Comparative effects of benidipine and amlodipine on proteinuria, urinary 8-OHdG, urinary L-FABP, and inflammatory and atherosclerosis markers in early-stage chronic kidney disease.
BACKGROUND
We examined the effects of 2 calcium channel blockers, benidipine (T-, L-, and N-type) and amlodipine (L- and N-type), on renal, inflammatory, oxidative, and atherosclerosis markers in hypertensive patients with mild chronic kidney disease (CKD).


METHODS
Forty hypertensive patients with CKD were assigned randomly to either of the 2 treatments: 8 mg benidipine once daily (n = 20, group A) or 5 mg amlodipine once daily (n = 20, group B). Treatment was continued for 12 months. Blood pressure, serum creatinine, estimated glomerular filtration rate, urinary protein excretion, urinary liver-type fatty acid-binding protein, interleukin-6, high mobility group box-1 protein, urinary 8-hydroxy-2'-deoxyguanosine, pulse wave velocity, intima-media thickness, and blood asymmetric dimethylarginine were monitored.


RESULTS
Blood pressure decreased equally in both groups (P < 0.001, at 6 and 12 months versus before treatment). Serum creatinine and estimated glomerular filtration rate changed little during the experimental period in each group. However, urinary protein excretion (P < 0.001), urinary liver-type fatty acid-binding protein (P < 0.001), urinary 8-hydroxy-2'-deoxyguanosine (P < 0.001), blood interleukin-6 (P < 0.001), blood high mobility group box-1 (P < 0.05), and pulse wave velocity (P < 0.01) decreased more in group A than in group B with 12 months of treatment. The percent reductions in intima-media thickness and blood asymmetric dimethylarginine were significantly greater in group A than in group B (P < 0.001).


CONCLUSIONS
Benidipine is more effective than amlodipine for protecting renal function and potentially for ameliorating atherosclerosis in hypertensive patients with mild CKD. T-type calcium channel blockers may be effective in patients with CKD.
Nakamura
Tsukasa
T
Department of Medicine, Shinmatsudo Central General Hospital, Chiba, Japan.
Sato
Eiichi
E
Fujiwara
Nobuharu
N
Kawagoe
Yasuhiro
Y
Ueda
Yoshihiko
Y
Sugaya
Takeshi
T
Yamagishi
Shoichi
S
Yamada
Shingo
S
Koide
Hikaru
H
D000080242:8-Hydroxy-2'-Deoxyguanosine; D000328:Adult; D017311:Amlodipine / Q000494:pharmacology*; D050197:Atherosclerosis / Q000378:metabolism; D015415:Biomarkers; D002121:Calcium Channel Blockers / Q000494:pharmacology; D003849:Deoxyguanosine / Q000031:analogs & derivatives* / Q000652:urine; D004095:Dihydropyridines / Q000494:pharmacology*; D050556:Fatty Acid-Binding Proteins / Q000652:urine*; D005260:Female; D006801:Humans; D007249:Inflammation; D007676:Kidney Failure, Chronic / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism*; D008297:Male; D011507:Proteinuria
D015415:Biomarkers; D002121:Calcium Channel Blockers; D004095:Dihydropyridines; C493319:FABP1 protein, human; D050556:Fatty Acid-Binding Proteins; D017311:Amlodipine; C061004:benidipine; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine