PT  - JOURNAL ARTICLE
AU  - PETER M. IZMIRLY
AU  - MARIANNA SHVARTSBEYN
AU  - SHANE MEEHAN
AU  - ANDREW FRANKS
AU  - ALAN BRAUN
AU  - ELLEN GINZLER
AU  - SHERRY X. XU
AU  - HERMAN YEE
AU  - TANIA RIVERA
AU  - CHARLES ESMON
AU  - LAURA BARISONI
AU  - JOAN T. MERRILL
AU  - JILL P. BUYON
AU  - ROBERT M. CLANCY
TI  - Dysregulation of the Microvasculature in Nonlesional Non-Sun-exposed Skin of Patients with Lupus Nephritis
AID  - 10.3899/jrheum.110878
DP  - 2012 Mar 01
TA  - The Journal of Rheumatology
PG  - 510--515
VI  - 39
IP  - 3
4099  - http://www.jrheum.org/content/39/3/510.short
4100  - http://www.jrheum.org/content/39/3/510.full
SO  - J Rheumatol2012 Mar 01; 39
AB  - Objective. Membrane endothelial protein C receptor (mEPCR) is highly expressed in peritubular capillaries of kidneys from patients with active and poorly responsive lupus nephritis (LN). We investigated the hypothesis that changes in the microvasculature are widespread with extension to the dermal vasculature. Methods. Skin biopsies from uninvolved skin (buttocks) were performed in 27 patients with LN and 5 healthy controls. Sections were stained with specific antibodies reactive with mEPCR, adiponectin, intercellular adhesion molecule-1 (ICAM-1), and CD31; then assessed by enumeration of stained blood vessels (percentage positive blood vessels) blinded to knowledge of clinical information. Results. There was a significant increase in the prevalence of blood vessels that stained for mEPCR and ICAM-1 in patients compared to controls [94% vs 59% (p = 0.045) and 81% vs 67% (p = 0.037), respectively]. Adiponectin staining and CD31 staining were similar between the groups (45% vs 43% and 98% vs 92%). Dermal staining for mEPCR was greater in patients with proliferative glomerulonephritis than in those with membranous disease (96% vs 60%; p = 0.029). A composite of poor prognostic renal markers and death was significantly associated with greater expression of mEPCR staining. Conclusion. These data are consistent with the notion that in patients with LN, activation of the microvasculature extends beyond the clinically targeted organ. The insidious expression of this widespread vasculopathy may be a contributor to longterm comorbidities.