Premature cardiovascular disease is the leading cause of morbidity and mortality in patients with end-stage renal failure. Natriuretic peptides, specifically brain natriuretic peptide, are released from the heart in response to chamber distension and thus increased in the presence of volume expansion and cardiac overload. Their physiological role is to cause vasodilatation and promote natriuresis to maintain volume homeostasis. Increasingly serum levels of brain natriuretic peptide are used to both diagnose and manage cardiovascular disorders. Furthermore, augmenting the beneficial hemodynamic actions of brain natriuretic peptide may have a therapeutic role in decompensated heart failure. However, the diagnostic role of serum brain natriuretic peptide levels in patients with advanced renal dysfunction remains to be defined. These patients have a high prevalence of left ventricular disorders, specifically left ventricular hypertrophy, which may reduce the diagnostic utility of brain natriuretic peptide. In addition, ventricular stretch may be determined by intravascular volume status rather than by cardiac dysfunction. Nonetheless, as the prognosis of patients with end-stage renal failure and co-existing heart failure is so poor, the availability of a further marker of cardiac ''distress'' may in the future become a useful diagnostic tool and in due course may become a primary goal for titration and tailoring of therapy.