Abstract: TH-PO965
Tubular Basement Membrane Deposits in Lupus Nephritis
Session Information
- Glomerular Trainee Case Reports
November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 1203 Glomerular Diseases: Clinical, Outcomes, and Trials
Authors
- Malik, Anum, Cleveland Clinic Foundation, Cleveland, Ohio, United States
- Abu Hweij, Roulan, Cleveland Clinic Foundation, Cleveland, Ohio, United States
- Herlitz, Leal C., Cleveland Clinic Foundation, Cleveland, Ohio, United States
- Nakhoul, Georges, Cleveland Clinic Foundation, Cleveland, Ohio, United States
Introduction
Glomerular lesions are the main renal finding in lupus nephritis (LN). Extraglomerular deposits can be observed in more than half of LN biopsies but are typically observed in conjunction with glomerular findings. We present a unique case of LN with tubulointerstitial inflammation secondary to prominent TBM immune deposits without glomerular activity.
Case Description
27 year old African American male with systemic lupus erythematosus (SLE) for 5 years, with biopsy proven LN class V, was admitted from nephrology clinic for work up of acute kidney injury. He was initially treated with hydroxychloroquine (HCQ) and prednisone at the time of his SLE diagnosis. On diagnosis of LN, 4 years later, mycophenolate mofetil (MMF) was added, which he was intolerant to and discontinued. He had 2 episodes of SLE flares for which rituximab was given. Azathioprine was added to his regimen of prednisone and HCQ after the second SLE flare. Prior to current presentation, the patient had started to taper his prednisone and was on 10mg daily. In this setting, his serum creatinine (SCr) rose to 4.32mg/dl from a baseline of 1.4-1.6mg/dl; C3 was low at 77; C4 was normal; dsDNA antibody was negative. He had an active urinary sediment. He was started on 125mg of methylprednisolone intravenously for 3 days. Renal biopsy was pursued to re-stage his LN and further determine the immunosuppression needed. Pathology showed active tubulointerstitial inflammation secondary to prominent TBM immune deposits without glomerular activity. He also had changes consistent with class V LN. He was discharged on oral prednisone 60mg daily, with a weekly 10mg taper, MMF 250mg daily, which he agreed to retry and HCQ 400 daily.
Discussion
Only 11 cases have shown predominant TBM LN in the literature. Studies have shown a correlation with TBM immune deposits and a twofold higher risk of end-stage renal disease or doubling of SCr after controlling for other factors. Thus, this finding is of prognostic significance. Treatment of predominant tubulointerstitial LN is not established. Most reported patients did not require cytotoxic immunosuppressive treatment and responded well to steroids alone.