The central hypothesis of this project is that Aliskiren causes a substantial decrease in MSNA in hypertensive patients with CKD.

Cardiovascular (CV) morbidity and mortality are frequently occurring problems in chronic kidney disease (CKD) patients. Apart from the so called traditional risk factors, also risk factors more or less specific to CKD contribute in the pathogenesis of these problems. There is strong evidence that the sympathetic hyperactivity, which often characterizes CKD, is one such factor. Previously, we have shown that angiotensin converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARB) reduce but not normalize this sympathetic hyperactivity. We re-analysed the cohort of patients who were investigated in the past and subsequently treated according to present guidelines. The results show that, despite of treatment, the unfavourable relation between sympathetic hyperactivity and clinical outcome still exits. This might mean that treatment is insufficient. In present study, we want to study the effect of Aliskiren 300mg on sympathetic nerve activity.

Inclusion Criteria:

• Patients with stable chronic kidney disease and hypertension: i.e. using antihypertensive drugs and/or blood pressure > 145/90 mmHg when off medication.
• Patients on ACE inhibitor or ARB

Exclusion Criteria:

• Patients with diabetes mellitus
• Patients on renal replacement therapy
• Pregnant patients Using of antihypertensive which cannot be stopped
• Patients on immunosuppressive therapy and active nephrotic syndrome