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)

Reference:

1. Clin Cornerstone. 2004;6(4):39-52
2. Acta Clin Belg. 2004 Jan-Feb;59(1):44-56