title: The effects of allopurinol on metabolic acidosis and endothelial functions in chronic kidney disease patients.
abstract: BACKGROUND
  Hyperuricemia and metabolic acidosis have emerged as important risk factors for progression of kidney disease. In this study, we aimed to investigate the effects of allopurinol on metabolic acidosis and endothelial functions in hyperuricemic stage 2-4 chronic kidney disease (CKD) patients.
  
  
  METHODS
  Thirty patients with stage 2-4 CKD and serum uric acid levels over 5.5 mg/dl were included in the study group. They were prescribed 300 mg/day per oral allopurinol treatment for three months. Age- and gender-matched CKD patients (n = 30) with similar clinical characteristics were taken as the control group and were not given allopurinol treatment. Endothelial functions were measured via flow-mediated dilatation (∆FMD %) over the forearm. pH and HCO3 levels in venous blood, Cr clearance and proteinuria levels were calculated in all patients at baseline and in the third month.
  
  
  RESULTS
  Serum uric acid levels significantly decreased in the study group from 7.9 ± 1.6 to 6.4 ± 1.7 (p < 0.001). Cr clearance (from 43.4 ± 20.1 to 51.4 ± 24.9, p = 0.011), serum bicarbonate levels (from 21.4 ± 3.4 to 23.0 ± 3.4, p = 0.007) and ΔFMD % values (from 5.8 ± 2.5 to 6.2 ± 2.7, p = 0.006) increased significantly in the allopurinol group. There were no significant changes except for ∆FMD % values (decreased from 6.27 ± 1.62 to 5.71 ± 1.90, p = 0.005) in the control group. ∆FMD % variations within the two groups were clearly significant in the repeated ANOVA general linear model.
  
  
  CONCLUSIONS
  We assume that decreasing uric acid levels with allopurinol treatment seems to be helpful in restoring endothelial functions, preventing metabolic acidosis and slowing down the progression of CKD.
authors.affiliation: Department of Internal Medicine, Süleyman Demirel University Faculty of Medicine, Isparta, Turkey.
authors.forename: Dilara
authors.initials: D
authors.lastname: Bayram
authors.affiliation: Division of Nephrology, Department of Internal Medicine, Süleyman Demirel University Faculty of Medicine, Cunur, 32200, Isparta, Turkey.
authors.forename: M
authors.initials: M
authors.lastname: Tuğrul Sezer
authors.affiliation: Division of Nephrology, Department of Internal Medicine, Süleyman Demirel University Faculty of Medicine, Cunur, 32200, Isparta, Turkey. salihinal@yahoo.com.
authors.forename: Salih
authors.initials: S
authors.lastname: İnal
authors.affiliation: Division of Nephrology, Department of Internal Medicine, Süleyman Demirel University Faculty of Medicine, Cunur, 32200, Isparta, Turkey.
authors.forename: Atila
authors.initials: A
authors.lastname: Altuntaş
authors.affiliation: Division of Nephrology, Department of Internal Medicine, Süleyman Demirel University Faculty of Medicine, Cunur, 32200, Isparta, Turkey.
authors.forename: Veysel
authors.initials: V
authors.lastname: Kıdır
authors.affiliation: Department of Biostatistics and Medical Informatics, Süleyman Demirel University Faculty of Medicine, Isparta, Turkey.
authors.forename: Hikmet
authors.initials: H
authors.lastname: Orhan
mesh_terms: D000138:Acidosis / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D000328:Adult; D000368:Aged; D000493:Allopurinol / Q000627:therapeutic use*; D001639:Bicarbonates / Q000097:blood; D003404:Creatinine / Q000097:blood / Q000652:urine; D004727:Endothelium / Q000187:drug effects* / Q000502:physiology; D005260:Female; D006074:Gout Suppressants / Q000627:therapeutic use*; D006801:Humans; D033461:Hyperuricemia / Q000188:drug therapy* / Q000209:etiology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D051436:Renal Insufficiency, Chronic / Q000097:blood / Q000150:complications*; D014527:Uric Acid / Q000097:blood; D014664:Vasodilation / Q000187:drug effects
chemical_list: D001639:Bicarbonates; D006074:Gout Suppressants; D014527:Uric Acid; D000493:Allopurinol; D003404:Creatinine
keywords: Allopurinol; Chronic kidney disease; Endothelial dysfunction; Hyperuricemia; Metabolic acidosis
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