THE IMPORTANCE OF MICROALBUMINURIA AS AN INDICATOR OF INCIPIENT DIABETIC NEPHROPATHY - THERAPEUTIC IMPLICATIONS

Nephropathy is the major life-threatening complication of insulin-depe ndent diabetes mellitus (IDDM). The clinical syndrome is characterized by persistent albuminuria (greater than 300 mg day), a rise in arteri al blood pressure, and a relentless decline in glomerular filtration r ate leading to end-stage renal failure. The availability of a radioimm unoassay for detecting albumin in low concentrations in urine has allo wed the study of urinary albumin excretion rates in diabetics well bef ore clinically persistent proteinuria develops. An albumin excretion r ate greater than that in normal subjects and lower than that in macroa lbuminuric subjects is called microalbuminuria (range 20-200 mu g/min or 30-300 mg/24 h). Although recent studies have challenged the predic tive value of microalbuminuria for later development of overt diabetic nephropathy, albumin excretion rate in the microalbuminuric range and its tracking (i.e. annual increase) are still considered reliable mar kers for prediction of later overt diabetic kidney disease. Overnight urinary collection is preferred for calculation of the rate of albumin excretion, but may be difficult to perform precisely. The albumin:cre atinine ratio of the first morning urine sample is a reliable screenin g method: the microalbuminuric range is considered to be 2.5-25 mg/mmo l or 30-300 mg/g (3.5 mg/mol has been proposed as lower limit in femal es because of their lower creatinine excretion). Irrespective of the p rocedure used, at least two samples over a 3-6-month period should tes t positive before microalbuminuria is confirmed and 'persistent microa lbuminuria' defined. If the albumin excretion rate is persistently in the microalbuminuric range it is of crucial importance to define strat egies and carry out interventions for prevention of decline in kidney function. The goal of achieving the best glycaemic control as early as possible in as many IDDM patients as is safely possible is particular ly important in microalbuminuric patients. Although it is unsafe to re duce dietary protein intake drastically, particularly in children and adolescents, moderate decrease of protein intake (i.e. 0.9-1.1/g/kg da y) is advisable in diabetic patients from the very beginning of the di sease. Timely treatment with an angiotensin-converting enzyme inhibito r, independently of rise in arterial blood pressure, should be conside red if improvement of glycaemic control and moderate decrease of dieta ry protein intake for 6-12 months have failed to reduce the albumin ex cretion rate. Screening programmes for microalbuminuria and early inte rvention can substantially modify the natural history of diabetic rena l involvement and disease and possibly reduce the incidence of end-sta ge renal failure.