Antihypertensive therapy remains the most effective strategy for slowing the progression of chronic kidney disease (CKD). However, in proteinuric nephropathies, calcium channel blockers (CCBs) are less effective than other antihypertensives unless normotension is achieved. This is because the glomerular capillaries, rather than larger vessels, are the primary site of hypertensive injury in proteinuric nephropathies. CCBs impair renal autoregulation, which protects glomerular capillaries against the transmission of systemic pressures. CCBs’ renoprotective inferiority in the comparator group likely accounts for the greater renoprotection observed with renin-angiotensin system blockade rather than blood pressure (BP)-independent renoprotective superiority. Nevertheless, CKD patients are at greater absolute risk for cardiovascular events rather than end-stage renal disease. Therefore, if the needed BP reductions cannot be achieved with other agents, it may be appropriate to use CCBs because of their antihypertensive effectiveness, provided care is taken to ensure normotension and to closely monitor proteinuria and renal disease progression.