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Proteins in the urine are classically associated with renal disease. In the past, it was considered to be the result of renal damage, in particular a filtration defect. Later, the concept of proteinuria being a marker, a mediator, or even a cause of renal damage was entertained. Apart from the pathophysiology, proteinuria can be used as a marker for therapeutic efficacy as far as renal protection is concerned, particularly in patients with diabetes. Recently, albuminuria has gained considerable interest outside the arena of nephrology or “diabetology.” Epidemiologists and cardiologists found that proteinuria, from high levels to even very small quantities of urinary albumin, are a very sensitive risk marker for cardiovascular (CV) disease. This supposedly “reno-cardiovascular interaction” has been the topic of many studies that have tried to unravel the mechanism by which urinary (renal?) albumin loss can predict CV disease. As such, albuminuria has to compete with existing CV risk markers such as hypertension, cholesterol, smoking, etc. More important, albuminuria competes with other new biochemical CV risk markers such as C-reactive protein and atrial or brain natriuretic peptide or even with renal filtration markers such as creatinine or cystatin-C. This issue’s Frontiers in Nephrology deals with the evidence of albuminuria’s being an important CV risk marker and possibly a