Cilnidipine, a dual calcium channel antagonist, is assumed to regulate hypertension via N- and L-type calcium
channel. The N-type calcium channel is associated with sympathetic nerve activation. This effect may improve the glomerular
hemodynamics in the injured nephron, and may mitigate the progression of renal injury. To clarify the effect of cilnidipine
in instances of already existing decreased renal blood flow, we examined the alteration of renal hemodynamics
before and after cilnidipine therapy in patients with advanced chronic kidney disease (CKD). Cilnidipine was administrated
daily to 17 CKD patients with hypertension for 12 months. Another 16 patients were similarly administered amlodipine
during this study, a long-acting L-type calcium channel antagonist has also been shown to be renoprotective.
Glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and protein excretion in 24-hour accumulated urine
were measured at the start and end of the study. The parameters of renal hemodynamics were calculated by Gomez’s estimation
equation. Systolic blood pressure decreased to 80 % of the level at the beginning of the study, and ERPF increased
to 127 % of the level at baseline. Glomerular capillary pressure on single nephron was reduced to 90 %, although
total GFR decreased within the non-statistical change. Especially, renal vascular resistance ratio (RA/RE) on single nephron
improved to 120 %. Cilnidipine improves ERPF and glomerular hypertension without worsening total renal function.
N- and L-type calcium channel antagonist is effective and safe for patients with advanced CKD as a result of improvement
of glomerular capillary resistance.