DIABETIC RENAL-DISEASE - MICROALBUMINURIA, IMPLICATIONS AND INTERVENTION

Diabetic nephropathy is the leading cause of end-stage renal failure i n the developed world. Proteinuria (''macroalbuminuria'' >200 mu g/min ; or >300 mg/24 h) heralds a phase of established renal pathology with inexorable decline to end-stage renal disease, although its progressi on can be delayed by antihypertensive medication, in particular the an giotensin-converting enzyme inhibitors (ACEI). Control of blood pressu re is vital; even if in the normal range, it is usually raised compare d with that in nondiabetic control groups. Reducing blood pressure can lower the rate of decline of the glomerular filtration rate by 90%. B efore established proteinuria there is a ''microalbuminuric'' (20-200 mu g/min, or 30-300 mg/24 h) phase, and during this time preventive in tervention may be effective. In so-called ''normotensive'' microalbumi nuric subjects antihypertensive medications, in particular the ACEI, s ignificantly reduce the progression to macroalbuminuria. Control of gl ycemia is important; recent evidence has shown that it is particularly important before the development of microalbuminuria; thereafter the role of glycemic control is not clear. Some researchers have suggested that protein restriction may be helpful, but more data are required. For the moment, improved glycemic control, in the normoalbuminuric dia betic subjects and treatment with ACEI after the onset of microalbumin uria would seem appropriate in light of knowledge today. Furthermore, any level of hypertension is totally unacceptable and should be treate d aggressively; the ACEI seem to be becoming the ''agents of choice.''