TY  - JOUR
T1  - Comparative Study of Serum and Urine Cell Free DNA, miRNA‐27b, as Novel Biomarkers with INF‐Y for Assessing Systemic Lupus Erythematosus and Lupus Nephritis Activity
AU - Kreem, Khalid
        AU - Altamemi, Ibrahim
        
JO  - ACE Journal of Research Studies in Biosciences
VL  - 6
IS  - 1
SP  - 1
EP  - 13
PY  - 2026
DA  - 2001/08/19
SN  - 2520-3916
DO  - 10.36478/acerjrsb. 2026.1.13
UR  - https://theacepublications.com/article-detail.php?art=277-ACE-JRSB
KW  - microRNA
KW  - miRNA‐27b
KW  - Cell‐free DNA (cf‐DNA)
KW  - interferon gamma (INF‐y)
KW  - Systemic lupus erythematosus (SLE). Lupus Nephritis (LN)
AB  - Systemic lupus erythematosus (SLE) disease
a condition as one of the causes of loss of tolerance
to several autoantigens triggering the involvement of
the immune system to the destruction of tissues.
One of the most disabling symptoms of systemic
lupus erythematosus (SLE) refers to lupus nephritis
(LN). It does also have a frequency‐of‐occurrence that
is dependent on some level of kidney inflammation.
The immune complexes accumulated in the mesangial,
subepithelial and subendothelial parts of the
glomeruli cause the kidneys damage by causing
several inflammatory, proliferative and fibrous
pathways in these regions. The patterns of
deposition of different immune complexes are
associated with different lupus types of nephritis
(LN) and their clinical chemistry symptoms. This
research paper set out to assess the use of blood
and urine cell‐free DNA (cfDNA) as a non‐invasive
lupus nephritis biomarker in patients. In addition,
serum microRNA‐27a and serum INF‐Y evaluated
whether there were any correlations with the
severity of the disease. The participants in this study
were divided into three groups and the number of
participants was 106. The initial group was patients
who had SLE and had 6 males and 27 females
(n=36). Moreover, 12 men, 24 women were patients
with nephritis (n=35). Lastly, 11 men, 24 women
were those who were not affected by SLE or
nephritis (n=35). Three groups participated in a
cross‐sectional study was conducted based on 106
participants was classified as follows: 36 patients with
SLE (6 men and 27 women), 35 patients with lupus
nephritis (12 men and 24 women), and 35 as a control
group (11 men and 24 women) without a history of
systemic disease. The study was conducted from
January 2024 to September 2024. All participants had
been selected from Al‐Sader Teaching Medical City
in Najaf province and private labs. The study
involved three groups: lupus nephritis (n=35),
systemic lupus erythematosus (SLE, n=36), and
healthy controls (n=35). The lupus nephritis group
included 12 males and 23 females, while the SLE
group had 9 males and 27 females. The healthy
control group had 11 males and 24 females. Across
all groups (n=106), there were 32 males and 74
females, showing a case‐control ratio of 2.03:1 for
71 diseased individuals compared to 35 healthy
controls. sex distribution did not differ significantly
among the groups (p=0.685). The age distribution in
the study groups showed the following: lupus
nephritis (n=35) had 9 under 20, 11 aged 20‐30, 9
aged 31‐40, 5 aged 41‐50, and 1 over 50. The
systemic lupus erythematosus (SLE) group (n=36)
included 4, 9, 14, 8, and 1 in the respective age
ranges. The healthy control group (n=35) comprised
1, 6, 15, 13, and 0 individuals. In total (n=106), there
were 14 participants under 20, 26 aged 20‐30, 38
aged 31‐40, 26 aged 41‐50, and 2 over 50. Statistical
analysis indicated significant association between age
group and group membership (p = 0.271). The levels
of pro‐inflammatory cytokine INF‐T was evaluated
across the three studied groups, where the median
levels were significantly higher in both the lupus
nephritis group (70.00, IQR = 429.00) and the SLE
group (48.00, IQR = 386.75) compared to the healthy
control group (0.70, IQR = 0.40), with an overall
statistically significant difference between groups (p
< 0.0001). The fold change of miRNA‐27b was
markedly reduced in the lupus nephritis group
(median = 0.00221, IQR = 0.00420) compared to
both the SLE group and healthy controls, which
showed nearly identical low levels (median =
0.00017, IQR = 0.00080 for both), also yielding a
highly significant p‐value (p < 0.0001). Serum cell‐free
DNA (cfDNA) levels between patients with lupus
nephritis and SLE, expressed as fold change relative
to healthy controls. In this analysis, the healthy
control group showed no detectable Ct values in
RT‐PCR, indicating minimal or undetectable cfDNA
levels; therefore, a default fold change value of 1
was assigned to the control group for quantification
purposes. The lupus nephritis group had a median
cfDNA fold change of 0.353 (IQR = 0.408), while the
SLE group showed a median of 0.291 (IQR = 0.000).
However, the difference between the two patient
groups was not statistically significant (p = 0.573).
The healthy control group again showed no
detectable Ct values in qPCR, indicating undetectable
cfDNA levels. The lupus nephritis group had a
median urine cfDNA fold change of 0.0306 (IQR =
0.073), while the SLE group showed a higher median
of 0.1518 (IQR = 0.162). A statistically significant
difference was observed between the two groups (p
= 0.036). In Conclusion This research illustrates the
potential of cell‐free DNA (cfDNA) and specific
microRNAs (miRNA‐27b) as non‐invasive biomarkers
for assessing lupus nephritis (LN) in patients with
systemic lupus erythematosus (SLE). The study
presents evidence of increased levels of
pro‐inflammatory cytokine(INF‐Y) in both SLE and LN
groups when compared to healthy controls,
highlighting a strong inflammatory response in these
conditions. Furthermore, the expression levels of
miRNA‐27b was significantly reduced in LN and SLE
patients, suggesting these microRNA might serve as
indicators of disease activity and severity. The
investigation also assessed cfDNA levels in blood and
urine samples. While serum cfDNA levels showed no
significant differences between LN and SLE groups,
urine cfDNA levels were notably higher in the SLE
cohort compared to LN patients, indicating that urine
cfDNA could be a more sensitive biomarker for
distinguishing between these two groups. These
findings underscore the importance of incorporating
cfDNA and specific microRNA markers into the
diagnostic and prognostic approaches for lupus
nephritis, highlighting their relevance in non‐invasive
disease monitoring. Future research should focus on
larger cohort studies and the molecular roles of
these biomarkers in the pathogenesis of lupus
nephritis and systemic lupus erythematosus. This
approach could lead to more accurate, personalized
treatment strategies and improved patient outcomes.
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