Objective Even though diabetes patients exhibit an increased oxidative stress, its correlation with diabetic nephropathy is not fully understood. The purpose of this study was to determine whether lipid peroxidation marker correlates well with eGFR and UACR in type 2 diabetes mellitus patients. Methods collected urine and serum samples of Indonesian type 2 diabetes mellitus outpatients with normo- and microalbuminuria at a Local  Clinic (from ages: 39–74 years). Urinary 8-iso-PGF2α was measured by ELISA, the serum malondialdehyde by TBARS assay, and urinary albumin by BCG albumin assay. eGFR was calculated using the corrected-Cockcroft–Gault (CG), MDRD, and CKD-EPI equation. Results The results showed that the increasing level of malondialdehyde was mildly correlated with the decline in eGFR (MDRD). In contrary, there was a significant positive correlation between 8-iso-PGF2α concentration and eGFR based on the corrected-CG, MDRD study, and CKD-EPI equation (r = 0.457, p < 0.001; r = 0.424, p < 0.001; r = 0.443, p < 0.001). This relationship still persisted in the normoalbuminuric subjects (n = 43) (r = 0.491, p = 0.001; r = 0.461, p = 0.002; r = 0.455, p = 0.002). The multivariate analysis showed that 8-iso-PGF2α together with fasting plasma glucose was the most predictive factor for the high 2-quantile eGFR (adjusted OR 1.001, (95% CI, 1.000–1.001)). However, there was no significant correlation between UACR with malondialdehyde (r = 0.268, p = 0.050) and 8-iso-PGF2α(r = −0.030, p = 0.808). UACR itself was inversely correlated with eGFR based on the corrected-CG, the MDRD, and CKD-EPI (r = −0.232, p < 0.05; r = −0.228, p < 0.05; r = −0.232, p < 0.05). Conclusions Increased 8-iso-PGF2α and malondialdehyde in type 2 diabetes mellitus patients may play a role in the pathophysiologic significance of diabetic nephropathy, even while considering the effect of potential confounders.