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Abstract: SA-PO724

Lupus-Like Nephritis Secondary to Non-steroidal Anti-inflammatory Drug (NSAID) Use: Case Report

Session Information

Category: Glomerular Diseases

  • 1303 Glomerular Diseases: Clinical‚ Outcomes‚ and Trials


  • Sharma, Sapna, St Barnabas Hospital, Bronx, New York, United States
  • Dhani Mohamed, Angelina, St Barnabas Hospital, Bronx, New York, United States
  • Greffie, Ermias Shenkutie, St Barnabas Hospital, Bronx, New York, United States
  • Paredes, William Mauricio, St Barnabas Hospital, Bronx, New York, United States
  • Ibrahim, Jamil, St Barnabas Hospital, Bronx, New York, United States
  • Flores Chang, Bessy Suyin, St Barnabas Hospital, Bronx, New York, United States

Membranous nephropathy (MN) is a disorder with thickening of the glomerular capillary wall, resulting from immune complex formation on the basement membrane which leads to loss of large amounts of proteins in the urine. MN accounts for 30% of cases of nephrotic syndrome in adults of which 80% are due to primary MN and 20% are secondary to medications such as NSAID and diseases such as systemic lupus erythematosus (SLE), hepatitis B, hepatitis C and malignancies. We present a case of Lupus-like nephritis secondary to NSAID use

Case Description

50-year-old male patient with diabetes, hypertension, asthma and obesity came to the hospital complaining of bilateral lower extremity swelling for 8 months. Physical exam was significant for generalized anasarca, chronic stasis changes in bilateral lower extremities, warmth and erythema of the left leg. His medications included lisinopril, hydrochlorothiazide, omeprazole, diclofenac 100 mg daily for over 8 months for joint pain. Initial serum creatinine was elevated to 9.2 mg/dl, Albumin was decreased to <1 gm/dl. 24-hour total urine protein was 27 g and diagnosis of nephrotic syndrome was made. Extensive workup for infectious causes were negative. Autoimmune workup was negative for antinuclear antibodies, Anti-dsDNA, and rheumatoid factor. This prompted a kidney biopsy which revealed full-house immunofluorescence with focal segmental sclerosing features, diffuse acute tubular injury and moderate interstitial inflammation. He required temporary hemodialysis and was subsequently started on pulse dose steroids for 3 days with subsequent tapering along with lisinopril and albumin. Serum creatinine plateaued around 4.5 mg/dl for which dialysis was discontinued and followed up in clinic


Membranous nephropathy with full-house immunofluorescence (IgG, IgA, IgM, C1q and C3) has been recently recognized in patients without features of SLE, called lupus-like nephritis. The insidious presentation of renal insufficiency with severe lower extremity edema, nephrotic syndrome and biopsy demonstrating full-house immunofluorescence, diffuse acute tubular injury and acute interstitial inflammation suggested NSAID induced MN in our patient. There are no clear guidelines on treatment for secondary MN due to NSAID use and need to be established along with awareness regarding long term effects