*2.2. Lipid Peroxidation Pattern in the Studied Groups*

We evaluated lipid peroxidation pattern by determining serum levels of 4-HNE (µg/mL), TBARs (µmol/L), MDA (ng/mL), F2-Isoprostan (pg/mL) and ImAnOx (µmol/L). 4-HNE levels had an increase with 28.9% in non-LN group (*p* > 0.05) and with 43.22% in LN group (*p* < 0.05), when compared with control group. TBARs levels were statistically significantly higher with 52.76% in non-LN group (*p* < 0.05) and with 71.35% in LN group (*p* < 0.01), when compared with control group. MDA increased with 93.3% in non-LN group (*p* < 0.05) and with 73.9% in LN group (*p* < 0.05) compared with control group. F2-Isoprostan also increased with 240% in LN group (*p* < 0.01) and with 334% in non-LN group (*p* < 0.01) compared with control group (*p* < 0.01). ImAnOx decreased with statistical significance with 33.6% in LN group (*p* < 0.01), and 14.3% in non-LN group (*p* < 0.01) compared with control group. When comparing LN and non-LN groups, we detected a statistically significant increase in F2-Isoprostan and TBARS and decrease in ImAnOx in LN group (*p* < 0.05). 4-HNE, TBARs and F2-Isoprostan had statistically significantly higher levels, while ImAnOx had statistically significantly lower levels in type IV lupus nephritis patients, when compared with SLE non-LN control group. When comparing SLE–LN patients with type IV lupus nephritis patients, we did not detect any statistically significant variations. All results are presented in Table 3.

## *2.3. DNA Oxidation in Studied Groups*

Oxidative DNA damage was evaluated by serum levels of 8-OHdG (ng/mL) and OGG1 status. 8-OHdG increased 1.16-fold in non-LN group (*p* < 0.01), 1.17-fold in LN group (*p* < 0.01), respectively 1.16 in type IV lupus nephritis (*p* < 0.05) compared with control group. There were no statistically significant variations between LN, type IV nephritis subjects and non-LN group. OGG1 did not vary significantly between non-LN and the control group, but in LN group it decreased 1.23-fold when compared with the control group (*p* < 0.001) and 1.28-fold when compared with non-LN group (*p* < 0.001). OGG1 did not vary significantly between SLE–LN and type IV LN subjects. All results are presented in Table 4.


**Table 3.** Lipid peroxidation pattern in the studied group.

4-HNE—4-hydroxy-2-nonenal, TBARs—Thiobarbituric acid reactive substances, MDA—Malondialdehyde, ImAnOX—Total antioxidative capacity, SLE—Systemic lupus erythematosus, LN—Lupus nephritis, *p*—Statistical significance, *p*1—Triple comparison of the groups, *p*2—Pairwise comparison of the groups, A—SLE non-LN, B—LN, C—type IV lupus nephritis, D—Control.

**Table 4.** DNA oxidation in studied groups.


8-OHdG—7,8-dihydro-8-oxo-2′ -deoxyguanosine, OGG1—8-oxoguanine-DNA-glycosylase, SLE—Systemic lupus erythematosus, LN—Lupus nephritis, *p*—Statistical significance, *p*1—Triple comparison of the groups, *p*2— Pairwise comparison of the groups, A—SLE non-LN, B—LN, C—type IV lupus nephritis, D—Control.

#### *2.4. Carbohydrate Oxidation in Studied Groups*

Carbohydrate oxidation status was evaluated by assessment of serum pentosidine (ng/mL) and AGE (ng/mL)- sRAGE (pg/mL) axis. Pentosidine levels were 249% higher in non-LN group (*p* < 0.01), 276% higher in LN group (*p* < 0.01), and 278% higher in the type IV nephritis cohort (*p* < 0.01) when compared with the control group. Pentosidine did not vary significantly between LN, non-LN group and type IV nephritis groups. AGE levels were 216% higher in non-LN group (*p* < 0.01), 243% in LN group (*p* < 0.01), and 267% in type IV nephritis (*p* < 0.01), when compared with control group. sRAGE decreased with 7.6% in non-LN group (*p* < 0.001), with 5.8% in LN group (*p* < 0.001), with 5.5% in type IV nephritis (*p* < 0.001), when compared with the control group. Pentosidine, AGE and sRAGE vary insignificantly both between LN–Non-LN group, and LN–Type IV nephritis group. All results are presented in Table 5.


**Table 5.** Carbohydrate oxidation in studied groups.

AGE—Advanced glycation end products, sRAGE—Soluble receptor for advanced glycation end products— Systemic lupus erythematosus, LN—Lupus nephritis, *p*—Statistical significance, *p*1—Triple comparison of the groups, *p*2—Pairwise comparison of the groups, A—SLE non-LN, B—LN, C—type IV lupus nephritis, D—control.
