Case Report: A Rare Presentation of NSAID-Induced Secondary Membranous Nephropathy in a Pediatric Patient

Abstract

Background: Membranous nephropathy (MN) is a common cause of nephrotic syndrome in adults, but it is responsible for <5% of nephrotic syndrome cases in children. MN has primary and secondary forms. Secondary MN is caused by viral infections, autoimmune diseases like lupus, or drugs. Non-steroid anti-inflammatory drug (NSAID)-induced secondary MN is rarely described in the pediatric population. Thus, the clinical presentation and time to recovery are vastly unknown in the pediatric subgroup. Clinical Presentation: We report a case of a 15-year-old female who presented with acute onset of nephrotic range proteinuria, significant hypoalbuminemia, hyperlipidemia, and lower extremity edema related to the presence of nephrotic syndrome. She had a history of ibuprofen use periodically for 6 months before presentation because of menstrual cramps and intermittent lower abdominal pain. After the presentation, we performed a renal biopsy that reported stage 1-2 MN, likely secondary. The phospholipase A2 receptor (PLA2R) antibody on the blood test and PLA2R immune stain on the renal biopsy sample were negative. We performed a comprehensive evaluation of the viral and immune causes of secondary MN, which was non-revealing. She had stopped ibuprofen use subsequent to the initial presentation. She was prescribed ACE inhibitor therapy. After 6 months of ACE inhibitor treatment, the proteinuria had resolved. Conclusion: Proteinuria can last for several weeks when NSAID induces secondary MN and nephrotic syndrome. With the widespread use of NSAIDs prevalent in the pediatric community, further studies are needed to evaluate and study the role of NSAIDs in this condition.

Keywords: ACE inhibitor; NSAID; membranous nephropathy; nephrotic syndrome; proteinuria.

Figure 1

H&E, 4X: The renal biopsy shows glomeruli with normal cellularity and no significant tubular atrophy or interstitial fibrosis.

Figure 2

Jones Silver, 40X: The glomerulus lacks well-developed “spikes” or “holes”.

Figure 3

IgG, 40X: The glomerulus demonstrates mesangial and diffuse global, granular capillary loop staining.

Figure 4

EM: The glomerulus demonstrates mesangial (arrow) and segmental small subepithelial electron-dense deposit.

Figure 5

EM: The glomerulus demonstrates mesangial and segmental small subepithelial electron-dense deposit (arrows).

Figure 6

Trends in proteinuria on ACE inhibitor therapy.