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Diabetic nephropathy is the single most frequent cause of end-stage renal disease (ESRD) in the western world, with an estimated cost in excess of 15. 6 billion per annum in the United States alone 1. In anticipation of an obesity-related diabetes epidemic, coupled with progressively growing rates of hypertension, these figures are forecast to rise exponentially. As both diabetes and renal disease are increasingly recognized as generalized vasculopathic states, there has been renewed interest in identifying potential vascular mechanisms influencing renal damage. The relationship between diabetes, hypertension and kidney disease is complex, progressive and reciprocal. In type 1 diabetes, the prevalence of microalbuminuria increases from the onset of disease, reaching 50% after 20 years 2, whilst in type 2 diabetes, it is stable at 20–25% 3. Microalbuminuria is a powerful marker for progression to overt nephropathy 4–6 and renal function continues to decline in 30% of microalbuminuric patients with either type 1 7 or type 2 diabetes 6. Whilst in patients with type 1 diabetes, good glycaemic control 8 or relative youth 7 is associated with the remission of microalbuminuria, in patients with type 2 diabetes, institution of antihypertensive therapy is also important 6. Once nephropathy is established however, ESRD occurs in 75% of individuals within 20 years 1; at which point the cardiac mortality risk is 20-fold higher than that of the general population 9. Thus, the stage at which diabetic renal disease is most likely to be arrested and even reversed is at the point at which microalbuminuria is detected by the clinician. The reversibility of microalbuminuria suggests an associated
Khavandi et al. (Fri,) studied this question.