Lupus nephritis (LN) is one of the most frequent and serious complications in the patients with
systemic lupus erythematosus. Autoimmune-mediated
inflammation in both renal glomerular and tubulointerstitial tissues is the major pathological finding of LN. In clinical practice, the elevated
anti-dsDNA antibody titer concomitant with reduced
complement C3 and C4 levels has become the predictive and disease-activity surrogate
biomarkers in LN. However, more and more evidences suggest that
autoantibodies other than
anti-dsDNA antibodies, such as anti-
nucleosome, anti-C1q, anti-C3b, anti-
cardiolipin, anti-endothelial cell, anti-ribonuclear
proteins, and anti-glomerular matrix (anti-
actinin)
antibodies, may also involve in LN. Researchers have demonstrated that the circulating preformed and in situ-formed
immune complexes as well as the direct cytotoxic effects by those cross-reactive
autoantibodies mediated kidney damage. On the other hand, many efforts had been made to find useful urine
biomarkers for LN activity via measurement of immune-related mediators, surface-enhanced
laser desorption/ionization time-of-flight mass spectrometry proteomic signature, and assessment of
mRNA and exosomal-derived
microRNA from urine sediment cell. Our group had also devoted to this field with some novel findings. In this review, we briefly discuss the possible mechanisms of LN and try to figure out the potential serum and urine
biomarkers in LN. Finally, some of the unsolved problems in this field are discussed.