Combination immunosuppressant therapy and lupus nephritis outcome: a hospital-based study

Abstract

Lupus nephritis (LN) is the leading cause of mortality in lupus patients. This study aimed to investigate the treatment outcome and renal histological risk factors of LN in a tertiary referral center. Between 2006 and 2017, a retrospective observational study enrolled 148 biopsy-proven LN patients. After propensity score matching, 75 cases were included for further analysis. The classification and scoring of LN were assessed according to the International Society of Nephrology/Renal Pathology Society. Treatment response was evaluated by daily urine protein and urinalysis at two years after commencing induction treatment and the development of end-stage renal disease (ESRD). In total, 50.7% patients achieved complete remission (CR) or partial remission (PR), while 49.3% patients were categorized as nonresponders. Therapeutic responses in terms of CR/PR rates were associated with Systemic Lupus Erythematosus Disease Activity Index scores (odds ratio (OR): 1.34, 95% confidence interval (CI): 1.12–1.60, p = 0.001). Moreover, higher baseline creatinine levels (hazard ratio (HR): 2.10, 95% CI: 1.29–3.40, p = 0.003), higher renal activity index (HR: 1.30, 95% CI: 1.07–1.58, p = 0.008) and chronicity index (HR: 1.40, 95% CI: 1.06–1.85, p = 0.017) predicted ESRD. Among pathological scores, cellular crescents (HR: 4.42, 95% CI: 1.01–19.38, p = 0.049) and fibrous crescents (HR: 5.93, 95% CI: 1.41–24.92, p = 0.015) were independent risk factors for ESRD. In conclusion, higher lupus activity was a good prognostic marker for renal remission. Renal histology was predictive of ESRD. Large-scale prospective studies are required to verify the efficacy of mycophenolate in combination with azathioprine or cyclosporine in LN patients.

Lupus Nephritis Biomarkers: A Critical Review

“…A more careful study of urine cells for the identification of molecules involved in kidney cell injury [211] can prove useful in monitoring the response to treatment, as the shed cells may provide a window into the events in the kidney tissue itself. Anti-CRP Clinical disease activity and responses to therapy in LN [34,35] Anti-ENO-1 (+) Diagnosis and prediction of LN [37,38,40] AaA (Low) Diagnosis [41] Anti-chromatin Diagnostic/predictive capacity in LN [48] PTEC-binding IgG (+) Clinical disease activity [167] PHACTR4 icx (+) Diagnosis [168] P3H1 icx (+) Diagnosis [168] RGS12 icx (+) Diagnosis [168] PTEC-binding IgG (+) Clinical disease activity [167] IgM (↑) Responses to therapy in LN [169] ANCAs Resistin (↑) Damage [190] CSF-1 (↓) Responses to therapy in LN [191] HNP1-3 (↓) Responses to therapy in LN [192] S100A8/A9 (↑) Responses to therapy in LN [193] S100A12 (↑) Responses to therapy in LN [193] Urine CSF-1 (↑) Histological disease activity [191] Periostin (↑) Damage [206] C9 (+) Prognosis [207] Podocyte foot process width (↓) Prognosis [169] Arteriolar C4d deposition (+) Prognosis [208] Cellular crescents (+) Prognosis [172] Fibrous crescents (+) Prognosis [172] Glomerular C3 deposition (+) Prognosis [212] IFTA (+) (≥25% of the surface cortical area)…”

Change of Renal Gallium Uptake Correlated with Change of Inflammation Activity in Renal Pathology in Lupus Nephritis Patients

“…Fifth, renal survival and patient survival were not assessed in this study. A recent study indicated that activity scores in LN histology were associated with end-stage renal disease [41]. Whether the degree of renal gallium uptake has a predicting role on renal survival in LN patients needs further study.…”

Drug Interactions in Autoimmune Systemic Lupus Erythematosus (SLE)

“…In research by Chen et al (2019), research was conducted on 149 patients who were separated into 4 groups based on the induction therapy given. Patients received systemic glucocorticoids and immunosuppressants with cyclosporine (50-100 mg/day) or azathioprine (25-50 mg/day) in combination with MPA in the so-called MPAcombination group.…”

“…However, in this study, hematuria and urine analysis were not measured so this study could not measure the clinical manifestations of the SLEDAI score. In addition, the samples obtained were only small and the SLEDAI score used to measure the success of therapy was the median SLEDAI score, not the SLEDAI score for each patient (Chen et al, 2019).…”