Open Access Research article

Clinicopathologic correlations of renal microthrombosis and inflammatory markers in proliferative lupus nephritis

Elena Gonzalo1, Oscar Toldos2, María P Martínez-Vidal3, María C Ordoñez4, Begoña Santiago1, Antonio Fernández-Nebro4, Estíbaliz Loza5, Isabel García6, Myriam León6, José L Pablos13 and María Galindo13*

  • * Corresponding author: María Galindo mgalindo@h12o.es

  • † Equal contributors

Author affiliations

1 Instituto de Investigación Hospital 12 de Octubre (i+12), Avenida de Córdoba sn, 28041 Madrid, Spain

2 Servicio de Anatomía Patológica, Hospital 12 de Octubre, Avenida de Córdoba sn, 28041 Madrid, Spain

3 Servicio de Reumatología, Hospital 12 de Octubre, Avenida de Córdoba sn, 28041 Madrid, Spain

4 Servicio de Reumatología, Hospital Regional Universitario Carlos Haya, Avenida Carlos Haya sn, 29010 Málaga, Spain

5 Unidad de Investigación de la Fundación Española de Reumatología, Sociedad Española de Reumatología, Calle Marqués del Duero 5, 1°, 28001 Madrid, Spain

6 Servicio de Anatomía Patológica, Hospital Regional Universitario Carlos Haya, Avenida Carlos Haya sn, 29010 Málaga, Spain

For all author emails, please log on.

Citation and License

Arthritis Research & Therapy 2012, 14:R126  doi:10.1186/ar3856

Published: 28 May 2012

Abstract

Introduction

Microthrombosis is often observed in lupus nephritis (LN) lesions, but its clinical significance is unknown. We evaluated the clinicopathologic correlations of renal microthrombosis and inflammatory markers in LN.

Methods

Kidney biopsies from 58 patients with systemic lupus erythematosus (SLE) proliferative nephritis were analyzed with immunohistochemistry (IHC) for intravascular platelet aggregates (CD61), macrophagic infiltration (CD68), and activated complement deposition (C4d). Clinical data at the time of kidney biopsy and follow-up were analyzed with regard to pathologic IHC data.

Results

Microthrombosis was present in 52% of the tissues. It was significantly more prevalent in patients with antiphospholipid antibodies (aPLs) (62% versus 42%). The presence of microthrombosis significantly correlated with higher macrophagic infiltration. Macrophagic infiltration but not microthrombosis was significantly correlated with C4d deposition. Only macrophagic infiltration showed a correlation with SLE and renal activity (proteinuria and active sediment), whereas neither the presence of CD61+ microthrombi nor the extent of C4d deposition correlated with LN severity or outcome.

Conclusions

Microthrombosis is associated with higher macrophagic infiltration in LN but does not seem to increase independently the severity of renal damage. Macrophagic infiltration was the best marker of SLE and renal activity in this LN series.