Abstract: TH-PO0505
Treatment of IgAN According to Kidney Lesions: A Randomized Controlled Trial (TIGER Study)
Session Information
- Glomerular Diseases: Clinical, Outcomes, and Therapeutics Research - IgAN
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- El Karoui, Khalil, Hopital Tenon, Paris, Île-de-France, France
- Maillard, Nicolas, CHU St Etienne, Saint Etienne, France
- Karras, Alexandre, Hopital Europeen Georges Pompidou, Paris, Île-de-France, France
- Hummel, Aurelie, Institut Necker Enfants Malades, Paris, Île-de-France, France
- Audard, Vincent, Henri Mondor Hospital Department of Nephrology, Creteil, France
- Alamartine, Eric, CHU St Etienne, Saint Etienne, France
- Joly, Dominique A., Institut Necker Enfants Malades, Paris, Île-de-France, France
- Elie, Caroline, Institut Necker Enfants Malades, Paris, Île-de-France, France
Background
The benefit of systemic corticosteroids in IgA nephropathy (IgAN) remains debated, while the potential impact in steroid response of stratification based on renal lesions is unknown. In this study, we evaluated whether early steroid therapy improves outcomes in patients with recent biopsy-proven IgAN and high-risk lesions.
Methods
TIGER is a multicenter, randomized, open-label trial comparing early corticosteroid therapy plus optimized nephroprotection versus nephroprotection alone in adults with IgAN and severe histological lesions. Inclusion required proteinuria >0.75 g/g and ≥2 positive items on the Oxford MEST-C classification from a biopsy performed within 45 days. The primary endpoint was treatment failure at 24 months, defined as proteinuria >0.5 g/g, or >20% decline in eGFR, or loss of >10 ml/min/1.73m2, or kidney failure, or renal transplantation, or death.
Results
The expected number of inclusions (122) was not reached. Fifty-nine patients were analyzed (30 control (Ctrl), 29 experimental (Exp); males 71%, caucasian 71%). Baseline characteristics and renal lesions were comparable between both groups (median eGFR 52 vs 59 ml/min/1.73m2; proteinuria 1.3 vs 1.5 g/g in Ctrl and Exp groups). Among patients in the Ctrl group, 15/30 (50%) received rescue steroid therapy (because of persistent proteinuria after month 6). At 24 months, treatment failure occurred in 63% Ctrl (including Ctrl with rescue steroid therapy) versus 48% Exp patients (RR 0.76, 95% CI 0.48–1.21; p=0.25). Regarding secondary outcomes, at 6 months, failure occurred in 70%Ctrl versus 41% Exp (RR 0.59, 95% CI 0.36–0.97; p=0.036). Moreover, mean proteinuria at month 9 (a validated surrogate endpoint of long-term evolution) was 0.72 (SD 0.73) vs 0.40 (SD 0.34) g/g (p=0.013), in Ctrl and Exp groups. At 24 months, persistent proteinuria >0.5 g/g was less frequent in Exp group (31% vs 53%, p=0.10). Over the entire follow-up, fewer patients in the Exp group reached failure criteria at any time (93% vs 68%, p=0.01). Renal function remained stable in both groups.
Conclusion
Although underpowered and not statistically significant for the primary endpoint, early steroid therapy was associated with improved short-term outcomes and greater reduction in proteinuria, a validated surrogate of long-term prognosis. These findings suggest a potential benefit of early, lesion-guided immunosuppression in high-risk IgAN.