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Updated: Jan 10, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
Published on: June 8, 2022
The Pathogenesis, Potential Biomarkers and Novel Therapeutic Strategies for Tubulointerstitial Nephritis in Systemic
Chang-Youh Tsai1, Tsai-Hung Wu2, Shuo-Ming Ou2
1Division of Immunology & Rheumatology, Department of Medicine, Fu-Jen Catholic University Hospital, College of Medicine, Fu Jen Catholic University, New Taipei City 24352, Taiwan.
Abstract:
Kidney diseases in patients with SLE include glomerulonephritis (GN), tubulointerstitial nephritis (TIN) and vasculitis alone or in combination. Immune complex (IC) deposition with complement activation in renal glomeruli causes lupus GN. However, IC deposition can also occur in the tubular basement membrane, renal interstitium, peritubular capillaries and arteries/arterioles to elicit inflammatory responses. TIN is usually associated with more severe GN with inflammation induced by IC. Immunopathologically, the aberrant presentation of T cell subpopulations, Th1, Th2, Th9, Th17, Treg and follicular T helper cells (Tfh), is closely implicated in TIN in SLE. In addition, M1/M2 macrophages and more specific dendritic cells (DCs) contribute to the inflammatory reactions of SLE-TIN. TIN may also present alone (isolated TIN) in apparently normal glomeruli or class I GN. It is intriguing that lupus nephritis constitutes two different pathological predilections, i.e., GN and tubulointerstitial inflammation. Alternatively, these two types may represent a continuous spectrum of inflammatory renal damages. In the present review, we will discuss in detail the pathology/immunopathogenesis, likely specific biomarkers/predictors and novel therapeutic designs for SLE-tubulointerstitial inflammation. In addition, we also raise several plausible investigation methods in SLE-tubulointerstitial inflammation that may help further elucidate this setting of perplexing renal diseases with rheumatic characteristics.
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