title: Azelnidipine reduces urinary protein excretion and urinary liver-type fatty acid binding protein in patients with hypertensive chronic kidney disease.
abstract: BACKGROUND
  Hypoxia plays a significant role in the pathogenesis and progression of chronic renal disease. Urinary liver-type fatty acid binding protein (L-FABP) levels reflect the clinical prognosis of chronic renal disease. The calcium channel blocker azelnidipine has anti-oxidative properties and these may contribute to the beneficial effects of this drug. The aim of the present study was to determine whether azelnidipine and/or amlodipine affected urinary protein excretion or the urinary levels of 8-OHdG and L-FABP in hypertensive patients with mild chronic kidney disease (CKD).
  
  
  METHODS
  Thirty moderately hypertensive chronic kidney disease patients were randomly assigned to 2 treatment groups: azelnidipine 16 mg once daily or amlodipine 5 mg once daily. Treatment was continued for 6 months. Urinary protein excretion and urinary levels of 8-OHdG and urinary L-FABP were measured before 3 and 6 months after the treatment period.
  
  
  RESULTS
  Both drugs exhibited comparable and significant effects on the systolic and diastolic blood pressure. Azelnidipine decreased heart rate significantly after 3 and 6 months whereas amlodipine increased it significantly after 3 and 6 months. Urinary protein excretion, urinary 8-OHdG and urinary L-FABP levels decreased significantly after 3 months (p < 0.05) and 6 months (p < 0.05) in the azelnidipine group. In contrast, amlodipine showed little effect on urinary protein excretion or the urinary levels of 8-OHdG and L-FABP throughout the experimental period.
  
  
  CONCLUSIONS
  Azelnidipine is renoprotective in hypertensive patients with mild CKD and this action is, at least in part, due to the anti-oxidative effect.
authors.affiliation: Department of Internal Medicine, Shinmatsudo Central General Hospital, Chiba, Japan.
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Nakamura
authors.forename: Takeshi
authors.initials: T
authors.lastname: Sugaya
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Kawagoe
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Suzuki
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Ueda
authors.forename: Hikaru
authors.initials: H
authors.lastname: Koide
authors.forename: Teruo
authors.initials: T
authors.lastname: Inoue
authors.forename: Koichi
authors.initials: K
authors.lastname: Node
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000328:Adult; D017311:Amlodipine / Q000494:pharmacology / Q000627:therapeutic use; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D001383:Azetidinecarboxylic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use*; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000652:urine; D004095:Dihydropyridines / Q000494:pharmacology / Q000627:therapeutic use*; D050556:Fatty Acid-Binding Proteins / Q000652:urine*; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000652:urine; D007676:Kidney Failure, Chronic / Q000188:drug therapy / Q000209:etiology / Q000652:urine; D008297:Male; D008875:Middle Aged; D011507:Proteinuria / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D002121:Calcium Channel Blockers; D004095:Dihydropyridines; D050556:Fatty Acid-Binding Proteins; D017311:Amlodipine; D001383:Azetidinecarboxylic Acid; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine; C061679:azelnidipine