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Patients with diabetic renal disease have a very bad prognosis. Hyperfiltration, related to poor metabolic control, occurs early on in the disease process.1 There is also an increase in albumin excretion which can be readily reversed by effective glycaemic control at clinical diagnosis (fig 1).
A phase is then entered during which most patients are normoalbuminuric. However, after approximately 10 years, some patients will develop microalbuminuria. The risk of progression from normal to microalbuminuria is closely related to poor metabolic control and also, to some extent, blood pressure elevation. In patients with type 1 or type 2 diabetes and microalbuminuria there is advanced structural damage in the kidney.
Later, patients develop overt nephropathy and in type 1 and type 2 diabetes there is a relentless decline in glomerular filtration rate (GFR).
Role of angiotensin converting enzyme inhibitors
In recent years there has been an increased focus on treating patients early to prevent future renal damage. Even before microalbuminuria has developed there is evidence of the benefits of angiotensin converting enzyme (ACE) inhibitors.
NORMAL ALBUMINURIA
In studies looking at renal haemodynamics, ACE inhibitors were used to treat patients with type 1 diabetes who had normal albumin excretion.2 A reduction in filtration fraction was observed with ACE inhibitor treatment suggesting that the pressure at the glomerular membrane was reduced. The albumin excretion rate was also reduced in these completely normo-albuminuric …