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Abstract: SA-PO1098

Non-Lupus Immune-Complex Glomerulonephropathy (ICGN) After Kidney Transplantation: A Report of 9 Cases

Session Information

Category: Pathology and Lab Medicine

  • 1502 Pathology and Lab Medicine: Clinical


  • Chin, Kuo-Kai, Stanford University School of Medicine, Stanford, California, United States
  • O'Shaughnessy, Michelle M., Stanford University School of Medicine, Stanford, California, United States
  • Grimm, Paul C., Stanford University School of Medicine, Stanford, California, United States
  • Troxell, Megan L., Stanford University School of Medicine, Stanford, California, United States
  • Cheng, Xingxing S., Stanford University School of Medicine, Stanford, California, United States

ICGN with positive immunofluorescence (IF) for IgG, IgA, IgG, C3, and C1q has been termed “non-lupus full-house nephropathy (FHN)” in the absence of clinical or serologic features of systemic lupus erythematosus (SLE). We describe characteristics and outcomes of ICGN with IgG, C3, and C1q +/- IgM/IgA deposits in the kidney allograft.


We retrospectively reviewed a single-institution pathology database from 2007-2017 to identify cases of allograft ICGN with IgG, C3 and C1q in the absence of SLE. Clinicopathologic and outcome data were derived from patient records.


Of 9 patients, most were non-white (89%), male (89%), and pediatric-adolescent (66%). None had ICGN as cause of ESRD. Median time from transplant to ICGN was 1.6 (range 0.5-5.2) years and 5/9 (56%) were identified on surveillance biopsy. Two of 7 patients had a positive donor-specific antibodies. By light microscopy, 7 cases had mesangial hypercellularity, and two had FSGS. At last follow-up (median 3.9 years, range 0.5-13.8), 7 of 9 patients (78%) had a stable serum creatinine with minimal proteinuria in 6. The remaining 2 patients had persistent allograft dysfunction. Four patients had subsequent biopsies with immunofluorescence: 3 (75%) showed persistent ICGN while 1 (25%) had resolution of immune complexes.


Post-transplant ICGN with IgG, C3 and C1q may be clinically silent and/or resolve spontaneously and in most cases appears to follow an indolent clinical course. Whether immune complex formation results from an auto- or allo-immune response remains to be elucidated.

Pt #AgeSexRaceNative Disease
(Bx, Y/N)
Years Post-TxIndicationLight Microscopy FindingsTherapy ChangeYears Post-BxFollow-Up
173MOtherDiabetic (N)5.2sCr 1.5, uPCR 2.9FSGS, MICD-HYNone3.9Death, sCr 0.8
220MPacific IslanderFSGS (N)1.6SurvMICD-HYNone2.5sCr 1.6
319MWhiteAlport (N)1.3SurvMICD-HYSteroid Pulse, increase MMF9.3sCr 0.7, uPCR 2.0
416MPacific IslanderUnknown (N)2.9sCr 1.5, uPCR 1.1MICD-HYIncrease MMF13.8sCr 3.1, uPCR 7.0
512MUnknownMethylmalonic Acidemia (N)0.5SurvMICD-HYAdd Steroid0.9sCr 0.6
64MBlackDenys-Drash (N)1.1SurvMICD-HYNone5.0sCr 0.8
719FOtherFSGS (Y)2.3sCr 1.3MICDNone4.1sCr 0.9, uPCR 0.12
832MAsianIgA (Y)1.0SurvMICD-HYNone0.6sCr 1.2, uPCR 0.29
960MUnknownHypertension (N)1.6sCr 1.9, uPCR 1.1FSGS, MICDSteroid Pulse0.5sCr 1.9

Tx = Transplant; Bx = biopsy; FSGS = Focal Segmental Glomerulosclerosis; HY = hypercellularity; sCr = serum creatinine, mg/dL; uPCR = urine protein-creatinine ratio, g/g; surv = surveillance; MICD = mesangial immune complex deposition; MMF = mycophenolate mofetil