ReviewFrontiers in immunology2026
Metabolic dysregulation and antibody-mediated rejection after kidney transplantation: interacting mechanisms and emerging clinical strategies.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Kidney transplantation (KT) improves survival in end-stage renal disease, but long-term outcomes are undermined by antibody-mediated rejection (ABMR) and metabolic complications. Recent insights suggest a mechanistic interplay between immune injury and metabolic dysregulation. Methods: This narrative review synthesizes current literature on the pathogenesis and clinical impact of antibody-mediated rejection (ABMR), the epidemiology of post-transplant metabolic syndrome-including post-transplant diabetes mellitus, dyslipidemia, and hypertension-and their bidirectional relationship. Emerging diagnostic tools and therapeutic strategies are also examined. Results: ABMR remains a leading cause of late graft failure. Concurrently, 30% ~ 50% of KT recipients develop metabolic syndromes within the first year, driven by immunosuppressive agents and underlying risk factors. Metabolic abnormalities enhance endothelial activation and complement-driven inflammation, aggravating ABMR. Conversely, immunosuppressive intensification to treat ABMR worsens metabolic profiles, forming a vicious cycle. Novel immunologic (e.g., complement inhibitors, anti-CD38 antibodies) and metabolic (e.g., SGLT2 inhibitors, GLP-1 receptor agonists) agents show promise, though data on long-term efficacy remain limited. Conclusion: Integrated immunometabolic strategies are essential for optimizing graft and patient survival. Future research should focus on personalizing immunosuppression and targeting metabolic health to break the feedback loop linking ABMR and metabolic disease.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.