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CS-15 Endothelial progenitor cells as a promising biomarker of systemic lupus erythematosus activity
  1. Gonzalo Silveira1,2,
  2. Sabrina Ranero2,3,
  3. Adriana Carlomagno1,
  4. Martín Rebella4,
  5. Sofía Grille2,3a and
  6. Álvaro Danza1a
  1. 1Clínica Médica ‘2’. Hospital Pasteur, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay
  2. 2Departamento Básico de Medicina, Hospital de Clínicas, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay
  3. 3Cátedra de Hematología. Hospital de Clínicas, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay
  4. 4Clínica Médica ‘C’. Hospital de Clínicas, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay
  5. aBoth authors contributed equally


Background Endothelial progenitor cells (EPC) and circulating endothelial cells (CEC) are cell populations mobilized from the bone marrow in response to endothelial damage. Its relationship with vascular risk damage and subclinical vascular damage in systemic lupus erythematosus (SLE) is being actively studied, but their role as an activity biomarker was not evaluated.

Aim to study EPC and CEC levels in SLE patients and compare them to healthy controls, as well as study their relationship with clinical and analytical markers of disease activity.

Methods A prospective, analytical, case-control study was conducted; in a center for systemic autoimmune diseases in Montevideo, Uruguay. EPCs and CEC levels were quantified by multiparametric flow cytometry. EPCs were defined as CD45low/-, CD34+, CD133+, CD31+, CD146+, CD3- and CEC as CD45low/-, CD34+, CD133-, CD31+, CD146+, CD3-.

Disease activity was assessed using ‘Systemic Lupus Erythematosus Disease Activity Index’ (SLEDAI) and ‘Physician’s Global Assessment’ (PGA), erythrocyte sedimentation rate (ESR), C reactive protein (CRP), complement (C3 and C4), double-stranded DNA (dsDNA) antibody levels and proteinuria.

Results 28 controls and 22 SLE patients age and sex matched were enrolled. Patients median ages was 29.5±11.5 years and controls were 36±11.25 years, (p=0.28). Sex ratio (female/male) was 22/2 and 24/4 in patients and controls (p=0.68).

SLE patients showed significantly lower levels of EPC (median 0.2202±0.4377 cells/µl vs 1.051±1.3849 cells/µl), p<0.0001, and lower levels of CEC (median 0.2321±0.49677 cells/µl vs 0.7043±0.5706 cells/µl), p=0.0004 than controls.

EPC levels correlated with proteinuria/creatininuria ratio (r=0.5386, p=0.0097) and with dsDNA level (r=0.5118, p=0.0211) in SLE patients.

EPC level was higher in patients with significant proteinuria (median 0.58710±1.5086 cells/µl vs 0.11502±0.42442 cells/µl), p=0.0474 (figure 1); and in patients with increased dsDNA level (median 0.5871±1.2562 cells/µl vs 0.1150±0.3504 cells/µl), p=0.0249.

No correlation was found with the levels of C3, C4, SLEDAI, as well as prednisone dose at the time of enumeration.

Conclusions EPS and CEC levels correlate with disease activity in SLE, particularly with renal involvement. Currently, we are enrolling more patients in order to confirm these results, but we postulate that, in the future, EPC may be used as a biomarker of disease activity.

Abstract CS-15 Figure 1

EPC and significant proteinuria

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