Cytomegalovirus (CMV) colitis, a complication in patients with inflammatory bowel disease (IBD), particularly ulcerative colitis (UC), is a significant diagnostic and therapeutic challenge due to its overlap with IBD flares. CMV reactivation in IBD is driven by chronic inflammation, compromised immune function, and use of immunosuppressive agents like corticosteroids. Risk factors include older age, pancolitis, and severe disease. Diagnosis hinges on endoscopy and histology, with tissue biopsy and immunohistochemistry as the gold standard. Quantitative tissue PCR may aid in differentiating latent from active infection. CMV colitis exacerbates IBD symptoms, prolongs hospitalization, and increases colectomy rates. Antiviral therapy, primarily ganciclovir, improves outcomes in patients with corticosteroid-refractory UC. Treatment focuses on tapering corticosteroids, optimizing biologic therapies such as infliximab, and a careful application of antivirals tailored to disease severity and viral load. Further research is needed to refine diagnostic thresholds and treatment strategies to mitigate CMV’s impact on IBD prognosis. Early identification and individualized management are critical to improving clinical outcomes and reducing morbidity.

Background: Acute kidney injury (AKI) is common in alcohol-associated hepatitis (AH) and associated with poor outcomes, yet the prognostic implications of AKI timing and early renal trajectory remain unclear. Methods: In this prospective multicenter cohort from the Global AlcHep Prospective Database, patients with AH were classified as no AKI, prevalent AKI at admission, or incident AKI during hospitalization. The primary outcome was 90-day mortality, using competing-risks regression with liver transplantation as the competing event. A 7-day landmark analysis assessed the prognostic impact of AKI trajectory among prevalent AKI patients. Results: Among 581 patients, 37% had prevalent AKI, and 11% developed incident AKI. The 90-day mortality was 18.2% (11 transplantations, 1.9%). Prevalent AKI was predominantly functional (84%), while incident AKI had a higher proportion of structural injury (44%). Despite lower baseline severity [median mDF 59.8 vs. 69.3 and lower rates of ACLF grade 3 (23.4% vs. 45.3%)], incident AKI conferred mortality of similar magnitude to prevalent AKI (sHR 2.18, 95% CI 1.19–3.99 vs. sHR 1.80, 95% CI 1.02–3.16). Among 7-day survivors (N=457), prevalent AKI without progression had mortality similar to no AKI (sHR 1.27, p =0.52), while prevalent AKI with progression carried the worst prognosis (sHR 3.34, 95% CI 1.44–7.77). Conclusion: Both prevalent and incident AKI independently predict mortality in AH. Incident AKI confers equivalent risk despite lower disease severity and a distinct etiologic profile with higher rates of intrinsic renal injury. Early renal trajectory refines risk beyond baseline AKI status, where absence of progression approximates outcomes of those without AKI, while progressive AKI identifies the highest-risk subgroup.