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.

Acute nephrotic-range glomerular proteinuria following ibuprofen intoxication in two cats

“…Interestingly, this type of renal injury in humans often occurs at therapeutic doses of NSAIDs, further highlighting its dose-independent nature. 7 , 8 , 14 …”

“…Interestingly, this type of renal injury in humans often occurs at therapeutic doses of NSAIDs, further highlighting its dose-independent nature. 7,8,14 Notably, there is often no clear-cut demarcation in humans between the two forms of NSAID renal toxicity and evidence of tubular necrosis and glomerular injury may be found in the same patient. 12 Given the short time course of AKI and complete resolution of proteinuria in both cats, no histopathology was performed to confirm glomerular damage.…”

Crocin improves the renal autophagy in rat experimental membranous nephropathy via regulating the SIRT1/Nrf2/HO-1 signaling pathway

“…Therefore, this study was designed to investigate the biological functions of crocin in MN development and detect whether the effect of crocin was mediated by the Sirt1/Nrf2/HO-1 pathways in PHN rats. Several studies have shown that angiotensin-converting enzyme (ACE) inhibitors can reduce proteinuria in patients with MN [ 42 , 43 ]. Enalapril is a potent, orally-active, long-acting, nonsulphydryl ACE inhibitor, can treat the proteinuria of membranous glomerulonephritis without detriment to systemic or renal hemodynamics [ 44 ].…”