Type 2 diabetes mellitus (T2DM) mediated renal dysfunction, or diabetic nephropathy (DN) is a progressive chronic complication which further increases the risk of T2DM mortality. Several studies have found reactive oxygen and nitrogen species (ROS/RNS) as key mediators of signal transduction during T2DM and DN leading to increased oxidative stress. Concurrent decreases in the capability of the cellular antioxidant defences to compensate for this T2DM-induced oxidative stress, results in elevated redox-mediated post-translational modifications (PTMs) of reactive cysteine residues. Here, we examined the cysteine redox-modified renal proteome in T2DM using rats that were fed either a standard CHOW (C) (12% fat) or high fat (HF) (42% fat) diet for 8 weeks with T2DM induced in 50% of the animals after 4 weeks utilising a low dose of streptozotocin (STZ; 35mg/kg); a pancreatic β-cell toxin. The remaining 50% were injected with a buffer vehicle (Cit). At the cessation of the feeding protocol, 9 animals per treatment group (C Cit; C STZ; HF Cit; HF STZ) were euthanised and kidneys excised. Tissue lysates were subjected to western blotting using anti-glutathione, anti-sulfenic acid, and anti-S-nitrosylation antibodies. Western blots revealed gross changes in glutathionylation, sulfenylation and nitrosylation PTMs associated with diet and pathology. To identify discrete sites targeted by these PTMs we performed isobaric tagging (TMT) and enriched for modified peptides using thiol-affinity chromatography, with subsequent analysis by LC-MS/MS on a Thermo Q-Exactive HF-X. Significantly modified proteins, changing in abundance between one or more treatment group in comparison to C Cit, were mapped to enriched regulatory pathways such as tricarboxylic acid cycle, phosphoinositol 3-kinase/protein kinase B pathway and glycolysis/gluconeogenesis pathway. Our data suggests that the rat renal redoxome is sensitive to diet and T2DM, indicating a possible physiological remodelling role for cysteine oxidation in DN.