title: Asymmetric dimethylarginine and lipid peroxidation products in early autosomal dominant polycystic kidney disease.
abstract: BACKGROUND
  Patients with autosomal dominant polycystic kidney disease (ADPKD) with normal renal function have endothelial dysfunction and decreased nitric oxide synthase activity in subcutaneous resistance vessels. We investigated asymmetric dimethylarginine (ADMA) as a marker of an inhibitor of nitric oxide synthase and the lipid peroxidation product 13-hydroxyoctadecadienoic acid (HODE) as a marker of oxidative stress in patients with early ADPKD.
  
  
  METHODS
  Cross-sectional study.
  
  
  METHODS
  Patients with early ADPKD (n = 27) and age-matched volunteers (n = 30) from a single academic medical center.
  
  
  METHODS
  Patients with ADPKD versus controls.
  
  
  METHODS
  Plasma (P) levels, urinary (U) excretion, and urinary clearance (C) of ADMA and HODE. Because of multiple comparisons, P for significance is considered less than 0.0167.
  
  
  RESULTS
  Patients with ADPKD had significantly increased P(ADMA) levels (604 +/- 131 versus 391 +/- 67 nmol/L; P < 0.01) and U(ADMA) excretion (22 +/- 4 versus 15.2 +/- 3 nmol/micromol creatinine; P = 0.01), decreased C(ADMA) (25 +/- 3 versus 33 +/- 4 mL/min; P = 0.01), increased P(HODE) levels (316 +/- 64 versus 230 +/- 38 nmol/L; P < 0.01) and U(HODE) excretion (467 +/- 67 versus 316 +/- 40 nmol/micromol creatinine; P < 0.01), and decreased plasma nitrite plus nitrate (P(NOx)) levels (21 +/- 5 versus 32 +/- 6 micromol/L; P < 0.01) and U(NOx) excretion (59 +/- 7 versus 138 +/- 27 micromol/micromol creatinine; P < 0.01).
  
  
  CONCLUSIONS
  Small sample size, cross-sectional nature of study, and limited number of markers of oxidative stress.
  
  
  CONCLUSIONS
  P(ADMA) and P(HODE) levels are increased in patients with early ADPKD. Increased P(ADMA) level is related to decreased C(ADMA) and is accompanied by oxidative stress.
authors.affiliation: Cardiovascular-Kidney-Hypertension Institute, Division of Nephrology and Hypertension and Angiogenesis Section, Lombardi Cancer Institute, Georgetown University, Washington, DC 20007, USA. dw32@georgetown.edu
authors.forename: Dan
authors.initials: D
authors.lastname: Wang
authors.forename: Svend
authors.initials: S
authors.lastname: Strandgaard
authors.forename: Malene L
authors.initials: ML
authors.lastname: Borresen
authors.forename: Zaiming
authors.initials: Z
authors.lastname: Luo
authors.forename: Stephanie G
authors.initials: SG
authors.lastname: Connors
authors.forename: Qing
authors.initials: Q
authors.lastname: Yan
authors.forename: Christopher S
authors.initials: CS
authors.lastname: Wilcox
mesh_terms: D000328:Adult; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood / Q000652:urine; D015415:Biomarkers / Q000097:blood / Q000652:urine; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D004791:Enzyme Inhibitors / Q000378:metabolism; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D008041:Linoleic Acids / Q000097:blood* / Q000652:urine*; D015227:Lipid Peroxidation; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000097:blood / Q000652:urine; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D018384:Oxidative Stress; D016891:Polycystic Kidney, Autosomal Dominant / Q000097:blood* / Q000378:metabolism
chemical_list: D015415:Biomarkers; D004791:Enzyme Inhibitors; D008041:Linoleic Acids; D009569:Nitric Oxide; C024348:13-hydroxy-9,11-octadecadienoic acid; C018524:N,N-dimethylarginine; D001120:Arginine; D019001:Nitric Oxide Synthase