Background & Aims: The association of liver biochemistry with clinical outcomes of SARS-CoV-2 infection is currently unclear and the utility of longitudinally-measured liver biochemistry as prognostic markers for mortality is unknown. We aimed to determine whether abnormal liver biochemistry, assessed at baseline and at repeat measures over time, was associated with death in hospitalised patients with COVID-19 compared to those without COVID-19, in a UK population. Approach & Results: We extracted routinely collected clinical data from a large teaching hospital in the UK, matching 585 hospitalised SARS-CoV-2 RT-PCR-positive patients to 1165 hospitalised RT-PCR-negative patients for age, gender, ethnicity and pre-existing comorbidities. 26.8% (157/585) of COVID-19 patients died, compared to 11.9% (139/1165) in the non-COVID-19 group (p<0.001). At presentation, a significantly higher proportion of the COVID-19 group had elevated alanine aminotransferase (20.7% vs. 14.6%, p=0.004) and hypoalbuminaemia (58.7% vs. 35.0%, p<0.001), compared to the non-COVID-19 group. Within the COVID-19 group, those with hypoalbuminaemia at presentation had 1.83-fold increased hazards of death compared to those with normal albumin (adjusted HR 1.83, 95% CI 1.25-2.67), whilst the hazard of death was ~4-fold higher in those aged >/=75 years (adjusted HR 3.96, 95% CI 2.59-6.04) and ~3-fold higher in those with pre-existing liver disease (adjusted HR 3.37, 95% CI 1.58-7.16). In the COVID-19 group, alkaline phosphatase (ALP) increased (R=0.192, p<0.0001) and albumin declined (R=-0.123, p=0.0004) over time in patients who died. Conclusion: In this UK population, liver biochemistry is commonly deranged in patients with COVID-19. Baseline hypoalbuminaemia and rising ALP over time could be prognostic markers for death but investigation of larger cohorts is required to develop a better understanding of the relationship between liver biochemistry and disease outcome.