Diabetic kidney disease (DKD) develops through maladaptive communication among glomerular, tubular, vascular and immune cells, but current clinical markers capture accumulated injury more readily than active molecular processes. Extracellular RNAs (exRNAs), including microRNAs, long noncoding RNAs, circular RNAs and messenger RNAs, are released in extracellular vesicles (EVs) or associated with ribonucleoproteins and lipoproteins. These carriers protect RNA against degradation and convey regulatory signals between cells, producing measurable molecular traces in urine and blood. In DKD models, exRNA pathways have been linked to podocyte loss, endothelial dysfunction, mesangial expansion, tubular stress, inflammation and fibrosis. Urinary EV-associated microRNAs have the most developed evidence from patient studies, with several varying alongside albuminuria or estimated glomerular filtration rate. Most of these studies are small and cross-sectional. Their findings are strongly affected by biofluid collection, EV enrichment, RNA normalization, treatment exposure and disease definition. Therapeutic studies remain preclinical, and effects of a nominated RNA must be separated from those of its carrier and co-packaged cargo. We critically assess biomarker and therapeutic evidence in relation to exRNA biology and renal cell-state transitions. The proposed staged translational framework addresses analytical validity, biological provenance, prospective clinical utility and scalable manufacturing. exRNA is therefore best viewed not as a single biomarker class, but as a platform whose value will depend on resolving cellular origin, context and causality.