Diabetic kidney disease is a leading cause of kidney failure worldwide and is easily detectable with screening examination. Diabetes causes hyperfiltration and activation of the renin-angiotensin aldosterone system by hemodynamic changes within the nephron, which perpetuates damaging physiology. Diagnosis is often clinical after detection of heavy proteinuria in a patient with diabetes,but can be confirmed by observation of histologic stages on kidney biopsy. Mainstays of treatment include angiotensin conversion or receptor blockade, mineralocorticoid receptor blockade, and tight glucose control. Newer agents favored in diabetic kidney disease are sodium glucose-cotransporters and glucagon-like peptide 1 receptor agonists, both for glycemic control and for various methods of reversing damaging physiology.