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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. |
