الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
In our study we aimed at estimating the serum level of interleukin -18 (IL-18) and urinary level of N-Acetyl-Beta-D-Glucosaminidase (uNAG) in a group of Egyptian SLE patients, and to determine their relations to SLE disease activity, classes of LN, histological activity and Chronicity indices, renal disease activity clinically, some other SLE related clinical manifestations and laboratory parameters, and drug therapy.
Our study was conducted on 72 SLE patients who were divided into two groups; 41 patients with LN and 31 patients designated as lupus non-nephritis, compared with 12 age and sex matched apparently healthy controls.Patients with other chronic renal diseases, overlap syndrome, chronic infections, UTI, patients undergoing haemodialysis or with a history of renal transplantation, DM, malignancy, cardiac surgery, and patients receiving nephrotoxic drugs (as aminoglycosides, anticonvulsants, antineoplastic drugs) were excluded.
All patients were subjected to: thorough history taking, therapeutic history especially CS therapy and DMARDs and NSAIDs, general and local examination, rheumatological assessment including disease activity by SLEDAI, and renal disease activity by the renal activity score, renal biopsy examination for patients with LN, routine laboratory investigations, and measurement of the levels of serum IL-18 and uNAG.
Results: Serum level of IL-18 were significantly higher in patients with LN > lupus non-nephritis > healthy controls. There was positive significant relation between IL-18 and SLEDAI, proteinuria, renal activity score and AI in patients with LN. There was no significant difference in the serum levels of IL-18 between WHO classes of LN. As regards uNAG activity, it was significantly higher in patients with LN more than lupus non nephritis patients and healthy controls. Tubular dysfunction with elevated uNAG was present in 6 lupus non-nephritis patients with no evidence of glomerular disease. There was positive significant relation between uNAG and proteinuria, P/C ratio, and renal activity score in patients with LN. No significant correlations were demonstrated between uNAG and SLEDAI or tubulo-interstitial index in patients with LN. There is no significant difference in the urinary levels of NAG between WHO classes of LN.
Conclusion and recommendations: IL-18 appears to have a pathogenic role in the development of SLE, and plays a crucial role in triggering inflammation in LN. Serum IL-18 levels could be a useful biomarker to assess the activity and progression of renal disease in SLE and its role in the pathogenesis of CNS SLE disease needs to be further elucidated. Therapeutic strategies devoted to down-regulate IL-18 may be helpful in treatment of LN. In addition, Determination of uNAG activity as a marker of tubular dysfunction may be a useful supplement to the routine biochemical analysis performed on the urine in cases of SLE. Increased uNAG activity in absence of proteinuria in lupus non-nephritis patients may predict the development of LN later on. Furthermore, in the presence of proteinuria, the increase in uNAG activity parallels the degree of renal disease activity. As no correlation was found between uNAG activity and tubulo-interstitial index in renal biopsy, it is suggested that tubular function study by estimating uNAG is probably a more sensitive indicator of tubulo-interstitial disease.