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Case Reports in Nephrology
Volume 2013, Article ID 268401, 3 pages
Case Report

Minimal Change Disease and IgA Deposition: Separate Entities or Common Pathophysiology?

1Department of Medicine, New York University, School of Medicine, New York, NY, USA
2Division of Nephrology, New York University, School of Medicine, New York, NY, USA
3Department of Pathology, New York University, School of Medicine, New York, NY, USA
4Nephrology Section, New York Harbor VA Medical Center, 111G New York DVAMC, 423 E. 23 Streat New York, NY 10010, USA

Received 5 April 2013; Accepted 4 May 2013

Academic Editors: J. Almirall, H. Matsukura, H. Schiffl, and H. Trimarchi

Copyright © 2013 Brandon S. Oberweis et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Introduction. Minimal Change Disease (MCD) is the most common cause of nephrotic syndrome in children, while IgA nephropathy is the most common cause of glomerulonephritis worldwide. MCD is responsive to glucocorticoids, while the role of steroids in IgA nephropathy remains unclear. We describe a case of two distinct clinical and pathological findings, raising the question of whether MCD and IgA nephropathy are separate entities or if there is a common pathophysiology. Case Report. A 19-year old man with no medical history presented to the Emergency Department with a 20-day history of anasarca and frothy urine, BUN 68 mg/dL, Cr 2.3 mg/dL, urinalysis 3+ RBCs, 3+ protein, and urine protein : creatinine ratio 6.4. Renal biopsy revealed hypertrophic podocytes on light microscopy, podocyte foot process effacement on electron microscopy, and immunofluorescent mesangial staining for IgA. The patient was started on prednisone and exhibited dramatic improvement. Discussion. MCD typically has an overwhelming improvement with glucocorticoids, while the resolution of IgA nephropathy is rare. Our patient presented with MCD with the uncharacteristic finding of hematuria. Given the improvement with glucocorticoids, we raise the question of whether there is a shared pathophysiologic component of these two distinct clinical diseases that represents a clinical variant.