Abstract: PO0128
Minimal Change Nephrotic Syndrome Superimposed on Anti-Glomerular Basement Membrane Antibody Glomerulonephritis: A Case Report
Session Information
- AKI Clinical, Outcomes, and Trials - 2
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Shibata, Yuko, Kyorin Daigaku, Mitaka, Tokyo, Japan
- Fukuoka, Kazuhito, Kyorin Daigaku, Mitaka, Tokyo, Japan
- Kaname, Shinya, Kyorin Daigaku, Mitaka, Tokyo, Japan
Group or Team Name
- Kyorin university school of medicine
Introduction
Background : The renal prognosis of anti-GBM glomerulonephritis (anti-GBM GN) is extremely poor as renal dysfunction often progresses acutely before the initiation of treatment. It is also known that once the disease activities are controlled by aggressive treatment, its recurrence is rare. Here we experienced a case of anti-GBM GN that improved from severe renal dysfunction but later relapsed. A possible cause was thought to be a rare complication of minimal change nephrotic syndrome (MCNS).
Case Description
A 30-year-old man was admitted to our hospital because of general malaise, fever, oliguria and renal dysfunction. The patient's laboratory data showed serum creatinine as high as 6.6 mg/dl and severe inflammation (C-reactive protein 20.6mg/dl). Anti-glomerular basement membrane antibody (anti-GBM Ab) was detected in his serum, leading to a diagnosis of anti-GBM GN. Treatment was initiated with high-dose glucocorticoid (GC) and plasma exchange therapy (PE), and the patient's renal function and oliguria improved rapidly and he was discharged 40 days after admission. Renal biopsy findings showed cellular crescents associated with linear IgG depositions along the glomerular tufts compatible with anti-GBM GN, but only about one-third of the glomeruli was involved, suggesting that it still remained an early stage of the disease. However, two months after discharge, he had a relapse and was readmitted due to severe proteinuria associated with positive anti-GBM Ab. On the second admission, he was treated with high-dose GC and PE combined by intravenous cyclophosphamide, and completed remission was achieved a few weeks later. Electron microscopy of the renal biopsy that returned later showed significant foot process effacement on podocytes in the apparently normal glomeruli without electron dense deposits.
Discussion
Considering clinical course and renal pathology findings, it is suggested that the present case was a rare complication of an early stage of anti-GBM GN and MCNS. Although the cause of concurrent development of anti-GBM GN and MCNS associated with anti-GBM antibody titers is unclear, it might have been precipitated by influenza infection or some unknown factor.