الفهرس 
Lupus Nephritis and its PathogenicityOnly 14 pages are availabe for public view
 |  | from | 183 |  |  |
| | | from | 183 | | |
Abstract
ystemic Lupus Erythematosus (SLE) is a complex autoimmune disease with heterogeneity in clinical manifestations and disease course, characterized by pathogenic autoantibody formation, immune complex deposition, and end-organ damage. Auto-antibodies attack normal tissues and organs, including the skin, joints, kidneys, brain, heart,
lungs and blood (Robert et al., 2010).
Lupus nephritis (LN) is a potentially devastating complication of systemic lupus erythematosus (SLE) (Schwartz et al., 2014).
Although all renal compartments including glomerular, tubulointerstitial, and vascular components may be injured by the disease however, the term lupus nephritis is mainly used to define the immune complex-mediated glomerulonephritis (GN) (Kiremitci and Ensari, 2014).
CD64 (cluster of differentiation 64) is a type of integral membrane glycoprotein known as Fc receptor that binds monomeric Ig-G with high affinity. It is more commonly known as Fc-gamma receptor 1 (FcγRI) (Hullet et al., 2002).
FcγRs have been implicated in the pathogenesis of several diseases, in particular the inflammatory autoimmune diseases such as, systemic lupus erythrematosus (SLE) and rheumatoid arthritis. These Fc receptors, therefore, play critical roles in host defense mechanisms against invading pathogens, in autoimmune diseases, and in cancer surveillance (Trinidad et al., 2006).
This study was carried out on 30 SLE patients attending the
inpatients’ departmentand outpatients’ clinics of the Rheumatology, Rehabilitation and physical medicine department of Benha University Hospitals. They were divided into two groups:
group Ia: they were 2 (14%) males and 13 (86%) females with disease duration ranging between 2-20 years with mean of 7.93±4.95 years.
group Ib: they were 3 (20%) males and 12 (80%) females with disease duration ranging between 2-15 years with mean of 6.4±4.11 years.
Together with 25 age and sex matched apparently healthy volunteers were recruited as a control group.
The aim of this work was to study the expression of FcγRI (CD64) on the surface of peripheral blood monocytes in SLE patients and their relationship to disease activity and lupus nephritis.
All patients were subjected to: full history taking, through clinical examination, laboratory assessment: CBC, ESR, CRP, ANA, Anti- ds DNS, C3, C4, protinuria (gm/24 hrs), serum creatinine, creatinine clearance, p/c ratio, assessement of disease activity SLEDAI score, r SLEDAI for LN cases and monocyte expression of CD 64 using flow cytometry.
In our study the mean monocyte expression of CD64 in SLE patients was 174.79 ± 61.38 % and 52.33 ± 28.71 % in healthy controls.There was a high significant increase in the mean monocyte expression of CD64 in SLE patients as compared to healthy subjects (p<0.001).In addition, there was significant increase in mean monocyte
expression of CD64 in SLE patients with LN (219.73 ± 52.94) as compared to SLE patients without LN (133.86 ± 37.55) (P < 0.05).
In our study; monocyte expression of CD64 was significantly elevated in SLE patients with renal manifestations in the form of (protinuria, elevated serum creatinine, increased P/C ratio and decreased creatinine clearance) (P<0.001) with non-statistically significant difference as regards other clinical manifestations. (P>0.05).
In this study:
High significant differences (p<0.001) between (SLE patients with & without LN) and control group as regard HB level, RBCs count, C3 levels, C4 levels, ESR and CRP being higher in SLE cases.
As regard the immunological profile, there was high significant difference (p<0.001) between SLE cases and control group as regard ANA positivity being positive in SLE cases than healthy control and anti ds DNA positivity being positive in SLE cases with LN than SLE cases without LN than healthy control.
As regard 24h urinary proteins and creatinine clearance there was a high significant difference (p<0.001) between SLE patients with LN compared to SLE without LN and control group and highly significant difference as regard P/C ratio being higher in SLE cases with LN when compared to SLE cases without LN and healthy control.
There was statistically significant difference as regard SLEDAI score being higher in SLE cases with LN than SLE cases without LN. (p<0.05).
There was highly statistically significant difference (p<0.001) in the mean CD64 expression levels between SLE cases being higher in SLE patients with LN class IV/V (219.46 ± 62.91) than SLE patients with LN class II/III (211.46 ± 43.38) (P<0.001).
There was highly statistically significant difference (p<0.001) in the mean CD64 expression levels between SLE cases being higher in SLE patients with LN class IV/V and SLE patients with LN class II/III than SLE patients without LN.
There was highly statistically significant difference (p<0.001) between SLE cases as regard expression levels of CD64 being higher in SLE cases with moderate, high and patients with very high disease activity compared to patients with no activity and in patients with high activity compared to patients with moderate activity.
There was statistically significant positive correlations between SLEDAI score (P<0.05) with (CRP, protinuria and P/C ratio) and there was highly statistically significant positive correlations (P<0.001) with (ESR and activity index).
There were statistically significant negative correlation between SLEDAI score and HB level, WBCs count and creatinine clearance and statistically highly significant negative correlation with C3 & C4 levels.
There were statistically hig significant positive correlation (p<0.001) betweenrSLEDAI and protinuria, protein creatinine ratio and activity index.
There were statistically significant (p<0.05) negative correlation between r SLEDAI score and C3 & C4 levels and statistically highly significantly negative correlations (p<0.001) with creatinine clearance.
Conclusion:
The changes in monocyte expression of CD64 in SLE patients support the hypothesis that CD64 may play a role in the pathogenesis of SLE generally and SLE with LN specifically.
Monocyte expression of CD64 could be used as potential marker in SLE patients reflecting disease activity.