Acute kidney injury (AKI) is a serious clinical condition that is linked to markedly higher rates of morbidity and mortality in cirrhosis patients. Its diagnosis is challenging due to overlapping clinical and laboratory features among causes such as hepatorenal syndrome (HRS), acute tubular injury (ATI), and prerenal hypovolemia. In order to address the distinct pathophysiology and clinical context of cirrhosis, the definitions and classification of AKI have changed over time, moving from RIFLE and AKIN to KDIGO and ICA-AKI. Because cirrhosis patients have altered muscle mass and fluid retention, traditional markers like serum creatinine (sCr) and urine output have significant limitations. Neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), interleukin-18 (IL-18), and cystatin C (CysC) are some of the new biomarkers that have shown promise in early AKI detection and in differentiating structural from functional kidney injury. NGAL and KIM-1 are sensitive indicators of tubular damage with potential prognostic implications. IL-18 reflects inflammatory injury, and CysC offers a more reliable measure of glomerular filtration. Incorporating these markers may improve early diagnosis, risk stratification, and treatment decisions, representing a key direction for future research in managing AKI in cirrhosis.

Background: Early rebleeding after endoscopic variceal ligation (EVL) represents a serious complication in patients with cirrhosis and is associated with poor short-term outcomes. This study aimed to identify independent predictors of early rebleeding after EVL, with a particular focus on distinguishing factors associated with variceal rebleeding from those related to post-banding ulcer (PBU) bleeding, and to assess predictors of six-week mortality. Methods: We conducted a retrospective cohort study including 217 cirrhotic patients who underwent first emergency EVL for an index episode of esophageal variceal bleeding at a tertiary referral center. Early rebleeding was defined as recurrent upper gastrointestinal bleeding occurring between days 6 and 42 after the index EVL. Results: Early rebleeding occurred in 38/217 patients (17.5%): 27/38 (71.1%) variceal rebleeding and 11/38 (28.9%) PBU rebleeding. In multivariable logistic regression analysis, lower hemoglobin (OR = 0.19, 95% CI: 0.067–0.539, p = 0.002) and a higher albumin–bilirubin (ALBI) grade (OR = 24.94, 95% CI: 1.134–548.342, p = 0.041) were independently associated with increased odds of early variceal rebleeding, whereas a higher number of bands applied during index EVL (OR = 0.52, 95% CI: 0.302–0.896, p = 0.019) was independently associated with reduced odds of rebleeding, with excellent model discrimination (area under the curve [AUC] 0.981; 95% CI: 0.959–1.000). For PBU rebleeding, lower fibrinogen level was the only independent predictor (OR = 0.957, 95% CI: 0.916–1.000, p = 0.047), with strong discriminative performance (AUC 0.945; 95% CI: 0.909–0.982). Model for End-Stage Liver Disease (MELD) score, serum albumin, platelet count, and PBU rebleeding independently predicted six-week mortality. Conclusions: Markers of liver function, along with endoscopic parameters, predict early rebleeding after EVL, emphasizing the importance of the complete assessment of cirrhotic patients for refined risk stratification and tailored post-EVL management.

Inflammatory bowel disease (IBD) includes Crohn’s disease (CD) and ulcerative colitis (UC), chronic immune-mediated conditions of the gastrointestinal tract characterized by alternating periods of disease activity and remission with a complex multifactorial pathogenesis. Persistent intestinal inflammation in IBD is a key driver of disease progression and is strongly associated with the development of complications such as dysplasia, colorectal cancer (CRC), intestinal strictures, and fistulas. It may also result in changes in anorectal function, identifiable and classifiable using high-resolution anorectal manometry. Histologic and endoscopic assessments are essential for the evaluation of intestinal inflammation. Cumulative inflammatory burden (CIB) is an important concept that quantifies inflammatory exposure in IBD over time by integrating the severity and duration of histologic inflammation across the disease course, highlighting the importance of long-term inflammatory activity in the development of CRC. Histologic healing may be an important therapeutic target in IBD to reduce the risk of long-term complications. In parallel, emerging precision medicine approaches aim to improve risk stratification and enable early, individualized interventions to reduce disease-related outcomes. Endoscopy also plays a fundamental role in monitoring high-risk patients and guiding treatment decisions. This review aims to characterize the main intestinal complications extending beyond the mucosa that are associated with cumulative chronic inflammation in patients with IBD, including dysplasia, CRC, strictures, fistulas, and anorectal dysfunction in an era increasingly focused on achieving complete mucosal healing. Particular attention is drawn to the significant role of persistent histologic and endoscopic inflammation in disease progression and development of complications, highlighting the specific features and associated risk factors of these disease-related outcomes. Throughout, this review emphasizes the fundamental role of endoscopy in the timely detection, monitoring, and therapeutic management of IBD-related complications, thereby reinforcing its role in comprehensive patient care.