The clinical syndrome of diabetic nephropathy is characterized by a progressive rise in albuminuria and arterial BP with a relentless decline in glomerular filtration rate (GFR) of approximately 10-14 mL/min/year. Even though arterial hypertension is an early and frequent phenomenon, normal BP is present in about 25% of the cases when kidney function is well preserved. In normotensive streptozotocin-diabetic rats, it has been demonstrated that angiotensin-converting enzyme (ACE) inhibition initiated at diabetes onset confers long-term protection against the development of diabetic glomerulopathy. Long-term use of ACE inhibitors (ACEIs) can delay the development of diabetic nephropathy in normotensive type 1 diabetic patients with persistent microalbuminuria.

Renoprotection - A beneficial effect on kidney function and structure, above and beyond that expected from the BP-lowering effect alone, has been demonstrated using ACE inhibition in diabetic nephropathies. In normotensive patients with type 1 and type 2 diabetes, ACEI therapy reduces the risk of developing diabetic nephropathy by 18%, defined as new-onset microalbuminuria or macroalbuminuria. It also improves all-cause mortality by 16% in patients with diabetes, including patients with or without hypertension. Studies showed that normotensive subjects with type 2 diabetes and microalbuminuria had higher morning BP than either of the normotensive subjects with type 2 diabetes and normal urinary albumin excretion or age-matched controls. Early documentation by ambulatory BP monitoring of an increase in morning BP warrants the use of ACEIs in a patient with type 2 diabetes, which prevents the development of diabetic nephropathy.