Recurrence of Immunotactoid Glomerulopathy with Monoclonal IgG3κ Deposits after Kidney Transplant

K Miki,K Iwadoh,T Murakami,M Sumida,K Honda

doi:10.17352/2640-7973.000006

Abstract

We report a case of rapid recurrence of immunotactoid glomerulopathy (ITG) with monoclonal IgG3κ deposits in a transplanted renal graft.

Highlights

Immunotactoid glomerulopathy (ITG), first reported by Korbet et al in 1985 as a glomerular deposition disease in which immunoglobulin-derived protein filaments deposit in the glomeruli and cause a range of nephritis [1], is a rare renal disease found in fewer than 1% of all kidney biopsies [2,3]. It exhibits pathological manifestations ranging from mesangial proliferative glomerulonephritis to membranoproliferative glomerulonephritis (MPGN)
ITG can be distinguished pathologically from other types of glomerulopathies accompanied with fibrillary deposits, such as fibrillary gromerulonephritis, lupus nephritis, cryoglobulinemia and light-chain deposition disease
ITG can engender proteinuria, microscopic hematuria and often hypertension, which might result in end stage renal disease necessitating renal replacement therapy in the long run [2]

Summary

Introduction

Immunotactoid glomerulopathy (ITG), first reported by Korbet et al in 1985 as a glomerular deposition disease in which immunoglobulin-derived protein filaments deposit in the glomeruli and cause a range of nephritis [1], is a rare renal disease found in fewer than 1% of all kidney biopsies [2,3]. Our patient with ITG experienced immediate recurrence after kidney transplantation. A 55-year-old man who developed nephrotic syndrome was diagnosed with ITG, proven by kidney biopsy in July 2004 He underwent steroid pulse therapy, his renal function deteriorated gradually. Steroid pulse therapy and plasmaphereses were performed for ITG recurrence At this time, serum protein electrophoresis showed a monoclonal peak of IgGκ. Total serum hemolytic complement (CH50) and C4 were normal, 33.8 U/mL (25.0–48.0 CH50/ml) and 17.1 mg/dL (15–40 mg/dL), respectively After this second round of treatment, s-Cr level fell to 1.5 mg/dL associated with improved clinical parameters of hematuria (40–50/HF) and proteinuria (0.43 g/day). RXM and BXM were administered in accordance with our protocol for ABOI-KTx, and plasmaphereses were frequently conducted postoperatively, the transplanted kidney function deteriorated progressively. The recurred ITG advanced to a stage where it did not effectively respond to any conventional treatment for aAMR

Discussion

Findings

Graft loss