The NIH funded SPRINT trial currently recruiting patients in the US may clarify this issue. It will randomize over 7500 patients with systolic BP to targets of o140mmHg or o120mmHg, deliberately including approximately 1750 patients over 75, and followed for cardiovascular, cognitive and kidney end points over a period of 9 years, commencing 2010.171,172 8.3: SHOULD A REDUCTION IN ALBUMINURIA BE A TARGET FOR TREATMENT WITH AGENTS THAT MODIFY BP? As outlined elsewhere in this Guideline, RAAS intervention is effective in not only lowering BP but also protecting individual patients with CKD from further decline in kidney function. Although the BP-lowering effect of RAAS inhibi- tion contributes to renoprotection, a component of the protective effect may be independent of the effect on BP. Thus, to achieve maximum renoprotection using a RAAS inhibitor, the clinician might consider monitoring the reduction in urine albumin excretion (an off target effect). This is particularly important in macroalbuminuric and microalbuminuric hypertensive subjects with type 2 diabetes, in whom the BP response to RAAS inhibitors may be discordant with the anti-albuminuric response.414,415 Studies in such patients indicate that those in whom urine albumin was lowered without significant lowering of BP gained some renoprotection, whereas patients who did not have urine albumin lowered in spite of BP-lowering did not have Thus, albuminuria may be an independent factor in renoprotection. In a prospective study supporting this concept, Hou et al.416 detected nearly 50% additional renoprotection with a dose of a RAAS inhibitor titrated to maximally reduce urine albumin levels as compared to a standard dose used for the BP lowering effect. There have been no RCTs assessing hard renal or cardio- vascular outcomes, in which patients have been randomized to different targets of urinary albumin excretion irrespective of BP. 8.4: SHOULD RAAS INHIBITION BE MAXIMIZED IN CKD PATIENTS? 