Background Moderate-to-severe tubulointerstitial damage (TID) is associated with poor renal outcomes in lupus nephritis (LN) independent of glomerular pathology1. Specific antibody profiles associated with TID in LN have not been identified. Unlike glomerular damage, TID is not associated with anti-dsDNA or complement levels1. An association between TID and the presence of anti-Ro/La antibodies has been proposed in Sjögren's syndrome2. Whether these antibodies are associated with TID in LN is not known.
Objectives To study an association between anti-Ro/La antibodies and moderate-to-severe TID in LN.
Methods We identified all patients who fulfilled ACR and/or SLICC criteria for SLE. Patients were included if they had an index renal biopsy consistent with LN between January 2005 and July 2015 and had complete data on TID and anti-Ro/La. Medical history, demographic and laboratory data were ascertained from chart review. TID was defined as the presence of moderate or severe tubular atrophy and/or interstitial fibrosis from the renal biopsy reports.
Results of the 157 LN patients, 39 (25%) had moderate/severe TID (Table). As expected, moderate/severe TID was associated with older age, class III/IV±V LN and lower estimated glomerular filtration rate (eGFR) at biopsy. Anti-Ro antibodies were present in 55 (47%) of patients with none/mild TID and 17 (44%) of patients with moderate/severe TID (p=0.74). Both anti-Ro and anti-La antibodies were present in 11 (9%) of patients with none/mild TID vs 11 (28%) of patients with moderate/severe TID (p=0.003). In the logistic regression model adjusted for age, eGFR and LN class, the presence of both anti-Ro and anti-La antibodies was associated with a 3-fold increase in the odds of TID, OR 3.1, 95% CI (1.1–9.1), p=0.04.
Conclusions The presence of anti-Ro and anti-La antibodies is associated with moderate/severe TID, independent of age, LN class and eGFR. Understanding the role of anti-Ro/La in the mechanisms underlying TID in LN may lead to novel preventive and therapeutic strategies.
Yu F, et al. Kidney Int 2010;77:820–9.
Francois H, et al. Nat Rev Nephrol, 2016;12(2):82–93.
Disclosure of Interest None declared