Microalbuminuria is defined as abnormally elevated urinary albumin excretion below the level of clinical albuminuria (albustix). This represents a urinary albumin excretion rate of 20-200 micrograms/min, equal to 30-300 mg/24 h. Urinary albumin excretion can vary as much as 40% with natural fluctuations, and so several tests should be done. Inexpensive radioimmunoassay, enzyme-linked immunosorbent assays or immunoturbidimetric assays are now routine in many clinical laboratories. The prevalence of microalbuminuria in essential hypertension and diabetes is about the same: 25% (range 14-31) and 20% (9-27), respectively. Increased transglomerular passage is the major mechanism of microalbuminuria in both the above-mentioned conditions; increased hydraulic glomerular capillary pressure and glomerular lesions probably both contribute. Microalbuminuria is highly predictive of the development of diabetic nephropathy but the predictive power in relation to hypertensive nephropathy remains to be established. However, in both conditions microalbuminuria is associated with an increased risk of retinopathy, left ventricular hypertrophy, fatal and non-fatal cardiovascular disease and all-cause mortality. The following mechanisms have been suggested as a link between microalbuminuria and these findings: endothelial dysfunction, insulin resistance, hyperinsulinemia, dyslipoproteinemia and a procoagulant state. Blood pressure lowering reduces microalbuminuria in essential hypertension and in diabetes mellitus. Long-term studies in diabetes suggest that angiotensin converting enzyme inhibitors postpone, and may even prevent, progression to overt clinical nephropathy in normotensive diabetic patients with persistent microalbuminuria. So far, there have been no long-term comparative trials on the beneficial effects of different antihypertensive drugs in hypertensive patients with microalbuminuria.