Abstract: SA-PO1217
Kidney Outcomes Associated with Nonsteroidal Anti-Inflammatory Drug (NSAID) Use in Patients with Spondyloarthritis: A Meta-Analysis
Session Information
- CKD: Biomarkers and Emerging Tools for Diagnosis and Monitoring
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: CKD (Non-Dialysis)
- 2302 CKD (Non-Dialysis): Clinical, Outcomes, and Trials
Authors
- Defante, Maria Luiza Rodrigues, UniRedentor, Itaperuna, RJ, Brazil
- Ximenes Mendes, Beatriz, Centro Universitario Christus, Fortaleza, CE, Brazil
- De Souza, Mariana, Hospital Israelita Albert Einstein, São Paulo, SP, Brazil
- De Souza, Kevlin, UniRedentor, Itaperuna, RJ, Brazil
- Austregesilo Athayde H Morais, Beatriz, Centro Universitario CESMAC, Maceió, AL, Brazil
- Martins Prizão, Vitoria, Universidade Estadual de Maringa, Maringá, PR, Brazil
- Dibo, Paula, The University of Alabama at Birmingham, Birmingham, Alabama, United States
Background
Nonsteroidal anti-inflammatory drugs (NSAIDs) are the mainstay of treatment for spondyloarthritis (SpA). Although NSAID-induced nephrotoxicity is well established in the general population, patients with SpA may carry a distinct risk profile due to chronic inflammation and comorbidities. However, SpA-specific data on the impact of continuous NSAID exposure on renal outcomes are limited.
Methods
We conducted a systematic review and meta-analysis of observational studies evaluating renal outcomes in patients with SpA undergoing continuous NSAID therapy. Proportions, odds ratios (OR), and mean differences (MD) with 95% confidence intervals (CI) were used.
Results
Ten studies involving 22,786 participants were included. The pooled prevalence of CKD among patients with SpA receiving continuous NSAID therapy was 8.71% (95% CI 5.40 to 13.7; Figure 1A). NSAID use was not associated with an increased risk of CKD compared to non-users (OR 1.24; 95% CI 0.73 to 2.10; p=0.42; Figure 1B). Serum creatinine levels showed no significant difference between baseline and follow-up periods after continuous NSAID exposure (MD 0.01 mg/dL; 95% CI -0.02 to 0.04; p=0.63; Figure 1C), while serum cystatin-C levels increased (MD 0.19 mg/dL; 95% CI 0.13 to 0.25; p<0.01; Figure 1D) and estimated glomerular filtration rate significantly declined (MD -17.36 mL/min/1.73 m2; 95% CI -25.66 to -9.06; p<0.01; Figure 1E).
Conclusion
Continuous NSAID use in patients with SpA was not associated with overt CKD; however, subclinical renal impairment may still occur, particularly when assessed using sensitive biomarkers.