Although end-stage renal disease (ESRD) currently affects only a small percentage (<0.2%) of the US population, its precursor, the mild and moderate forms of chronic kidney disease (CKD), affects 11% of the population, with significant growth in both ESRD and CKD anticipated in the rapidly aging US population. The primary diagnoses in the majority of ESRD patients are diabetes and hypertension. Results of clinical studies demonstrate that the level of proteinuria and sympathetic activation contribute to the progression of CKD to ESRD. There are sufficient clinical data to demonstrate that the dihydropyridine calcium channel blocker (DHP CCB) class of antihypertensives such as amlodipine and nifedipine, although effective in reducing systemic hypertension, lack activity in reducing proteinuria or attenuating sympathetic activity. Experimental studies and a limited number of clinical studies suggest that non-DHP CCBs, including verapamil and diltiazem, have a mechanism of action that differs from DHP CCBs. Non-DHP CCBs could potentially attenuate sympathetic activity and reduce protein excretion in patients with CKD.