AP-HP (Assistance Publique des Hôpitaux de Paris), Groupe Hospitalier Henri-Mondor, Department of Nephrology and Renal Transplantation, Créteil, France.
AP-HP (Assistance Publique des Hôpitaux de Paris), Groupe Hospitalier Henri-Mondor, Department of Pathology, Créteil, France.
PLoS One. 2018 Nov 15;13(11):e0207066. doi: 10.1371/journal.pone.0207066. eCollection 2018.
Lupus glomerulopathies are classified into various histological patterns, which probably result from different pathophysiological origins. Podocyte injury can be demonstrated in lupus nephritis but its clinical relevance is far little appreciated and is often masked by proliferative lesions and inflammatory cell infiltrations. Two patterns of podocyte lesions may be considered, either occurring in the context of renal inflammation or reflecting podocyte dysfunction in non-proliferative and non-inflammatory glomerulopathies. This distinction remains elusive since no reliable biomarker discriminates between both entities. CMIP was recently found induced in some glomerular disease but its expression in different lupus nephritis classes has not been investigated. Twenty-four adult patients with lupus nephritis, including non-proliferative (n = 11) and proliferative (n = 13) glomerulopathies were analyzed. Clinical, biological and immunological data were compared with immunomorphological findings. We analyzed by quantitative and qualitative methods the expression of CMIP in different histological classes. We found CMIP abundance selectively increased in podocytes in class II and class V glomerulopathies, while in proliferative forms (class III and class IV), CMIP was rarely detected. CMIP was not expressed in cellular crescents, endothelial cells or mesangial cells. CMIP colocalized with some subsets of B and T cells within glomerular or interstitial mononuclear cell infiltrates but never with macrophages. Hematuria is rarely present in lupus glomerulopathies expressing CMIP. There was no correlation between classical immunological markers and CMIP expression. Thus, CMIP induction in lupus nephritis seems restricted to non-proliferative glomerulopathies and may define a specific pattern of podocyte injury.
狼疮性肾小球病变可分为多种组织学类型，这可能源于不同的病理生理起源。在狼疮肾炎中可以观察到足细胞损伤，但它的临床相关性远未被充分认识，并且常被增生性病变和炎症细胞浸润所掩盖。可以考虑两种足细胞病变模式，一种发生在肾脏炎症的背景下，另一种反映非增生性和非炎症性肾小球病变中的足细胞功能障碍。这种区别仍然难以捉摸，因为没有可靠的生物标志物可以区分这两种实体。CMIP 最近在一些肾小球疾病中被发现诱导，但在不同的狼疮肾炎类型中其表达尚未被研究。分析了 24 名成人狼疮肾炎患者，包括非增生性（n=11）和增生性（n=13）肾小球病变。比较了临床、生物学和免疫学数据与免疫形态学发现。我们通过定量和定性方法分析了 CMIP 在不同组织学类型中的表达。我们发现 CMIP 在 II 型和 V 型肾小球病变中的足细胞中选择性增加，而在增生性形式（III 型和 IV 型）中很少检测到 CMIP。CMIP 不在细胞性新月体、内皮细胞或系膜细胞中表达。CMIP 与肾小球或间质单核细胞浸润中的一些 B 和 T 细胞亚群共定位，但从不与巨噬细胞共定位。在表达 CMIP 的狼疮性肾小球病变中，血尿很少见。经典免疫标志物与 CMIP 表达之间没有相关性。因此，CMIP 在狼疮肾炎中的诱导似乎仅限于非增生性肾小球病变，并可能定义了一种特定的足细胞损伤模式。
