Renal dysfunction is a significant marker of advanced liver disease (ALD), as evidenced by the presence of creatine on the model for end-stage liver disease (MELD), which is the primary clinical model used to predict transplant-free survival in patients with cirrhosis. Patients with pretransplantation renal dysfunction have higher morbidity than patients without and are more prone to developing endstage renal disease after transplantation [1]. Moreover, renal dysfunction can persist after liver transplantation, and in a recent study, the majority of patients with glomerular filtration rate (GFR) < 30 achieved an improvement in their renal function but also maintained impaired kidney function (chronic kidney disease stage III-V) after 3-5 years of follow-up [2]. Patients with GFR < 30 should be evaluated for the possibility of a simultaneous liver and kidney transplantation (SLKT) (with guidelines even proposing automatic approval for these patients), with patients in this group showing increased survival with SLKT compared to liver transplantation [3].Creatinine and creatinine-based estimation of GFR are the primary measurements by which renal function is assessed in clinical practice, with the Chronic Kidney Disease Epidemiology Collaboration equation (CKD-EPI) [4] and the Modification of Diet in Renal Disease equations (MDRD-4 and MDRD-6) [5] being the most prominent. However, there are several reasons due to which these methods present suboptimal accuracy in patients with cirrhosis [6][7][8]. Cystatin-C, a protein almost entirely filtered by the kidneys, has been proposed as a more suitable marker of GFR in patients with cirrhosis. Many studies have reported better estimation of GFR with Cystatin-C-based equations [9][10][11][12][13][14][15]. However, Cystatin-C is not available in most institutions, and even in those used, its measurement is significantly more expensive than the