We are currently confronted with an epidemic of renal failure caused by diabetic nephropathy. It has become apparent that blood pressure is a major determinant of the risk of developing diabetic nephropathy; individuals with a genetic predisposition to hypertension are at increased risk of developing diabetes and diabetic nephropathy. Antihypertensive medication has an impact on development of diabetes; beyond blood-pressure lowering, the risk of diabetes is further reduced by blockade of the renin–angiotensin system (RAS). In experimental studies, blockade of the RAS in the pre-diabetic stage ameliorates the severity of subsequent diabetic nephropathy. Guidelines recommend a target blood pressure of 130/80 mmHg for diabetic patients without proteinuria and some guidelines recommend a target of less than 125/175 mmHg for diabetic patients with proteinuria. Above a systolic blood pressure of approximately 110 mmHg, the risk of progression of diabetic nephropathy increases progressively with increasing blood pressure. Blood-pressure lowering and blockade of the RAS delays or prevents onset of microalbuminuria, slows worsening of microalbuminuria and attenuates progression of diabetic nephropathy, even in advanced stages. In addition to blood pressure, proteinuria is a treatment target and should be reduced to below 1 g/24 h.