Inflammatory bowel disease (IBD) can extend beyond the gastrointestinal tract, affecting extraintestinal organs and significantly increasing morbidity and mortality. Despite early studies revealing kidney involvement in nearly a quarter of patients with IBD, renal manifestations have been notably overlooked. Among these manifestations, nephrolithiasis, obstructive uropathy, and fistula formation between the bowel and urinary tract are the most reported occurrences. Additionally, renal parenchymal involvement in IBD, including glomerulonephritis (GN), tubulointerstitial nephritis, and amyloidosis, has been documented. GN is particularly noteworthy, as a significant proportion of patients progress to end-stage kidney disease (ESKD). Although GN has long been recognized as a potential extraintestinal manifestation (EIM) of IBD, it has often been dismissed as an anecdotal association. Recently, several studies highlighted the clinical correlation between GN and IBD, suggesting a pathogenic interplay involving gut inflammation, dysbiosis, and intrinsic glomerular processes. Thus, our objective is to elucidate the basis of IBD-related nephropathies, with a specific focus on IgA nephropathy (IgAN) and the gut–kidney axis.

Background: Managing extraintestinal manifestations (EIMs) in inflammatory bowel disease (IBD) patients remains challenging due to considerable heterogeneity in diagnostic criteria and the lack of a standardised definition and validated diagnostic pathways. Delays in recognising and treating EIMs can lead to significant disease progression. Therefore, early detection and treatment are crucial. Objectives: We aimed to assess the effectiveness of a dedicated immune-mediated inflammatory diseases (IMIDs) clinic in reducing EIM diagnostic delays and improving patients’ outcomes. Design: A single-centre observational study was conducted, including IBD patients presenting with EIMs red flags. Methods: We compared the EIMs diagnostic delay between patients who attended a multidisciplinary IMID outpatient clinic (IMID-G) and those who attended individual referral specialists representing the standard outpatient clinic group (SOC-G). We further evaluated the impact of diagnostic timing on 18-month clinical outcomes, including therapeutic changes, steroid and immunosuppressant use and biological therapy switch/swap. Results: We enrolled 238 IBD patients, 127 in the IMID-G and 111 in the SOC-G. The average time to EIM diagnosis was 2.48 ± 1.8 and 5.36 ± 2.3 months for the IMID and SOC-Gs (Δ = 2.88 months, p = 0.005). The majority of patients received a diagnosis of peripheral arthritis (IMID-G = 37.5%; SOC-G = 33.7%) and spondyloarthropathy (IMID-G = 32.1%; SOC-G = 33.7%). No significant difference was observed in the rates of EIMs between the two groups (88.2% in IMID-G vs 92.8% in SOC-G, p = 0.27). Regarding therapeutic changes, the IMID-G reported a mean time to the first therapeutic change driven by the specialist referral of 2.96 ± 1.8 months, compared to 6.09 ± 2.5 months in the SOC-G, showing a significant difference ( p = 0.007). The IMID-G had a higher frequency of biological therapy switching/swapping and adding immunosuppressive treatment than the SOC-G ( p = 0.008 and p = 0.04, respectively). Survival curves revealed a significant reduction in diagnostic delay and time to treatment in the IMID-G compared to the SOC-G (log-rank test, p < 0.001). Conclusion: Attending a dedicated IMID clinic can enhance the diagnostic process for EIMs in IBD patients, thereby reducing diagnostic delays and allowing early interventions to avoid disease progression.

Background: Bowel urgency (BU) is reported by over 80% of patients with ulcerative colitis (UC) and 60% of those with Crohn's disease (CD). However, the impact of advanced therapies on BU has not been consistently evaluated. Objectives: To assess the effect of advanced therapies on BU improvement in patients with UC and CD. Methods: This retrospective cohort study included all consecutive patients with confirmed UC or CD who started an advanced therapy with available data regarding BU before and after induction therapy between 2023 and 2024 at two tertiary centers. BU was assessed using the numeric‐rating‐scale urgency score (NRS‐us), with BU defined as NRS‐us ≥ 3. The primary endpoint was BU improvement (NRS‐us ≤ 3 or reduction of at least two points) after the induction phase. Multivariate logistic regression analysis identified factors associated with BU improvement. Results: A total of 159 patients were included (56% male; 65% UC; median age: 36 years (Interquartile range [IQR] 27–25)). TNFα inhibitors were the most frequently used agents (49.6%). At baseline, the median NRS‐us was 7. After induction, 50.9% of patients achieved BU improvement, with a mean reduction of 2.3 ± 2.9 points. BU improvement was significantly associated with clinical remission (false‐discovery‐rate [FDR] = 0.009 in CD and FDR = 0.010 in UC), normalization of fecal calprotectin (FDR = 0.001), CRP (FDR = 0.008), and bowel wall thickness on intestinal ultrasound (FDR = 0.001). No significant differences were observed between therapeutic classes. Conclusion: BU improved in approximately half of IBD patients following induction with advanced therapies. Its improvement correlated with clinical, biochemical, and ultrasound remission, supporting the incorporation of BU assessment into routine clinical monitoring.