Macrophage Migration Inhibitory Factor in Systemic Lupus Erythematosus and its Expression in Lupus Nephritis

Document Type : Original Article

Authors

1 Health Radiation Research Departments Faculty of Medicine Ain Shams University

2 National Centre for Radiation Research & Technology; Physical Medicine & Rehabilitation Department

3 Ain Shams University; Early Cancer d Dtection Unit Department, Ain Shams University Hospitals.

4 Early Cancer d Dtection Unit Department, Ain Shams University Hospitals.

Abstract

Objective: the aim of this study was to access the potential involvement of MIF in SLE, its relationship with corticosteroid dose, also, to measure serum and urinary MIF levels in SLE as well as detecting renal MIF expression in SLE GN.
Methods: Serum and urine MIF concentrations were measured by enzyme-linked immunosorbent assay in 20 SLE female patients with lupus nephritis , World Health Organization class II, III, IV, with mean age of 35.1510.42 years and in 10 normal healthy, age matched, female volunteers. All patients were subjected to detailed clinical assessment and laboratory investigations. Serum and urinary MIF concentrations were measured by ELISA technique. Renal MIF expression was assessed by immunostaining of biopsy tissue. Univariate and multivariate regression analysis were used to examine the associations between serum and urine MIF concentrations, renal MIF expression, disease-related indices of SLE and corticosteroid use.
Results: A statistically significant 2.98-fold-increase was detected in mean urinary MIF (U MIF) levels in SLE patients compared to controls. While, mean Serum MIF (S MIF) showed no significant difference between cases & control. Both S & U MIF concentrations were positively correlated with SLICC/ACR DI but not with SLEIDAI. Corticosteroid doses showed a highly positive correlation with S MIF, serum creatinine & SLICC/ACR DI. Also a positive correlation was found between the different histopathologic grades of renal affection & the U MIF. Immunohistochemistry staining of all normal kidney specimens showed that MIF is constitutively weakly expressed by some glomerular & parietal epithelial cells & by most tubular epithelial cells. In contrast, there was a significant increase in glomerular & tubular MIF protein staining in SLE nephropathy. This increased MIF expression correlated positively with both S MIF and U MIF, SLICC/ACR DI & the daily steroid dose
Conclusion: This study shows that serum MIF is over-expressed in SLE patients and that the urine MIF concentration is significantly increased in SLE World Health Organization class IV patients and correlates with the degree of renal injury. Thus, urine MIF levels reflect MIF expression within the kidney.




 

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