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SAT0413 Urinary Lipocalin-2 as a Biomarker of Renal Disease Activity in Patients with Lupus Nephritis: A Prospective Study
  1. N. M. Gamal1,
  2. N.M. Mustafa1,
  3. E. A.M. Abda1,
  4. O. Afifi2,
  5. N. Fathi1
  1. 1Rheumatology and Rehabilitation department
  2. 2Clinical pathology department, Assiut University Hospital-Faculty of Medicine, Assiut, Egypt


Background Lupus nephritis (LN) is a common manifestation among patients with systemic lupus erythematosus (SLE), occurring in over 50%. One major determinant of poor prognosis among patients with SLE is renal involvement (1). Available renal biomarkers that measure the degree of SLE renal disease activity are too insensitive to allow for early identification of patients with active SLE nephritis, prohibiting early initiation of therapy to avoid permanent renal damage (2). Lipocalin-2 was regarded a novel biomarker in various types of acute kidney injury and chronic kidney diseases (3,4).

Objectives The aim of this study was to detect the levels of urinary lipocalin-2 excretion in SLE patients, to determine its association with SLE disease activity focusing on nephritis and to assess its value in predicting changes of SLE disease activity.

Methods The study included 50 adult SLE patients met 1997 revised ACR classification criteria for SLE and 20 matched healthy controls. Patients were clinically and laboratory evaluated. Activity was assessed using SLEDAI score. SLE patients were classified into 2 groups (with LN and without LN) based on renal parameters of SLEDAI score. Urinary lipocalin-2 levels were measured using ELISA in SLE patients and controls. Twenty five of included patients were enrolled in a longitudinal study one year after the initial visit. SLEDAI score, laboratory investigation and urinary lipocalin-2 levels were assessed and compared with their initial values.

Results Urinary lipocalin-2 levels were significantly higher in SLE patients (13.2±2.44 ng/ml) compared with normal controls (1.70±0.23 ng/ml) (p=0.004). Among SLE patients, urinary lipocalin-2 levels were significantly higher in patients with LN (22.95±4.41 ng/ml; n=22) than in those without LN (5.39±1.54 ng/ml; n=28) (p=0.000). Urinary lipocalin-2 of patients with LN correlated significantly with the renal SLEDAI score (r=0.790, p=0.000), but not with extrarenal disease activity. Within follow up group, urinary lipocalin-2 levels showed significant difference when compared between with and without LN groups (p =0.016). Change in total and renal SLEDAI scores were associated with change of urinary lipocalin-2 levels within follow up group but none of these changes reached statistical significance.

Conclusions Urinary lipocalin-2 is a potential biomarker for renal disease activity in adult SLE patients and its serial measurements may be valuable in predict worsening of SLE disease activity.


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Disclosure of Interest None declared

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