The clinical significance of arteriolitis in renal allograft biopsies 

Index

Christopher O.C. Bellamy and Parmjeet S. Randhawa

Department of Pathology, Edinburgh University Medical School, Edinburgh, Scotland, UK (COCB), and Division of Transplantation Pathology, Department of Pathology, University of Pittsburgh, PA, USA (PSR)

Background
The Banff 1997 classification of renal allograft pathology identifies arteriolitis in kidney allograft biopsies as a finding of uncertain significance, although allowance is made for coding the lesion. We have sought to improve our understanding of arteriolitis, by correlating its occurrence with histopathological and clinical parameters.

Methods
Allograft kidney biopsies showing arteriolitis were identified by a text search on archived biopsy reports at the University of Pittsburgh. Arterioles were defined as small vessels satisfying 3 criteria: (1) wall thickness no more than 3 myocytes thick, (2) vessel diameter less than 1/3 that of an adjacent glomerulus in the biopsy, and (3) discontinuous or absent elastica. Arteriolitis was recognized when there was mural infiltration by lymphocytes; luminal adhesion to arteriolar endothelium by lymphocytes was not sufficient for the diagnosis of arteriolitis. A total of 20 biopsies from 19 patients, collected over a 5½ year period, were felt to show arteriolitis, and these formed the study set. Histologic findings in these biopsies and previous or subsequent specimens from these patients were categorized according to the Banff 1997 working formulation. Serum creatinine levels were obtained from the electronic medical records of these patients. Follow-up was available for all 19 patients.

Results
From the 20 biopsies, 10 (50%) showed type IIA rejection, 7 (35%) showed type IA rejection, and 3 (15%) showed borderline change, suspicious for the diagnosis of acute rejection. Of the 3 cases with borderline change, 1 patient showed type IIA rejection in the next biopsy 24 days later, and a second showed type IA rejection on the following biopsy 42 days later. None of the 7 patients with type IA rejection had previous or subsequent type II acute rejection. Hence, in all 11 of 20 biopsies (10 of 19 patients) showing arteriolitis were associated with type IIA rejection (intimal arteritis) in the index or immediately subsequent biopsy. On follow-up, graft loss due to acute rejection occurred in 1/19 (5%) patients, 27 days after the index biopsy, and graft loss due to chronic rejection occurred in 4/19 (21%) patients, 62-224 (median 126) days after index biopsy. Chronic allograft nephropathy developed in a further 4/19 (21%) patients, 15-1134 (median 157) days after index biopsy. The remaining 10/19 (53%) patients followed for 7-1902 (median 773) days have serum creatinine ranging from 1.2-5.5 (median 1.5) mg/dl. All patients with graft loss had shown type IIA rejection on a previous biopsy. However, of the patients developing chronic allograft nephropathy without graft loss, 3/4 showed type IA rejection, and 1/4 showed type IIA rejection in prior biopsies.

Conclusion
Arteriolitis frequently coexists with acute rejection, often type IIA rejection, and is associated with poor graft outcome. Other causes of arteriolitis described in the literature such as drug toxicity, Henoch-Schonlein purpura and crescentic glomerulonephritis appear to be uncommon entities in the setting of renal transplantation, and were not encountered in this series.

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