Dhingra Sadhna, Qureshi Raza, Abdellatif Abdul, Gaber Lillian W, Truong Luan D
Department of Pathology and Genomic Medicine, The Methodist Hospital, Houston,TX, USA.
Department of Medicine Renal Section, Baylor College of Medicine, Houston, TX, USA.
Histol Histopathol. 2014 May;29(5):553-65. doi: 10.14670/HH-29.10.553. Epub 2013 Nov 29.
SLE-associated tubulointerstitial injury (SLE TIN) is increasingly recognized in two forms, i.e., secondary and primary. The secondary form coexists with lupus glomerulonephritis, whereas the primary form develops against the background of no or mild glomerular or vascular involvement. Secondary SLE TIN is frequent, but its frequency and severity correlate with the class of the associated lupus glomerulonephritis (GN), being almost universal in Class IV lupus GN and less frequent in GN of other classes. Although the presence of underlying GN may mask its clinical manifestation, secondary SLE TIN has a major prognostic implication for the renal outcome. Yet, SLE TIN is not factored in the current therapy-focused International Society of Nephrology/Renal Pathology Society schema of renal lupus classification, and its management remains to be elucidated. The pathogenesis of secondary SLE TIN is either immunologic, i.e., the tubulointerstitial injury being mediated by SLE-related immunologic mechanisms akin to those responsible for lupus GN; or non-immunologic, i.e., a nonspecific tubulointerstitial injury secondary to any type of advanced glomerular lesion, regardless of etiology. Primary SLE TIN is rare with about 15 reported cases. It has a rather uniform and distinctive clinical manifestation including acute kidney injury with no or mild proteinuria. It responds well to steroid and usually carries a good prognosis. Its pathogenesis is almost certain immunologic, with immunoglobulin/complement deposits along the tubular basement membrane in each reported case. In spite of these profound clinical implications, the current review underlies a limited knowledge on the pathobiology of SLE TIN.
系统性红斑狼疮相关的肾小管间质损伤（SLE TIN）越来越多地被认识到有两种形式，即继发性和原发性。继发性形式与狼疮性肾小球肾炎共存，而原发性形式则在无或轻度肾小球或血管受累的背景下发生。继发性SLE TIN很常见，但其发生率和严重程度与相关狼疮性肾小球肾炎（GN）的类型相关，在IV型狼疮性GN中几乎普遍存在，在其他类型的GN中则较少见。尽管潜在的GN可能掩盖其临床表现，但继发性SLE TIN对肾脏预后具有重要的预后意义。然而，SLE TIN并未被纳入当前以治疗为重点的国际肾脏病学会/肾脏病理学会的狼疮性肾炎分类方案中，其管理仍有待阐明。继发性SLE TIN的发病机制要么是免疫性的，即肾小管间质损伤由与狼疮性GN相关的免疫机制介导，类似于导致狼疮性GN的机制；要么是非免疫性的，即继发于任何类型的晚期肾小球病变的非特异性肾小管间质损伤，无论其病因如何。原发性SLE TIN很少见，仅有约15例报告病例。它具有相当一致和独特的临床表现，包括急性肾损伤且无或轻度蛋白尿。它对类固醇反应良好，通常预后良好。其发病机制几乎肯定是免疫性的，在每个报告病例中，免疫球蛋白/补体沿肾小管基底膜沉积。尽管有这些深刻的临床意义，但目前的综述表明对SLE TIN病理生物学的了解有限。
