DNA damage in a patient with Systemic Lupus Erythematosus and Nephropathy- A Case Report

Gurleen Kaur Tung, Gursatej Gandhi



Systemic Lupus Erythematosus (SLE) is a complex, multisystem autoimmune inflammatory disease. The inflammatory response in SLE exacerbates oxidative stress which tends to promote lipid peroxidation, protein oxidation and damage to DNA. Documentation of manifestation of DNA damage in SLE patients is scarce and related studies have not come to attention from this part of the world, therefore the present study showcases a case report on SLE.


Assessment of DNA damage in peripheral blood leukocytes and oxidative stress biomarkers in blood sera of a 12y-old male presenting with SLE and nephropathy (on dialysis therapy) was made.


Basal DNA damage in PBL scored as percent DNA in tail was higher (51.48%) compared to levels (40.38%) in an age-and sex-matched healthy control. Quantitative measures of DNA damage revealed DF of 96 vs. 94 and DI of 317 vs. 208 in the case and the control, respectively. Serum lipid peroxidation as estimated from MDA level was 3x higher (1.759µmol/l) compared to its level in a healthy control (0.571µmol/l). OSI was slightly higher in the patient (0.134 arbitrary units) compared to that in the control (0.132 arbitrary units). The atherogenic indices were higher in the present case compared to ratios in the control.


The results from the case report on increased oxidative stress, dyslipidemia, genetic damage and atherogenic indices support observations from earlier studies and imply onset of other complications in patients with SLE. The assessment of various blood-based biomarkers (as carried out in the present case) in SLE patients may assist in disease diagnosis, prognosis and optimal disease management.


Genetic damage, lupus nephritis, oxidative stress

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DOI: http://dx.doi.org/10.7439/ijbr.v6i7.2213

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