Lupus: Open Access
Open Access

Stronger Correlation between Interleukin 18 and Soluble Fas in Lupus Nephritis Compared with Mild Lupus

Hanifa Wadood^{* *}Correspondence: Hanifa Wadood, Department of Pharmaceutical Biotechnology, Sudan University of Science & Technology, Khartoum, Sudan, Email:

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About the Study

In SLE patients, abdominal pain may also be a sign of underlying vasculitis and thrombosis, which, if left untreated, can result in life-threatening ischemia and perforation. The case study that follows depicts a young woman who developed lupus enteritis and lupus panniculitis as her first signs of SLE. It highlights the value of early disease recognition, the diagnostic value of abdominal CT, and the most recent lupus enteritis treatment guidelines. One of the main causes of morbidity in people with Systemic Lupus Erythematosus is Lupus Nephritis (LN) (SLE). It has been hypothesized that a number of cytokines and apoptotic markers, including soluble Fas (sFas) and IL-18, contribute to the pathogenesis of LN. Previous research verified that sFas and IL-18 serum concentrations are elevated in SLE. Only a few research, nevertheless, have hypothesized a link between IL-18 and sFas. This work was intended to build on our earlier investigation into the relationship between those markers in order to assess that relationship in LN. In this study, 46 individuals without major organ involvement and 32 patients with just LN were involved.

A major SLE consequence is lupus nephritis. The most frequently noted abnormality in lupus nephritis is proteinuria. Although the exact cause of LN is unknown, a number of factors have been suggested in its onset and development. The imbalance of apoptosis and the excessive production of many cytokines, including IL-18, are two significant elements that are thought to be implicated. The harmful role of IL-18 and the Fas/ Fas ligand pathway in autoimmune illnesses like lupus has been highlighted by researchers. Apoptosis mediated by Fas and IL-18 may also be related to one another due to IL-18's proapoptotic properties, according to current research. Specific cells can express more Fas/Fas ligand when exposed to IL-18.

The superfamily of tumour necrosis factor/nerve growth factors includes Fas (Apo/1-CD95) and its ligand. An essential component of the autoimmune process is IL-18, which expresses Fas/Fas ligand. Although the roles of IL-18 and sFas in the pathogenesis of LN have been clarified individually, there is minimal proof that sFas and IL-18 are related related in autoimmune disorders. Only a small number of research noted that infections could increase serum levels of sFas and IL-18 by augmenting or increasing the apoptotic turnover of defence cells. Only a small number of studies on autoimmune illnesses have included this correlation. The impact of IL-18 on participants with Adult- Onset Still's Disease (AOSD), SLE, and healthy participants' peripheral blood lymphocyte apoptosis. We also showed in our earlier research that sFas and increases in IL-18 are correlated with lupus disease activity.

There is a sizable and expanding body of literature that discusses the roles of IL-18 and sFas separately in lupus nephritis, and some researchers have mentioned the local production of IL-18 in glomeruli that has local consequences in the pathogenesis of LN. However, the relationship between these two serum indicators in LN has received much too little study. As a followup to our earlier research, we carefully looked at the relationship between sFas and IL-18 blood concentrations in lupus nephritis in comparison to moderate lupus in this work. Whether the association between sFas and IL-18 in LN is stronger than that correlation in moderate lupus was the major focus of the current study. To achieve this, we chose and compared two patient groups: those with lupus nephritis who did not have any other major organ involvement, and those with mild lupus who did not have any major organ involvement. 78 SLE patients participated in this prospective case-control, cross-sectional study, of which 75 (96.2%) women and 3 (3.8%) males were female.

In the case or severe SLE group, 32 patients (41%) had proteinuria of more than 500 mg in a 24-hour urine collection, and 46 patients (59%) had no kidney involvement, as indicated by normal urinary sedimentation, a creatinine clearance of more than 80%, and the absence of a prior history of renal involvement (control or mild SLE group).

By meeting at least four of the updated SLE diagnostic criteria from the American College of Rheumatology (ACR), all patients have been given an SLE diagnosis. Proteinuria of more than 500 mg in a 24-hour urine collection sample, nephritic hematuria or pyuria, or a GFR of less than 80% were considered signs of renal involvement in this investigation.

Patients' demographic information, including significant test results and medications, were documented on a given checklist.

Each participant completed the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) questionnaire. Women who were pregnant or nursing, people with a history of cancer (past or present), concurrent infections, recent trauma, smokers, people who were addicted to drugs or alcohol, people with overlap syndromes, people with chronic renal failure, and people with other systemic issues unrelated to SLE-like a history of hepatitis or liver disease-were all excluded from the study. We also excluded all individuals with Glomerular Filtration Rates (GFR) less than 80% since lower GFR raises blood sFas concentrations.

Therefore, this study's objective was to assess the serum levels of sFas and IL-18 in lupus renal involvement.

The current investigation shown that lupus patients with proteinuria have considerably greater serum levels of sFas and IL-18 than those without proteinuria. Additionally, compared to patients without LN, the association between sFas and IL-18 is noticeably stronger in LN patients. Additionally, sFas serum readings are more accurate predictors of proteinuria than IL-18. The significance of the pathogenic function played by these two indicators in kidney damage is highlighted by the higher connection between sFas and IL-18 in LN compared with moderate lupus.