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Soluble Fms-like Tyrosine Kinase Associated with Preeclampsia in Pregnancy in Systemic Lupus Erythematosus

UMAIR QAZI, CHUN LAM, S. ANANTH KARUMANCHI, and MICHELLE PETRI

ABSTRACT.

Objective. Placental synthesis of soluble Fms-like tyrosine kinase (sFlt-1) is responsible for the increased level of serum sFlt-1 in preeclampsia. sFlt-1 binds to the receptor-binding domain of placental growth factor (PlGF) and vascular endothelial growth factor (VEGF), acting as an endogenous inhibitor of VEGF and PlGF signaling in endothelial cells. It has been hypothesized that increased circulating sFlt-1 contributes to the endothelial dysfunction, hypertension, and proteinuria of preeclampsia. We examined the association of sFlt-1 and preeclampsia in pregnancies in patients with systemic lupus erythematosus (SLE).

Methods. A case-control study was performed using stored serum samples. Cases were SLE pregnancies with later preeclampsia and controls were SLE pregnancies without later preeclampsia.

Results. The 52 SLE pregnancies occurred from 1998 to 2001. Nine (17%) pregnancies met the definition of preeclampsia and an additional 9 (17%) met the definition of superimposed preeclampsia. sFlt-1 concentration was significantly higher in SLE pregnancies with preeclampsia (1768 ± 196 pg/ml) than in those without (1177 ± 143 pg/ml) (p = 0.0185).

Conclusion. Our study shows for the first time that sFlt-1 is associated with preeclampsia in patients with SLE, as previously shown in the general pregnancy population. This suggests that SLE pregnancies at risk for preeclampsia can be identified early in the pregnancy by sFlt-1, thus identifying them for high-risk obstetric referral and appropriate monitoring. (J Rheumatol First Release Feb 15 2008)

Key Indexing Terms:

SYSTEMIC LUPUS ERYTHEMATOSUS
PREGNANCY
PREECLAMPSIA

From the Department of Medicine, Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland; and Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.

Supported by the Kirkland Scholar Program. The Hopkins Lupus Cohort is supported by NIAMS R01 AR43737 and the Johns Hopkins University General Clinical Research Center M01-RR00052.

U. Qazi, MD, MPH; M. Petri, MD, MPH, Division of Rheumatology, Johns Hopkins University School of Medicine; C. Lam, MD; S.A. Karumanchi, MD, Department of Nephrology, Beth Israel Deaconess Medical Center.

Address reprint requests to Dr. M. Petri, Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 7500, Baltimore, MD 21205, USA. E-mail: mpetri@jhmi.edu

Accepted for publication November 3, 2007.