Table 4.
Summary of previous studies characterizing transplant immune-complex glomerulopathy (ICG) that cannot be readily classified under a known entity
| Author, journal, yr | Sample size (% all screened biopsies) | Case definition | Other IF features | Comparison to our case definitions | Key conclusions |
|---|---|---|---|---|---|
| Giannico et al.,6Human Pathology 2015 | 28 (3.5%) | Mesangial glomerulopathy without known history of ICG, and excluding IgA-dominant | 23 of 28 IgM dominant. 5 of 28 IgG dominant. 17 of 18 had concomitant C3/C1q. | All our categories except IgA-rich. Encompasses FH | High prevalence of concurrent rejection, both T-cell mediated (36% vs. 7% in control) and ABMR (25% vs. 4%). Rate of progression to graft failure (5 of 28) was not different from that in control (7 of 28), median follow-up 24 months. Authors hypothesize that ICG may not be clinically significant in terms of graft survival. |
| Lloyd et al.,7Human Pathology 2018 | 12 (1.7%) | Immune complexes not attributable to cause of native kidney failure | Typically codominant IgG and IgM; C1q present in 50% | All our categories except IgA-rich. Similar case-finding process | High prevalence of concurrent rejection (75%), including ABMR with DSAs (67%). High rate of progression with graft failure (7 of 12), median follow-up 36 mo. Authors hypothesize that the underlying mechanism for de novo ICG may be alloimmunity. |
| Said et al.,1Modern Pathology 2010 | 24 (0.1%) | C1q 2+ or higher, excluding native MPGN or lupus | Most also had C3, IgG, and IgM | All our categories except IgA-rich and C1q-poor | Lower prevalence of concurrent rejection compared with other studies (5 of 24); 50% had infection in the preceding 6 mo, but no evidence of infection-related GN on histology. Benign course in the absence of a second glomerular lesion |
| Kanai et al.,2BMC Nephrology 2018 | 5 (1.2%) | C1q 2+ or higher, no to mild proteinuria/hematuria | All cases had IgG, IgM, and C3 | qFH | Long-term mesangial C1q deposits accompanied by IgG, IgM, and C3 may be clinically silent. |
| Gough et al.,3Archives of Pathology and Laboratory Medicine 2005 | 9 (7.6%) | IgM immune complexes not otherwise attributable | +IgM with and without C3 | C1q-poor | Earlier onset of ICG (within 1 yr) compared to other studies. Viral infection in 2 of 9, no control group |
| Grau et al.,13Transplantation 2016 | 8 | Convenience sample of 51 transplant glomerulopathy cases. Included cases with immune complexes not otherwise attributable | Typically IgM-positive with variable C1q and C3 | Cases with CWD | In patients with known transplant glomerulopathy, ICG is present in 16% of cases and represents alloimmune response against non-MHC epitopes or mesangial targets. |
ABMR, antibody-mediated rejection; CWD, capillary wall duplication; DSA, donor-specific antibody; FH, full-house; GN, glomerulonephritis; IF, immunofluorescence; MPGN, membranoproliferative glomerulonephritis; qFH, quasi-full-house.