title: Benazepril slows progression of renal dysfunction in patients with non-diabetic renal disease.
abstract: OBJECTIVE
  The present study examined the effects of benazepril, an angiotensin-converting enzyme inhibitor, on the progression of renal insufficiency in patients with non-diabetic renal disease.
  
  
  METHODS
  Fifteen patients with non-diabetic renal disease whose serum creatinine (Cr) ranged from 1.5 to 3.0 mg/dL were given either benazepril (2.5-5 mg) or placebo once daily for 1 year in a random crossover manner. In both periods, antihypertensive medications were increased if blood pressure was greater than 130/85 mmHg. Blood sampling and urinalysis were performed bimonthly throughout the study period.
  
  
  RESULTS
  Blood pressure was similar when comparing the benazepril and the placebo periods (128+/-12/83+/-6 vs 129+/-10/83+/-7 mmHg). Serum Cr significantly increased from 1.62+/-0.18 to 1.72+/-0.30 mg/dL (P=0.036) during the placebo period, while there was no statistically significant increase in serum Cr during the benazepril period (from 1.67+/-0.17 to 1.71+/-0.27 mg/dL). The slope of decrease of the reciprocal of serum Cr was steeper in the placebo period than in the benazepril period (-0.073+/-0.067 vs-0.025+/-0.096/year, P=0.014). Urinary protein excretion was lower during the benazepril period than during the placebo period (0.57+/-0.60 vs 1.00+/-0.85 g/gCr, P=0.006). Serum K was significantly higher in the benazepril period than in the placebo period (4.4+/-0.5 vs 4.2+/-0.5 mEq/L, P<0.001), but no patient discontinued benazepril therapy as a result of hyperkalemia.
  
  
  CONCLUSIONS
  Long-term benazepril treatment decreased the progression of renal dysfunction in patients with non-diabetic renal disease by a mechanism that is independent of blood pressure reduction.
authors.affiliation: Department of Hypertension and Cardiorenal Medicine, Dokkyo Medical University, Mibu, Tochigi, Japan. isimitu@dokkyomed.ac.jp
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Ishimitsu
authors.forename: Akira
authors.initials: A
authors.lastname: Akashiba
authors.forename: Tomoko
authors.initials: T
authors.lastname: Kameda
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Takahashi
authors.forename: Satoshi
authors.initials: S
authors.lastname: Ohta
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Yoshii
authors.forename: Junichi
authors.initials: J
authors.lastname: Minami
authors.forename: Hidehiko
authors.initials: H
authors.lastname: Ono
authors.forename: Atsushi
authors.initials: A
authors.lastname: Numabe
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Matsuoka
mesh_terms: D000328:Adult; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D001552:Benzazepines / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D003401:Creatine / Q000097:blood; D018592:Cross-Over Studies; D005260:Female; D006801:Humans; D007668:Kidney / Q000187:drug effects* / Q000502:physiology; D007674:Kidney Diseases / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011507:Proteinuria / Q000652:urine; D051437:Renal Insufficiency / Q000517:prevention & control*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D001552:Benzazepines; D003401:Creatine; C044946:benazepril