Immune-complex deposits in “pauci-immune” glomerulonephritis: a case report and brief review of recent literature Mireille El-Ters1, Umadevi Muthyala2, Marie D. Philipneri3, Fadi A. Hussein3, Krista L. Lentine3,4 Case report 1Department Internal Medicine, Saint Louis University School of Medicine, St. Louis, USA 2Division of Endocrinology, Saint Louis University of Medicine, St Louis, USA 3Division of Nephrology, Saint Louis University School of Medicine, St. Louis, USA 4Center for Outcomes Research, Saint Louis University, St. Louis, USA Submitted: 22 August 2009 Accepted: 22 September 2009 Arch Med Sci 2010; 6, 4: 633-637 DOI: 10.5114/aoms.2010.14479 Copyright © 2010 Termedia & Banach A b s t r a c t Anti-neutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis is considered a “pauci-immune” disease, characterized by absent or mild glomerular tuft staining for immunoglobulin and/or complement. We describe a 72-year-old man with progressive renal failure over five months who was found to have P-ANCA associated crescentic glomerulonephritis. Renal biopsy also revealed immunofluorescence staining for Immunoglobulin G and C3. Treatment comprised corticosteroids, cyclophosphamide, and plasmapheresis but unfortunately kidney function did not recover, likely due to substantial interstitial fibrosis at diagnosis. This case illustrates that serologic evaluation for ANCAs should not be discounted when immune deposits are present. Prompt diagnosis is warranted. Key words: anti-neutrophil cytoplasmic antibodies, glomerulonephritis, immune deposits. Introduction Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis is associated with rapidly declining renal function, and often leads to end-stage renal disease (ESRD) or death if not treated promptly and aggressively [1]. The disease is typically characterized by “pauci-immune” cresentic glomerulonephritis. However, there are a few reports of ANCA-associated glomerulonephritis with immune deposits in the literature, and the exact role of these deposits is not well understood [2-4]. Case report A 72-year-old man with hypertension and chronic obstructive pulmonary disease was referred to our institution for evaluation and management of renal failure. He had been followed at an outside facility with progressively deteriorating renal function over several months. Serum creatinine was 1.6 mg/dl 5 months previously, and rose to 3.8 mg/dl in the next 3 months. Initially, renal insufficiency was attributed to prostatic outlet obstruction. However, renal function did not improve with attempts to relieve obstruction by prostatectomy. Nephrotic-range proteinuria was also detected at 3.6 g of urinary protein per day. On presentation to our institution, physical Corresponding author: Krista L. Lentine, MD, MS Center for Outcomes Research Saint Louis University 3545 Lafayette Avenue Salus Center St. Louis, MO, 63104, USA E-mail: lentne.krista @stanfordalumni.org