The level of albuminuria in CKD predicts not only the prognosis with respect to kidney function but also morbidity and mortality from CVD events including Urinary albumin excretion is influenced by BP and by many of the agents used to reduce BP, particularly ACE-Is and ARBs. The concept of using albuminuria as a surrogate marker for CKD progression and CVD outcomes is widely accepted, with the reduction of urine albumin levels often being regarded as a target for therapy. This would mean that treatment would be escalated to reduce albuminuria to a preferred level, regardless of BP. Treating to an albumin target usually involves an escalation of RAAS blockade, which can be achieved by restricting dietary salt intake, increasing doses of an ACE-I or an ARB, combining the two classes of medication, or by adding a thiazide diuretic, an aldosterone- receptor blocker or a direct renin inhibitor (DRI). While a strong case has been made for targeting a reduction of albuminuria, particularly with agents that interfere with the RAAS, there have been no large studies in CKD patients reporting long term differences in GFR or CVD outcomes where reduction in urinary albumin levels (regardless of BP) was the primary objective. There is also uncertainty as to whether the dose of a particular agent that is required to achieve BP control is necessarily the same as the dose required for albuminuria reduction.24 The Work Group thus decided that it was premature to recommend an albuminuria reduction target strategy for all cases of CKD but felt this deserved further discussion in Chapter 8. Cardiovascular outcomes. Recognition that premature CVD is a major cause of death in CKD has led to CVD risk management becoming a recognized component of the care of the CKD patient. 