Urinary excretion of albumin exceeds normal values in 10 to 25% of patients with essential hypertension. The level of albuminuria is highly correlated with arterial pressure, and more closely with ambulatory arterial pressure. The interaction between albuminuria and arterial pressure is enhanced by overweight, smoking, protein intake, insulin resistance, lipid abnormalities, and possibly genotypes of the components of the renin-angiotensin system. The renal mechanisms of microalbuminuria are not well elucidated. Notably, an increase in filtration fraction suggestive of intraglomerular hypertension was observed in patients with hyperfiltration. Microalbuminuria may be a marker of diffuse vascular abnormalities predisposing to cardiovascular disease and/or hypertensive renal disease heralding future renal failure, but its predictive value needs to be tested in more long-term follow-up studies. Antihypertensive treatment has a varied influence on albuminuria; angiotensin-converting enzyme inhibitors may correct this abnormality (at least partially) better than other agents.