Diabetic kidney microvascular injury is a major chronic complication that increases the risk of chronic kidney disease progression and cardiovascular events. Albuminuria plays a central role in diabetic kidney disease because it serves as an early marker of renal microvascular damage and reflects disease severity along a continuous spectrum driven by the combined effects of metabolic disturbances and hemodynamic alterations. Albuminuria staging based on the urine albumin-tocreatinine ratio (uACR) facilitates assessment of kidney involvement and risk stratification; however, biological variability should be acknowledged, and repeat confirmation is recommended before establishing a diagnosis of persistent albuminuria. Importantly, a non-albuminuric phenotype of diabetic kidney disease exists; therefore, combined assessment of uACR and estimated glomerular filtration rate (eGFR) is essential in routine practice. Factors associated with albuminuria and renal microvascular injury include diabetes duration, glycemic control and HbA1c variability, as well as comorbidities and baseline characteristics such as overweight/obesity, smoking, dyslipidemia, hypertension, older age, and male sex. Emerging evidence also suggests modulatory roles of the gut microbiome, non-alcoholic fatty liver disease, gene-expression regulatory mechanisms, and genetic susceptibility. Without appropriate intervention, albuminuria may progress to varying degrees, indicating worsening renal injury and representing an important therapeutic target. From a treatment perspective, renin–angiotensin system inhibition remains foundational particularly in patients with hypertension and albuminuria, while newer agents, including sodium–glucose cotransporter 2 (SGLT2) inhibitors and the non-steroidal mineralocorticoid receptor antagonist finerenone—have strengthened a multi-mechanistic kidney-protective strategy aimed at reducing albuminuria and slowing diabetic kidney disease progression.