calcium channel blockers and the kidney
Last reviewed 01/2018
- 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 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
- 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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