Transplant glomerulopathy (TG) is a morphologic lesion of renal allografts that is histologically identified by glomerular basement membrane (GBM) duplication and/or multilayering.

[7][8][9] TG is thought to be a morphologic expression of chronic antibody-mediated rejection (ABMR) in most cases and is well-documented as being correlated with a buildup of donor-specific antibodies (DSAs), particularly against HLA class II antigens.

But TG is not exclusive to chronic ABMR; in one-third to one-fourth of cases, thrombotic microangiopathy (TMA), hepatitis C, and possibly T cell-mediated rejection (TCMR) appear to be the alternative etiologies.

[12] Out of all the suggested mechanisms, the one that has been documented the most is the correlation between donor-specific antibody against the human leukocyte antigen (anti-HLA-DSA), antibody-mediated mediated rejection (ABMR), and endothelial damage that results in the development of TG.

Severe nodular hyaline arteriolosclerosis, arterial fibrous intimal thickening, and progressive interstitial fibrosis and tubular atrophy are typically linked to advanced TG.

[22] Immunofluorescence (IF) results for TG show no diagnostic staining for IgG, IgA, or C1q, as well as mild-to-moderate glomerular mesangial along with capillary wall deposition of IgM and C3.