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Título: Tubulointerstitial nephritis in systemic lupus erythematosus: innocent bystander or ominous presage
Fecha de publicación: 2014
Editorial: F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
Cita bibliográfica: Histology and Histopathology, vol. 29, nº 5, (2014)
ISSN: 1699-5848
Materias relacionadas: CDU::6 - Ciencias aplicadas::61 - Medicina
Palabras clave: Systemic lupus erythematosus
Primary lupus tubulointerstitial nephritis
Secondary lupus tubulointerstitial nephritis
Resumen: 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 therapyfocused 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.
Autor/es principal/es: Dhingra, Sadhna
Qureshi, Raza
Abdellatif, Abdul
Gaber, Lillian W.
Truong, Luan D.
URI: http://hdl.handle.net/10201/68600
Tipo de documento: info:eu-repo/semantics/article
Número páginas / Extensión: 13
Derechos: info:eu-repo/semantics/openAccess
Aparece en las colecciones:Vol.29, nº 5 (2014)

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