Key result
Induction immunosuppressive therapy in lupus nephritis is linked to ~90% higher odds of EF recovery.
Why the study?
SLE, especially lupus nephritis, significantly increases cardiovascular risk, but clear guidelines for cardiovascular disease prevention and management in this population are lacking.
Does induction immunosuppressive therapy improve structural cardiac lesions in patients with active lupus nephritis?
Cohort (n=64)
Does induction immunosuppressive therapy improve structural cardiac lesions in patients with active lupus nephritis?
Odds Ratio: 1.9
p-value: p=<0.001
Immunosuppressive induction therapy with mycophenolate mofetil or cyclophosphamide is associated with significant short-term echocardiographic improvement of structural cardiac lesions in patients with active lupus nephritis.
Indicates substantial cardiac involvement in active LN; leaves open whether targeted screening modifies outcomes.
Background SLE, and especially lupus nephritis (LN), significantly increases cardiovascular (CV) risk. Despite the magnitude of the problem, clear and homogeneous guidelines specifically focused on CV disease prevention and management are still lacking. This study assessed the degree of affection of cardiac structures in patients with active LN and its outcomes with induction therapy. Methods A Prospective study included 64 active LN patients. Screening of cardiac affection was done by the Echo for all patients at the beginning of the study. The patients who had evident cardiac lesions were assessed by echo after 3 months with termination of induction immunosuppressive therapy to assess cardiac outcomes. Results The prevalence of cardiac lesions was 23.4% (15 patients) in active LN. It was the following; mean ejection fraction (EF) (54 ± 10%), global hypokinesia 33.3% (5 patients), mild to moderate pericardial effusion (PE) 73.3. % (11 patients) Moderate to severe mitral valve regurgitation (MVR) 66.7% (10 patients), mild aortic regurgitation (AVR) 13.3% (2 patients) moderate to severe tricuspid valve regurgitation (TVR) 33.3% (5 patients) & elevated right ventricular systolic pressure (RVSP) 33.3% (5 patients). Baseline EF was negatively correlated with serum creatinine (r-value = -0.301) p-value 0.016. After 3 months of active LN management, there were significant improvements in EF, PE, and severe MVR p-values < 0.001, 0.027, and 0.015 respectively. EF was improved with either Mycophenolate mofetil or Cyclophosphamide p-values 0.011, and 0.012 respectively while PE was improved by Mycophenolate mofetil p-value 0.026. MVR was significantly improved by Cyclophosphamide p-value 0.029. Management of active LN carries recovery of EF 1.9 times (odds ratio:1.9), PE 15 times (odds ratio:15), and MVR 64 times (odds ratio:64). TVR, AVR, and RVSP were independent cardiac lesions with active LN. Conclusion Structural cardiac lesions are highly prevalent in active LN, and effective induction therapy of active LN for 3 months is positively linked to cardiac improvement.
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Abdel-Wahab et al. (2026) conducted a cohort in Active lupus nephritis (n=64). Induction immunosuppressive therapy vs. Baseline (pre-treatment) was evaluated on Recovery of ejection fraction (OR 1.9, p=<0.001). Induction immunosuppressive therapy for active lupus nephritis over 3 months significantly improved ejection fraction (OR 1.9, p<0.001), pericardial effusion, and mitral valve regurgitation.
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