Description

Systemic lupus erythematosus (SLE) is a chronic inflammatory multisystem autoimmune disease characterized by pathogenic autoantibodies production against nuclear structures. SLE affecting mainly women of childbearing age and is characterized by unpredictable flares and remissions. Disease severity varied from a mild episodic disorder to a rapidly progressive life-threatening illness. The kidney is the most commonly involved visceral organ in SLE Lupus nephritis (LN) is one of the most serious manifestations of SLE since it is associated with significant morbidity and mortality and affects up to 60% of SLE patients. Nephritic syndrome and acute kidney injuries can complicate LN and increase the risk of end stage renal disease (ESRD) . Early diagnosis of renal involvement in SLE patients is important to improve the long-term outcome and increase the survival rate .

LN is diagnosed by either the presence of proteinuria (>0.5 g/day), active urinary sediment (with red blood cell, granular, tubular and/or mixed casts), or an unexplained rise in serum creatinine. A renal biopsy is known to be the gold standard for the diagnosis of LN because it gives information and details about the pattern and severity of kidney affection as well as the exclusion of other mimics of LN . Each of these factors weighs heavily on treatment choices. However, kidney biopsy is an invasive technique, and it is contraindicated in some situations such as bleeding and infection, associated with renal biopsy .

Therefore, identifying new noninvasive biomarkers of LN severity and outcome is mandatory. IL-17 is a potent pro-infammatory cytokine that amplifes T-cell activation and stimulates fibroblast cells, endothelial, and epithelial cells to produce several pro-infammatory mediators, including IL-1β, IL-6, and TNF-α. IL-17 receptor signaling enhances the expression of multiple pro-infammatory mediators. Hence, IL-17 enhances the production of neutrophil-attracting chemokines .

Few studies focused on the importance of IL-17 in SLE, particularly LN, and its relation to different disease activity parameters, so we aimed to explore its relation with uric acid and homocysteine in LN.

Also, Lupus nephritis (LN) is closely associated with hyperuricemia, and uric acid is the metabolite of purine that is excreted mainly in urine and considered a risk factor for renal involvement in systemic lupus erythematosus (SLE).

We postulated that patients with lupus nephritis are more likely to have elevated homocysteine levels. Homocysteine is metabolized by two alternative pathways, including its remethylation and transsulfuration. Elevated serum homocysteine can occur in 5 to 10 percent of the population. Increased serum homocysteine levels are seen in approximately 15% of patients with systemic lupus erythematosus.