Immunostaining for galactose-deficient immunoglobulin A is not specific for primary immunoglobulin A nephropathy

Immunostaining for galactose-deficient immunoglobulin A is not specific for primary immunoglobulin A nephropathy
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DOI:
10.1093/ndt/gfz152
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发表时间:
2020-12-01
影响因子:
6.1
通讯作者:
Satoskar, Anjali A.
Satoskar, Anjali A.
中科院分区:
医学1区
文献类型:
--
作者:
Cassol, Clarissa A.;Bott, Cherri;Satoskar, Anjali A.

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背景原发性免疫球蛋白A肾病(IgAN)的特征是IgA 1显性或共显性肾小球沉积,推测为半乳糖缺乏(Gd)。然而,肾小球伊加沉积也可以发生在非肾脏疾病,如肝硬化,银屑病和炎症性肠病(“继发性IgA”)或在其他病理活检中偶然发现。类似IgAN的肾小球肾炎可在细菌感染(主要是葡萄球菌感染)患者中发生[葡萄球菌感染相关性肾小球肾炎(SAGN)]。没有特异性的组织学特征来区分这些,但分化对于适当的管理至关重要。本研究的目的是调查是否最近描述的抗体Gd-IgA 1(KM-55)可以帮助区分原发性IgA肾病与其他条件与肾小球伊加沉积,特别是SAGN。我们对因临床指征接受肾活检并发现有肾小球伊加沉积的患者进行了回顾性队列研究。我们评估了100例活检,包括原发性IgAN(n = 44),继发性IgAN(n = 27),SAGN(n = 13),偶发性伊加沉积(n = 8)和狼疮性肾炎(n = 8)。原发性和继发性IgAN的Gd-IgA染色强度和阳性病例比例无差异。SAGN和偶发性伊加沉积病例的Gd-IgA染色强度显著低于原发性IgAN,但高达69%的SAGN病例呈阳性(尽管较弱)。Gd-IgA染色不仅存在于原发性IgAN中,而且存在于继发性IgAN、SAGN和偶发性伊加的活检中。弱染色或阴性染色可能有利于SAGN,特别是在感染的情况下,或在没有肾炎症状或存在其他无关肾小球病变的情况下偶然出现伊加。然而,单独的Gd-IgA阳性染色对于原发性IgAN的诊断不够特异。
Background. Primary immunoglobulin A nephropathy (IgAN) is characterized by IgA1-dominant or codominant glomerular deposits, postulated to be galactose deficient (Gd). However, glomerular IgA deposition can also occur in nonrenal diseases such as liver cirrhosis, psoriasis and inflammatory bowel disease ('secondary IgAN') or be an incidental finding in biopsies with other pathologies. A glomerulonephritis resembling IgAN can develop in patients with bacterial, mainly staphylococcal infections [staphylococcal infection-associated glomerulonephritis (SAGN)]. There are no specific histological features to distinguish between these, but differentiation is critical for appropriate management. The aim of this study was to investigate whether a recently described antibody to Gd-IgA1 (KM-55) could aid in differentiating primary IgAN from other conditions with glomerular IgA deposition, especially SAGN.Methods. We performed a retrospective cohort study of patients who underwent kidney biopsy for clinical indications and were found to have glomerular IgA deposits.Results. We evaluated 100 biopsies, including primary IgAN (n = 44), secondary IgAN (n = 27), SAGN (n = 13), incidental IgA deposition (n = 8) and lupus nephritis (n = 8). There was no difference in Gd-IgA staining intensity or the proportion of positive cases between primary and secondary IgAN. SAGN and cases with incidental IgA deposits had significantly lower Gd-IgA staining intensity than primary IgAN, but up to 69% of SAGN cases were positive (albeit weaker).Conclusions. Gd-IgA staining is present not only in primary IgAN, but also in biopsies with secondary IgAN, SAGN and incidental IgA. Weak or negative staining may favor SAGN, especially in the setting of infection, or incidental IgA in the absence of nephritic symptoms or in the presence of other unrelated glomerular pathologies. However, positive staining for Gd-IgA alone is not specific enough for a diagnosis of primary IgAN.