Salle V, Cordonnier C, Schmidt J, Mazière C, Smail A, Attencourt C, Mabille M P, Mazière J C, Makdassi R, Choukroun G, Diouf M, Duhaut P, Ducroix J P
Department of Internal Medicine, Amiens University Hospital, Amiens, France.
Department of Pathology, Amiens University Hospital, Amiens, France.
J Clin Pathol. 2016 Jun;69(6):533-6. doi: 10.1136/jclinpath-2015-203139. Epub 2015 Oct 28.
To evaluate vascular expression of annexin A2 (ANXA2) and its subunit S100A10 in lupus nephritis (LN).
The present histological study included 14 patients with LN and 11 controls (patients with non-lupus 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).
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.
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.
评估狼疮性肾炎(LN)中膜联蛋白A2(ANXA2)及其亚基S100A10的血管表达情况。
本组织学研究纳入了14例LN患者和11例对照(非狼疮性肾病患者)。对狼疮患者的肾活检标本进行狼疮性肾小球肾炎评分(根据国际肾脏病学会/肾脏病理学会2003年分类法)以及血管病变评分(如微血栓和抗磷脂综合征肾病(APSN))。通过组织切片免疫组化评估肾小球和肾小管周围毛细血管中ANXA2和S100A10的表达。染色强度评分范围为0(无表达)至4(强表达)。
LN患者首次肾活检时的中位年龄(范围)为36岁(18 - 49岁)。6例患者观察到血管病变(包括2例APSN患者)。我们观察到肾小球和肾小管周围毛细血管中ANXA2表达强烈,而S100A10表达较弱。然而,1例APSN患者显示S100A10强表达。LN患者和对照在肾小管周围毛细血管中S100A10表达方面存在显著差异。我们还观察到有肾血管病变的LN患者和无肾血管病变的LN患者在肾小管周围毛细血管中ANXA2表达方面存在统计学差异。
LN中血管病变的存在似乎与ANXA2的血管表达显著差异有关。LN中ANXA2的血管表达略高。LN中S100A10的血管表达略低(2例APSN患者中的1例除外)。需要进一步研究ANXA2作为活动性LN生物标志物或LN血管病变的潜在价值。