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Abstract: TH-PO662

Not All Lupus Nephritis Is "Complement"-ary

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Trials


  • Parkinson, William M., Brooke Army Medical Center, Fort Sam Houston, Texas, United States
  • Rayman, Ryan, Brooke Army Medical Center, Fort Sam Houston, Texas, United States
  • Guan, Andy, Brooke Army Medical Center, Fort Sam Houston, Texas, United States
  • Denapoli, Thomas S., Pathology Reference Laboratory, San Antonio, Texas, United States
  • Wickham, Jesse M., Brooke Army Medical Center, Fort Sam Houston, Texas, United States

Lupus nephritis (LN) is a common but serious manifestation of Systemic Lupus Erythematous (SLE) that can lead to high morbidity and mortality, ultimately affecting up to 50% of patients with SLE. Typically, LN presents early in the clinical course of SLE, often within the first 3 years after diagnosis. Although the clinical manifestations of LN vary greatly, from nearly asymptomatic to rapidly progressive glomerulonephritis (RPGN), the typical presentation of LN includes edema, hypertension, proteinuria, and microscopic hematuria in patients with known SLE. We present a case with a classical presentation of lupus nephritis that did not follow the typical serologic findings.

Case Description

A 19-year-old white female with no significant past medical history presented to her primary care with 6-month history of intermittent bilateral itching leg pain and a 20lb weight gain. She initially attributed her leg pain to a high level of physical activity. Pain was worse between her knees and ankles and only temporarily alleviated with rest, massage, and ice. Over the past month, she developed new bilateral swelling in her legs. She denied history of recent illness, chest pain, SOB, congestion, malar rash, photosensitivity, oral ulcers, joint pains, or any history of kidney disease. Initial labs were significant for elevated lipid panel, ESR, and TSH with hypoalbuminemia. Urine analysis showed 3+ proteinuria with micro positive for >50% dysmorphic RBC and acanthocytes. Complements were normal suggesting against lupus nephritis. However, subsequent ANA came back positive with dsDNA 36 and anti-chromatin. The patient underwent a kidney biopsy and was diagnosed with Class IV +V lupus nephritis.


In the work up of Nephritic syndrome we classically teach a targeted approach to serologic testing to avoid unnecessary (and potentially costly) labs. Complements are often used in the initial lab work up to assist in limiting serologic labs as a differentiating factor between complement mediated/immune complex mediated glomerulonephritis. In the above case, we initially had a lower suspicion for lupus nephritis due to normal complements. We were later surprised to find + ANA and biopsy confirmed class IV +V lupus nephritis. This case highlights the need to keep a broad differential diagnosis in the work up of Nephritic syndrome, and the limitations of Complement.