Vascular expression of annexin A2 in lupus nephritis

被引:9
|
作者
Salle, V. [1 ]
Cordonnier, C. [2 ]
Schmidt, J. [1 ]
Maziere, C. [3 ]
Smail, A. [1 ]
Attencourt, C. [2 ]
Mabille, M. P. [2 ]
Maziere, J. C. [3 ]
Makdassi, R. [4 ]
Choukroun, G. [4 ]
Diouf, M. [5 ]
Duhaut, P. [1 ]
Ducroix, J. P. [1 ]
机构
[1] Amiens Univ Hosp, Dept Internal Med, F-80054 Amiens 1, France
[2] Amiens Univ Hosp, Dept Pathol, Amiens, France
[3] Amiens Univ Hosp, Biochem Lab, INSERM, U1088, Amiens, France
[4] Amiens Univ Hosp, Dept Nephrol, Amiens, France
[5] Amiens Univ Hosp, Div Clin Res & Innovat, Amiens, France
关键词
THROMBOCYTOPENIA SYNDROME; SEVERE FEVER;
D O I
10.1136/jclinpath-2015-203139
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Aims To evaluate vascular expression of annexin A2 (ANXA2) and its subunit S100A10 in lupus nephritis (LN). Methods The present histological study included 14 patients with LN and 11 controls (patients with nonlupus kidney diseases). Kidney biopsies from patients with lupus were scored for lupus glomerulonephritis (according to the International Society of Nephrology/Renal Pathology Society 2003 classification) and vascular lesions (such as microthrombi and antiphospholipid syndrome nephropathy (APSN)). ANXA2 and S100A10 expression in glomerular and peritubular capillaries was evaluated by immunohistochemistry on tissue sections. The staining intensity score ranged from 0 (no expression) to 4 (intense expression). Results In patients with LN, the median age (range) at first kidney biopsy was 36 (18-49). Vascular lesions were observed in six patients (including two with APSN). We observed intense expression of ANXA2 in glomerular and peritubular capillaries while expression of S100A10 was weaker. However, one of the patients with APSN showed strong S100A10 expression. Patients with LN and controls differed significantly in terms of S100A10 expression in peritubular capillaries. We also observed a statistical difference between patients who had LN with renal vascular lesions and those without renal vascular lesions in terms of ANXA2 expression in peritubular capillaries. Conclusions The presence of vascular lesions in LN appears to be associated with significant differences in the vascular expression of ANXA2. Vascular expression of ANXA2 was somewhat higher in LN. Vascular expression of S100A10 was somewhat lower in LN (except one of the two patients with APSN). Further studies of ANXA2's putative value as a biomarker of active LN or of vascular lesions in LN are required.
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页码:533 / 541
页数:10
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