title: Impact of serum uric acid on renal function and cardiovascular events in hypertensive patients treated with losartan.
abstract: High serum uric acid level (SUA) and chronic kidney disease (CKD) are risk factors for cardiovascular events (CVEs). However, their interactions as cardiovascular risk factors remain unknown. This subanalysis of the Japan Hypertension Evaluation with Angiotensin II Antagonist Losartan Therapy (J-HEALTH) study included 7629 patients, in whom the serum creatinine level was measured at least twice. The study examined the impact of hyperuricemia (SUA ≥7 mg dl(-1)) on CVE according to the level of renal dysfunction and whether early changes in SUA predicted future glomerular filtration rates (GFRs). The mean follow-up period was 3.1 years. The patients were divided into three groups according to the baseline estimated GFR (eGFR): groups A, B and C with eGFR <45, 45-59 and ≥60 ml min(-1) per 1.73 m(2), respectively. eGFR increased from 38.1 to 57.6, from 52.8 to 67.5 and from 74.7 to 80.7 ml min(-1) per 1.73 m(2) in groups A, B and C, respectively. In non-hyperuricemic patients, the CVE rate was 10.83, 4.98 and 4.21/1000 person-years in groups A, B and C, respectively, while in hyperuricemic patients, the corresponding values were 14.18, 17.02 and 5.93. Thus, hyperuricemia increased the risk of CVE only in group B (relative risk (RR) 3.43 (95% confidence interval (CI) 1.55 to 7.60); P<0.002). The final change in the eGFR was negatively correlated with the change in SUA from baseline to year 1 (P<0.001). CVEs were more frequent in those with a decrease in eGFR. Hyperuricemia may be a major determinant of increased cardiovascular risk in CKD stage 3A, and SUA may be involved in the progression of CKD. Changes in the GFR influence the rate of CVE.
authors.affiliation: Department of Medicine, Division of Nephrology, Tohoku University School of Medicine, Endocrinology and Vascular Medicine, Aoba-ku, Sendai, Japan. ishisho@med.tohoku.ac.jp
authors.forename: Sadayoshi
authors.initials: S
authors.lastname: Ito
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Naritomi
authors.forename: Toshio
authors.initials: T
authors.lastname: Ogihara
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Shimada
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Shimamoto
authors.forename: Heizo
authors.initials: H
authors.lastname: Tanaka
authors.forename: Nobuo
authors.initials: N
authors.lastname: Yoshiike
mesh_terms: D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000009:adverse effects / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D002319:Cardiovascular System / Q000187:drug effects*; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology*; D007668:Kidney / Q000187:drug effects*; D007677:Kidney Function Tests; D016014:Linear Models; D019808:Losartan / Q000009:adverse effects / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011507:Proteinuria / Q000378:metabolism; D014527:Uric Acid / Q000097:blood*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; D014527:Uric Acid; D019808:Losartan