title: Valsartan reduces serum cystatin C and the renal vascular resistance in patients with essential hypertension.
abstract: A high level of albuminuria and increased renal vascular resistance are associated with hypertensive renal damage. In this study, the authors investigated the effect of the angiotensin II receptor blocker, valsartan, on renal function and intrarenal hemodynamics in non-diabetic patients with essential hypertension. A prospective three-month study of the effects of valsartan, 40-80 mg/day, was performed in 30 hypertensive patients. As an assessment of renal function, serum creatinine, urine albumin/creatinine (Alb/Cr) ratio, and serum cystatin C levels were evaluated. Doppler ultrasonography of the kidney was performed for the evaluation of renal hemodynamics. Peak-systolic, end-diastolic, and mean velocities of interlobar arteries were evaluated, and the pulsatility index (PI) and resistive index (RI) were calculated. It was determined that patients with microalbuminuria had higher levels of serum cystatin C, PI, and RI compared to patients without microalbuminuria. Valsartan treatment significantly reduced systolic and diastolic blood pressure and decreased the Alb/Cr ratio. Serum creatinine was not changed, whereas serum cystatin C levels were significantly reduced. Valsartan treatment significantly decreased the PI in all patients and both PI and RI in patients with microalbuminuria. These results suggest that the angiotensin II receptor blocker, valsartan, is able to improve renal function by reducing renal vascular resistance in hypertensive patients, especially in patients with microalbuminuria, and may prevent future renal failure in patients with essential hypertension.
authors.affiliation: The Second Department of Internal Medicine, Ehime University School of Medicine, Toon City, Ehime, Japan.
authors.forename: Sanae
authors.initials: S
authors.lastname: Watanabe
authors.forename: Takafumi
authors.initials: T
authors.lastname: Okura
authors.forename: Mie
authors.initials: M
authors.lastname: Kurata
authors.forename: Jun
authors.initials: J
authors.lastname: Irita
authors.forename: Seiko
authors.initials: S
authors.lastname: Manabe
authors.forename: Ken-Ichi
authors.initials: K
authors.lastname: Miyoshi
authors.forename: Tomikazu
authors.initials: T
authors.lastname: Fukuoka
authors.forename: Akiko
authors.initials: A
authors.lastname: Gotoh
authors.forename: Kazuo
authors.initials: K
authors.lastname: Uchida
authors.forename: Jitsuo
authors.initials: J
authors.lastname: Higaki
mesh_terms: D000328:Adult; D000368:Aged; D000419:Albuminuria / Q000188:drug therapy; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood / Q000652:urine; D001783:Blood Flow Velocity / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D003404:Creatinine / Q000097:blood / Q000652:urine; D055316:Cystatin C; D015891:Cystatins / Q000097:blood*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D007564:Japan; D007668:Kidney / Q000098:blood supply / Q000000981:diagnostic imaging / Q000378:metabolism; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011673:Pulsatile Flow / Q000187:drug effects; D012079:Renal Circulation / Q000187:drug effects*; D013777:Tetrazoles / Q000037:antagonists & inhibitors / Q000627:therapeutic use*; D016896:Treatment Outcome; D018608:Ultrasonography, Doppler; D014633:Valine / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors / Q000627:therapeutic use; D000068756:Valsartan; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; D015415:Biomarkers; C525030:CST3 protein, human; D055316:Cystatin C; D015891:Cystatins; D013777:Tetrazoles; D000068756:Valsartan; D003404:Creatinine; D014633:Valine