Going out to detect incipient diabetic nephropathy rather than waiting until it has supervened--a reversal in policy.

Persistent albuminuria (>300 mg/24 h or 200 ug/min) is the hallmark of diabetic nephropathy, which can be diagnosed clinically if the following additional criteria are fulfilled: presence of diabetic retinopathy and no clinical or laboratory evidence of kidney or urinary tract disease other than diabetic glomerulosclerosis [1]. This clinical definition of diabetic nephropathy is valid both in insulin dependent diabetic (IDDM) and noninsulin dependent diabetic (NIDDM) patients. Albuminuric NIDDM patients without retinopathy require further evaluation, that is, kidney biopsy, since the chances for diabetic and non-diabetic glomerulopathy are approximately fifty-fifty [2]. The clinical syndrome termed diabetic nephropathy is characterized by persistent albuminuria, early blood pressure elevation, a relentless decline in GFR, and high risk of cardiovascular morbidity and mortality. Diabetic nephropathy has become a leading cause of end-stage renal disease (ESRD) in the world. Both IDDM and NIDDM patients contribute to the increase in ESRD. Prevention of diabetic nephropathy, or at least the postponement or slowing down of the disease process has emerged as a key issue. In the past years six sets of recommendations on the prevention of diabetic nephropathy, with special reference to microalbuminuria, have been published, as reviewed by Mogensen et al. [3]. Since the six programs proposed differ, an agreed unifying, global strategy for screening and treatment of diabetic patients with persistent microalbuminuria has been advocated [3]. This report focuses on microalbuminuria because this is the first clinical sign of risk of diabetic nephropathy and other vascular complications and prevention is best achieved at this early stage.