Dihydropiridine CCBs like amlodipine and cilnidipine decrease proteinuria or have neutral effects instead of increasing it.
It is hypothesized that the nonDHP CCB, diltiazem CD reduces glomerular membrane permeability to high molecular weight species compared to the DHP CCB, nifedipine. Hence, the nonDHP CCB will reduce proteinuria. This change in membrane permeability is assessed by changes in glomerular size and charge selectivity.
There´s another point of view no clashing with the hypothesis of Solanke above: dihydropiridines like nifedipine, nitrendipine,anlodipine, manidipine, clinidipine, lercanidipine and others cause vasodilation only in gromerular afferent artery whilst the non-dihydropiridines (diltiazem, verapamil) make the same in afferent and efferent artery improving glomerular function and diminishes proteinuria
If there is a significant BP reduction with a dihydropyridine CCB (DPCCB), then there can be a significant reduction in albuminuria- as in a European systolic hypertension study from >15 yrs ago with nitrendipine). Most studies do not show that though (see a review in Kid Int 2004;65:1-12). Another factor that has been demonstrated with non-DPCCBs is a reduction in GBM permeability. Ultimately though the outcome studies have not shown benefit in reducing ESRD with CCBs, although mostly done with DPCCB, and hence they are not recommended to be used without an ACEI or ARB being co-administered at the maximum anti-hypertensive dose.
I recommend this paper which discusses different actions of calcium channel blockers in the vascular bed and can point out the differences
Article Dihydropyridine calcium channel blockers in the elderly with...
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