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Publications

Journal Article Epublish

PubMed: 40221666 DOI: 10.1186/s12882-025-04108-0

Factors associated with worsening interstitial fibrosis/tubular atrophy in lupus nephritis patients undergoing clinically indicated repeat kidney biopsy.

BMC Nephrol 26(1):189

Authors: Daming Shao, Alejandra Londoño Jimenez, Maria Salgado Guerrero, Shudan Wang, Anna Broder

Affiliations

  • Division of Rheumatology, University of Chicago Medical Center, Chicago, IL, USA.
  • Division of Rheumatology, McFarland Clinic, Ames, IA, USA.
  • Division of Rheumatology, Columbia University Irving Medical Center, New York, NY, USA.
  • Division of Rheumatology, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, NY, USA.
  • Division of Rheumatology, Hackensack University Medical Center, Hackensack, NJ, USA.

Abstract

BACKGROUND

Lupus nephritis (LN) is one of the most severe manifestations of systemic lupus erythematosus (SLE). Interstitial fibrosis/tubular atrophy (IFTA) on kidney biopsies strongly predicts progression to end-stage renal disease although factors associated with IFTA progression remained unknown. This study aimed to evaluate the demographic, clinical, and histopathological factors at the time of index kidney biopsies that are associated with worsening IFTA on repeat biopsies and identify potential biomarkers of worsening interstitial damage.

METHODS

Patients with LN Class I to V or mixed LN on index biopsies who underwent a clinically indicated repeat biopsy between 2004 and 2020 were identified. None-mild IFTA was defined as < 25% acreage of the interstitium affected by fibrosis and atrophy, and moderate-severe IFTA was defined as ≥ 25% of the interstitium affected. Patients with none-mild IFTA on index biopsies who progressed to moderate-severe IFTA on repeat biopsies were defined as progressors. Patients with none-mild IFTA on both biopsies were defined as non-progressors.

RESULTS

Seventy-two patients who underwent clinically indicated repeat kidney biopsies were included, and 35 (49%) were identified as progressors. Compared to non-progressors, progressors had a higher proportion of proliferative LN (26 [74%] vs. 18 [49%], p = 0.04) and crescents (9 [26%] vs. 3 [8%], p = 0.045) on index biopsies. There was no difference regarding the time to repeat biopsy or the baseline characteristics, including eGFR, presence of hypertension and diabetes, urine protein to creatinine ratio, or the initial treatments.

CONCLUSIONS

Proliferative LN and the presence of crescents on index biopsies were associated with subsequent IFTA progression on repeat biopsies. This association indicates that glomerular damage is one of the major drivers of tubulointerstitial scarring in SLE. IFTA progression may, in turn, be the driving factor of poor treatment response and progression to chronic kidney disease.

MeSH

Kidney Diseases, Atrophy, Fibrosis, Lupus Nephritis, Kidney, Biopsy, Therapeutics, Nephritis