Hypertension is 2-3 times more prevalent in CKD as compared to the general population. Enhancement of renal sympathetic nerve activity during renal ischemia and norepinephrine overflow from the kidney after reperfusion are responsible for the development of ischemic acute kidney injury. Angiotensin receptor antagonists and Angiotensin -converting enzyme inhibitors are unable to normalize sympathetic hyperactivity in patients with hypertensive chronic renal failure in spite of lowering blood pressure. Moxonidine is considered to differ from the other centrally acting sympatholytic drugs. Fifty patients of CKD were enrolled in the moxonidine group and forty nine patients were enrolled in the clonidine group in this open label randomized study. A significant reduction in SBP and DBP was observed in both the treatment groups as compared to baseline. A significant difference between treatment groups was observed. Moxonidine caused a significantly greater reduction of SBP and DBP as compared to clonidine at the end of 3 months. Serum Creatinine was significantly lower after treatment in the moxonidine group as compared to the clonidine group. eGFR after 3 months of treatment was significantly higher in the  moxonidine group. Moxonidine can be a preferred sympatho-inhibitory drug in renal failure patients.

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Vikash Khandelia

Assistant Professor Department of Nephrology,

Government Medical College Kota, Rajasthan, India