Abstract. Data from recent clinical trials show that lowering of BP reduces the rate of renal function loss in chronic renal disease. There is evidence supporting the assertion that BP lowering obtained by intervention in the renin-angiotensinaldosterone system (RAAS) has an additive renoprotective effect in both diabetic and nondiabetic renal diseases. However, to dissociate BP-dependent and non-BP-dependent action of RAAS blockade, the relevant trials are in many cases flawed by design, resulting in BP differences between the comparative antihypertensive strategies. This review discusses whether the relevant literature allows for the conclusion that RAAS intervention has renoprotective effects in addition to its effects on BP. In particular, the main evidence for a specific renoprotective action of RAAS blockade is provided by its consistent antiproteinuric action, which cannot completely be attributed to the reduction in BP. Indeed, other strategies that lower proteinuria without having an antihypertensive effect, such as lowering dietary protein intake or the use of nonsteroidal antiinflammatory drugs, appear to have a renoprotective effect as well. Interestingly, a consistent finding across different intervention studies is that the more proteinuria is reduced the better the kidney appears to be protected. Therefore, it is concluded that agent-characteristics of RAAS intervention (i.e., antiproteinuric properties) independently influence renal function loss in addition to its BP-lowering effect. Future studies should further explore the renoprotective benefit of non-antihypertensive intervention measures, alone and in combination with antihypertensive strategies.Antihypertensive therapy has always been the cornerstone of renoprotective intervention. Recent large trials particularly indicate that intervention in the renin-angiotensin-aldosterone system (RAAS) appears to be effective in retarding the decline of renal function loss in both diabetic and nondiabetic renal diseases. In nondiabetic patients, the AIPRI (1) and REIN (2) studies showed that angiotensin-converting enzyme (ACE) inhibitors delay the progression of renal function loss. Lewis et al. (3) showed a renoprotective effect of ACE inhibitors in type 1 diabetic patients. Moreover, two recent studies, RENAAL (4) and IDNT (5), demonstrated angiotensin-II (AngII)-receptor (type 1) antagonists to be renoprotective in type 2 diabetics.The above-mentioned trials, comprising thousands of patients, can be taken as impressive evidence for RAAS intervention to be superior to other treatment strategies. However, whether the effects of RAAS intervention are due to the specific pharmacologic RAAS blockade as such or due to their antihypertensive potency is a crucial question. This issue is still open, because in many of the above trials, the obtained BP levels were lower in the patients treated with an agent that intervenes in the RAAS compared with the control groups. The current review focuses on this particular question, that is, is renoprotection obtain...