title: Serum uric acid levels and renal damage in hyperuricemic hypertensive patients treated with renin-angiotensin system blockers.
abstract: BACKGROUND
  A correlation between hyperuricemia and renal target organ damage (TOD) was shown in hypertensive patients, locally mediated by the activation of renin-angiotensin system (RAS). We investigated whether high serum uric acid (UA) levels could negatively affect tubulointerstitial damage in hyperuricemic essential hypertensive patients with normal renal function, on treatment with RAS-blocking drugs.
  
  
  METHODS
  We studied 40 patients with World Health Organization stage I-II essential hypertension, 9 with high serum UA levels (hyperuricemic group) and 31 with normal serum UA levels (normouricemic group, either normouricemics, n = 15, or formerly hyperuricemics in chronic allopurinol treatment, n = 16). All patients were on RAS-blocking drugs (either angiotensin-converting enzyme inhibitors or angiotensin II receptors blockers). Evaluation of renal TOD included urinary albumin excretion (UAE), Doppler ultrasound renal resistive index (RRI) and renal volume-to-resistive index ratio (RV/RRI) measurements.
  
  
  RESULTS
  Hyperuricemics had significantly higher RRI and lower RV/RRI values than normouricemics. Creatinine clearance and UAE were similar between groups. Linear regression analysis showed that RV/RRI values were inversely related to serum UA levels (r = -0.57, P < 0.01). The logistic regression analysis selected serum UA as an independent predictor of decreased RV/RRI (odds ratio 4.45, 95% CI 1.47-13.45, P = 0.01).
  
  
  CONCLUSIONS
  In hyperuricemic hypertensives normal serum UA levels are associated with normal RV/RRI, integrated marker of tubulointerstitial damage and renal arteriolopathy, independently of RAS activation.
authors.affiliation: Department of Medical and Surgical Critical Care, University of Florence, Florence, Italy. berniandrea@inwind.it
authors.forename: Andrea
authors.initials: A
authors.lastname: Berni
authors.forename: Maria
authors.initials: M
authors.lastname: Boddi
authors.forename: Elisa Bissoni
authors.initials: EB
authors.lastname: Fattori
authors.forename: Ilaria
authors.initials: I
authors.lastname: Cecioni
authors.forename: Sabino
authors.initials: S
authors.lastname: Berardino
authors.forename: Francesca
authors.initials: F
authors.lastname: Montuschi
authors.forename: Marco
authors.initials: M
authors.lastname: Chiostri
authors.forename: Loredana
authors.initials: L
authors.lastname: Poggesi
mesh_terms: D000328:Adult; D000368:Aged; D000493:Allopurinol / Q000494:pharmacology; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D033461:Hyperuricemia / Q000097:blood / Q000150:complications* / Q000188:drug therapy; D007668:Kidney / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D012084:Renin-Angiotensin System / Q000187:drug effects*; D014527:Uric Acid / Q000097:blood
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D014527:Uric Acid; D000493:Allopurinol