title: Hyperuricemia is associated with progression of IgA nephropathy.
abstract: OBJECTIVE
  IgA nephropathy (IgAN) is one of the world's most common glomerular diseases. Hyperuricemia was recently defined as risk factor for chronic kidney disease. We aimed to investigate the impact of baseline serum uric acid levels on progression of IgAN.
  
  
  METHODS
  A total of 93 patients with IgAN were screened. Demographic information and biochemical data were recorded. eGFR (using the CKD-EPI = Chronic Kidney Disease Epidemiology Collaboration formula) was used as renal function marker. Baseline and sixth month eGFR values were calculated. Progression of renal disease was defined as the difference between baseline eGFR and sixth month eGFR (delta eGFR).
  
  
  RESULTS
  Mean age of the patients was 40 ± 11 years (60% were males). Baseline mean eGFR was 77.9 ± 30.2 mL/min, and baseline mean serum uric acid was 5.65 ± 1.68 mg/dL. Importantly, baseline serum uric acid levels were found to be associated with the change in eGFR (r = 0.252, p = 0.01). In multivariate analysis (adjusted R(2) = 0.171, p = 0.031), adjusting for age, gender, baseline eGFR, blood pressure, baseline albumin concentration and ACEI and/or ARB use revealed that the baseline serum uric acid levels significantly predicted the change in eGFR.
  
  
  CONCLUSIONS
  Baseline serum uric acid concentration is directly proportional to the rate of decline in renal functions in patients with IgAN. Uric acid-lowering treatments may be beneficial for the prevention of progression of IgAN. However, randomized controlled studies are needed for this purpose.
authors.affiliation: Department of Internal Medicine and Nephrology, Goztepe Training and Research Hospital, Istanbul Medeniyet University, 34730, Kadikoy, Istanbul, Turkey.
authors.forename: Ali
authors.initials: A
authors.lastname: Bakan
authors.forename: Alihan
authors.initials: A
authors.lastname: Oral
authors.forename: Omer Celal
authors.initials: OC
authors.lastname: Elcioglu
authors.forename: Mumtaz
authors.initials: M
authors.lastname: Takir
authors.forename: Osman
authors.initials: O
authors.lastname: Kostek
authors.forename: Abdullah
authors.initials: A
authors.lastname: Ozkok
authors.forename: Semih
authors.initials: S
authors.lastname: Basci
authors.forename: Abdullah
authors.initials: A
authors.lastname: Sumnu
authors.forename: Savas
authors.initials: S
authors.lastname: Ozturk
authors.forename: Murat
authors.initials: M
authors.lastname: Sipahioglu
authors.forename: Aydın
authors.initials: A
authors.lastname: Turkmen
authors.forename: Luminita
authors.initials: L
authors.lastname: Voroneanu
authors.forename: Adrian
authors.initials: A
authors.lastname: Covic
authors.forename: Mehmet
authors.initials: M
authors.lastname: Kanbay
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate; D005922:Glomerulonephritis, IGA / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D006801:Humans; D033461:Hyperuricemia / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D012189:Retrospective Studies; D012307:Risk Factors; D014527:Uric Acid / Q000097:blood*
chemical_list: D015415:Biomarkers; D014527:Uric Acid