Study of the impact of Microalbuminuria on the morbidity and mortality of the acute coronary syndrome in diabetic patients

Microalbuminuria (MA) is a well- known risk factor for coronary artery disease (CAD) in diabetics and non diabetics. It is associated with higher cardiovascular mortality, especially in diabetics. However, there are few data linking angiographic severity of CAD to microalbuminuria. Diabetics with MA had higher fasting glucose and glycosylated hemoglobin levels than diabetics without MA. Thus patients with MA have more severe angiographic CAD than those without MA. This relation is independent of other risk factors and is particularly evident in patients with DM.Among patients with type 2 diabetes, the reported prevalence of microalbuminuria at 10 years is between 25 to 40 percent. Some patients have microalbuminuria at the time of diagnosis, which may be due to previously undiagnosed diabetes or some other disease that is responsible for the microalbuminuria.Microalbuminuria is defined as persistent urinary albumin excretion between 30 and 300 mg/day (20 to 200µg/min). Macroalbuminuria referred to albumin excretion above 300 mg/day (200 µg/min).With type 2 diabetes, microalbuminuria is associated with declining kidney function, progression to macroalbuminuria, and increased long-term mortality. However, remission to normoalbuminuria may occur. Factors associated with remission include short duration of microalbuminuria, better glycemic control, better blood pressure control, and use of ACE inhibitors or angiotensin receptor blockers.The mechanism by which microalbuminuria is associated with cardiovascular disease is not well understood. However, microalbuminuriaty appears to be a signal that the vasculature, particularly the endothelium, is not functioning normally. Among diabetic patients, the degree of coronary endothelial dysfunction appears to be greater in patients with microalbuminuria and may be related to hyperglycemia-induced alterations in extracellular matrix, such as decreased density of heparan sulfate proteoglycans. This abnormality can lead to increased microvascular permeability, resulting in microalbuminuria at the glomerulus and perhaps increased lipoprotein deposition in peripheral vessels.