderate, implying that there are other factors that influence the development of fibrosis and its progression, so metabolic control and other factors in patients with MALFD are highly relevant to prevent fibrosis progression.