Publication: Tubulointerstitial nephritis in systemic lupus erythematosus: innocent bystander or ominous presage
Authors
Dhingra, Sadhna ; Qureshi, Raza ; Abdellatif, Abdul ; Gaber, Lillian W. ; Truong, Luan D.
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Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
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DOI
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info:eu-repo/semantics/article
Description
Abstract
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.
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Citation
Histology and Histopathology, vol. 29, nº 5, (2014)
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