Email updates

Keep up to date with the latest news and content from Arthritis Research & Therapy and BioMed Central.

This article is part of the supplement: Lupus 2012: New targets, new approaches

Meeting abstract

Renal flare as a biomarker of incident and progressive chronic kidney disease in patients with lupus nephritis

S Parikh, A McKinley and BH Rovin*

  • * Corresponding author: BH Rovin

Author affiliations

Wexner Medical Center at Ohio State University, Columbus, OH, USA

For all author emails, please log on.

Citation and License

Arthritis Research & Therapy 2012, 14(Suppl 3):A45  doi:10.1186/ar3979

The electronic version of this article is the complete one and can be found online at: http://arthritis-research.com/content/14/S3/A45


Published:27 September 2012

© 2012 Parikh et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Introduction

Flares of lupus nephritis (LN) cause acute kidney injury (AKI), even if serum creatinine (SCr) does not increase. Although classic forms of AKI, such as ischemia, have long been thought to heal without long-term sequelae, it is now clear that AKI events predispose patients to chronic kidney disease (CKD). It was therefore postulated that renal flare (RF) in LN patients promotes CKD.

Methods

To determine whether RF frequency and duration can be used as markers of new CKD or progression of established CKD, we correlated RF with starting and ending SCr levels in the Ohio SLE Study (OSS) cohort.

Results

New-onset CKD occurred in 12/41 patients over a median follow-up of 4.5 years. The CKD group had more RF events than the non-CKD group: 31 (2.59/patient) versus 17 (0.59/patient), respectively, and spent more time in RF (Table 1). Only 8% of the CKD group versus 59% of the non-CKD group had no RF. In OSS patients with established CKD, those who progressed had more RF events than nonprogressors: 13 (1.63/patient) versus 2 (0.29/patient), respectively. In the nonprogressor group 71% had no RF, compared with 37.5% of progressors. Progressors had a significant change in SCr over the study period (P = 0.0078). Differences in number of RF and RF duration were not significant between the two groups but tended to be higher in the progressors (Table 2).

Conclusion

In patients with LN, the frequency and duration of RF are biomarkers of new CKD and progression of existing CKD. As new LN therapeutic regimens are developed, targeting RF prevention should be an important goal.