title: Addition of aliskiren to olmesartan ameliorates tubular injury in chronic kidney disease patients partly by reducing proteinuria.
abstract: BACKGROUND
  Tubular injury is more important than glomerulopathy for renal prognosis in chronic kidney disease (CKD) patients. Numerous studies have demonstrated the active participation of the renin-angiotensin system (RAS) in CKD. However, whether addition of aliskiren, a direct renin inhibitor, to olmesartan improves renal tubular injury in CKD patients is unknown.
  
  
  METHODS
  This study compared the effects of aliskiren (300 mg daily), olmesartan (40 mg daily), and its combination therapy on urinary L-fatty acid binding protein (L-FABP), a marker of tubular injury in stage I or II CKD patients. It also examined which clinical variables were independently correlated with tubular damage.
  
  
  RESULTS
  Olmesartan or aliskiren monotherapy for 6 months comparably decreased blood pressure (BP) and proteinuria. BP and proteinuria levels were reduced more by combination therapy than by either monotherapy. Olmesartan or aliskiren decreased urinary L-FABP level, and combination therapy produced more incremental reduction in L-FABP level relative to each monotherapy. Multiple stepwise regression analysis revealed that BMI, low-density lipoprotein (LDL)-cholesterol and proteinuria were independently related to urinary L-FABP level.
  
  
  CONCLUSIONS
  The present study demonstrated that addition of aliskiren to olmesartan decreased urinary L-FABP level partly via reduction of proteinuria in stage I or II CKD patients.
authors.affiliation: Division of Nephrology, Department of Internal Medicine, Shinmatsudo Central General Hospital, Chiba, Japan.
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Nakamura
authors.forename: Eiichi
authors.initials: E
authors.lastname: Sato
authors.forename: Mayuko
authors.initials: M
authors.lastname: Amaha
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Kawagoe
authors.forename: Sayaka
authors.initials: S
authors.lastname: Maeda
authors.forename: Sho-ichi
authors.initials: S
authors.lastname: Yamagishi
mesh_terms: D000328:Adult; D000577:Amides / Q000494:pharmacology / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D004359:Drug Therapy, Combination; D050556:Fatty Acid-Binding Proteins / Q000652:urine; D005260:Female; D005650:Fumarates / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology / Q000627:therapeutic use*; D007676:Kidney Failure, Chronic / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control*; D007684:Kidney Tubules / Q000187:drug effects / Q000473:pathology*; D008297:Male; D011507:Proteinuria / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control*; D012044:Regression Analysis; D013777:Tetrazoles / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D000577:Amides; D000959:Antihypertensive Agents; D050556:Fatty Acid-Binding Proteins; D005650:Fumarates; D007093:Imidazoles; D013777:Tetrazoles; C446481:aliskiren; C437965:olmesartan