Received February 14, 2008
Accepted on May 15, 2008

ORIGINAL ARTICLES

Pauci-immune and Immune Glomerular Lesions in Kidney Transplants for Systemic Lupus Erythematosus

Shane M. Meehan ^*1, Anthony Chang ^*, Amandeep Khurana , Rajendra Baliga , Pradeep V. Kadambi , and Basit Javaid

Departments of *Pathology and Medicine, Section of Nephrology, University of Chicago, Chicago, Illinois; and Department of Medicine, Division of Nephrology, Stanford University School of Medicine, Stanford, California

¹ To whom correspondence should be addressed. E-mail: shane.meehan{at}uchospitals.edu.

	Abstract

Background and objectives: Glomerular lesions in allografts in recipients with end-stage nephritis resulting from systemic lupus erythematosus (SLE) were examined to determine the spectrum of glomerular pathology in recurrent glomerulonephritis (GN).

Design, setting, participants, & measurements: A total of 156 biopsy samples, from 49 serial allografts in 43 recipients with end-stage lupus nephritis, were examined by light microscopy, and by immunofluorescence and electron microscopy in selected cases. These were compared with control allografts (n = 35).

Results: Glomerular lesions best explained by recurrent lupus nephritis were observed in 19 of 49 allografts (38.8%) in lupus recipients. Three categories of glomerulopathies were identified: 1) immune complex glomerulopathies, including mesangial GN (28%) and membranous GN (4%); 2) atypical glomerulopathies, including acute proliferative GN (32%) and focal segmental glomerulosclerosis (12%), with scant immune deposits in glomerular capillaries, frequent endothelial tubuloreticular inclusions, and thrombotic microangiopathy; and 3) transplant-associated glomerulopathies (24%).

Conclusions: Allografts from recipients with SLE had typical immune complex-mediated GN and atypical pauci-immune, proliferative GN and segmental glomerular sclerosis. Atypical glomerulopathies like these suggest a role for nonimmune complex-mediated glomerular injury in recurrent lupus GN.