Advances in antibody-mediated rejection of renal allografts
TL;DR
This review summarizes current concepts in AMR pathogenesis, diagnosis, and emerging therapy, using phenotype-guided assessment to separate expert-consensus practice from randomized evidence, observational experience, and experimental interventions.
Abstract
Antibody-mediated rejection (AMR) remains a major obstacle to long-term kidney allograft survival. It does not arise from a single pathway. Preformed or de novo donor-specific antibodies (DSA), endothelial injury, microvascular inflammation, complement-dependent and complement-independent mechanisms, and chronic remodeling may each contribute, often in different combinations. Recent Banff updates, biopsy-based transcriptomics, DSA assessment, and donor-derived cell-free DNA (dd-cfDNA) testing have made AMR phenotypes easier to recognize. Still, these tests are most useful when interpreted together rather than treated as separate answers. The same caution applies to treatment. Plasma exchange, intravenous immunoglobulin, B-cell or plasma-cell directed agents, complement inhibition, IL-6 pathway blockade, and optimization of maintenance immunosuppression differ in the strength of their evidence, the patients they may help, their toxicities, and their feasibility in routine practice. This review summarizes current concepts in AMR pathogenesis, diagnosis, and emerging therapy, using phenotype-guided assessment to separate expert-consensus practice from randomized evidence, observational experience, and experimental interventions.