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Abstract Number: 2796

Low Versus High Dose Glucocorticosteroid Used in Lupus Nephritis:  Is There a Difference

Haifa Al-Sheikh1, Dafna D. Gladman1, Jiandong Su1 and Murray Urowitz2, 1Rheumatology, Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital and University of Toronto, Toronto, ON, Canada, 2Medicine, Toronto Western Hospital and University of Toronto, Toronto, ON, Canada

Meeting: 2016 ACR/ARHP Annual Meeting

Date of first publication: September 28, 2016

Keywords: glucocorticoids and lupus nephritis

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Session Information

Date: Tuesday, November 15, 2016

Title: Systemic Lupus Erythematosus – Clinical Aspects and Treatment - Poster III: Biomarkers and Nephritis

Session Type: ACR Poster Session C

Session Time: 9:00AM-11:00AM

Background/Purpose: The exact dose of glucocorticoids (GC) needed for the management of lupus nephritis in an individual patient is unknown. We aimed to compare the renal outcomes between patients with lupus nephritis (LN) treated early with high or low dose glucocorticoids (GC).

Methods:   Inception patients (enrolled within one year of diagnosis) aged ≥ 18 years that were newly diagnosed with LN and followed for at least 3 years after LN formed our cohort. Patients are followed prospectively at 2-6 month intervals according to a standard protocol which includes complete history, physical examination and laboratory evaluation. Patients were divided into two groups based on the maximum dose of GC used at the time of LN diagnosis (including one visit before or one after LN). Group 1 patients were treated with a high-dose (>35 mg/d) and group 2 with a low-dose (<35 mg/d) GC. Disease activity was measured by the SLEDAI-2K and accumulated damage by the SLICC/ACR damage index (SDI). All information necessary to complete the SLEDAI-2K and the SDI is collected prospectively. Specific GC-related damage was documented by the presence of any of the following: cataracts, osteonecrosis or osteoporosis. Outcomes were: all cause mortality, SDI increase, and renal outcomes, including: complete renal remission, partial renal remission, renal flare, and end-stage renal disease.

Results:    Of 786 inception patients in our cohort, 198 patients met LN definition and had 3 or more years of follow-up after LN. 99 (50.5%) patients received a high dose of GC (HD) with a mean dose of 55.6 ± 17.9 mg/d, and 97 (49.5%) patients received a low dose (LD) with a mean dose of 20.6 ± 8.8 mg/d. The majority of the patients (84%) were female. The mean disease duration from SLE to LN was longer in LD group (1.6 ± 2.4 years compared to 0.8 ± 2.2 years in the HD, p = 0.015). The HD group had higher disease activity than LD group as shown in table-1. The mean cumulative GC dose 6 months after LN was comparable between both groups 7.0 ± 8.3g in LD group and 8.2 ± 7.6g in the HD group (p= 0.31). Cumulative doses were similar five years after LN (22.3 ± 13.4g in LD group and 24.8 ± 14.2g HD group (p= 0.20). The mortality rate, renal outcomes, accumulated damage, and GC-related side effects were similar in both groups.  Multivariable logistic regression analysis showed that age at LN and SDI were associated with increased mortality while the use of antimalarial agents had a protective effect. Moreover, age at LN and use of immunosuppressive medications were associated with an increase in damage, while the use of a low versus high doses of GC had no impact on any of the renal outcomes.

Conclusion: High dose GC was used in patients with more active disease but this was tapered more rapidly as the cumulative GC dose at 6 months and 5 years was similar in both groups, with comparable side effects and good renal outcomes and diseases control. GC dose sufficient to control active disease should be used early and tapered quickly for best results and least side effects.  

Table 1:  Disease characteristics at LN
Variable

Low Dose Group

N=97

High Dose Group

N=99

P-value

SLEDAI-2K

10.49 ± 6.96

15.55 ± 9.66

<0.001

Renal SLEDAI

5.03 ± 4.59

7.27 ± 5.09

0.001

Non-Renal SLEDAI

5.46 ± 4.43

8.27 ± 8.02

0.003

Low-complement

52 (53.6%)

62 (62.6%)

0.201

High ds-DNA

56 (60.9%)

57 (60.0%)

0.903

Serum creatinine (>140μmol/l)

7 (7.3%)

27 (27.3%)

<0.001

Antimalarial

56 (57.7%)

37 (37.4%)

0.004

Immunosuppression (IS)

54 (55.7%)

70 (70.7%)

0.029

Renal Biopsy

 

 

<0.001

     II Mesangial

23 (41.1%)

14 (20.6%)

 

     III Focal proliferative

14 (25.0%)

15 (22.1%)

 

     IV Diffuse prolferative

 8 (14.3%)

33 (48.5%)

 

     V Membranous

8 (14.3%)

6 (8.8%)

 

     VI Glomerosclerosis

3 (5.4%)

0 (0.0%)

 

       


Disclosure: H. Al-Sheikh, None; D. D. Gladman, None; J. Su, None; M. Urowitz, None.

To cite this abstract in AMA style:

Al-Sheikh H, Gladman DD, Su J, Urowitz M. Low Versus High Dose Glucocorticosteroid Used in Lupus Nephritis:  Is There a Difference [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10). https://acrabstracts.org/abstract/low-versus-high-dose-glucocorticosteroid-used-in-lupus-nephritis-is-there-a-difference/. Accessed .
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