Calcium channel blockers and the kidney
- the primary diagnoses in the majority of end-stage renal disease (ESRD) patients are diabetes and hypertension
- results of clinical studies demonstrate that the level of proteinuria and sympathetic activation contribute to the progression of chronic kidney disease (CKD) to ESRD
- clinical data to demonstrate that the dihydropyridine calcium channel blocker (DHP CCB) class of anti-hypertensives 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
- studies suggest that CCB do not worsen the progression of renal disease but may rather provide benefit when systemic BP has been tightly normalised
- non-dihydropyridine calcium channel blockers (NDHP), diltiazem and verapamil, slow the progression of type 2 diabetic nephropathy with overt proteinuria almost to a similar extent as observed with ACE-I (2)
- CCB may have an advantage in combination with ACE-I and/or ARB (2)
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