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Asymmetric dimethylarginine and lipid peroxidation products in early autosomal dominant polycystic kidney disease

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

  • Dan Wang
  • S. Strandgaard
  • M.L. Borresen
  • Z.M. Luo
  • S.G. Connors
  • Q. Yan
  • C.S. Wilcox
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. Study Design: Cross-sectional study. Setting & Participants: Patients with early ADPKD (n = 27) and age-matched volunteers (n = 30) from a single academic medical center. Factor: Patients with ADPKD versus controls. Outcomes & Measurement: 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/Amol 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/mu mol creatinine; P < 0.01), and decreased plasma nitrite plus nitrate (P-NOx) levels (21 +/- 5 versus 32 +/- 6 mu mol/L; P < 0.01) and U-NOx excretion (59 +/- 7 versus 138 +/- 27 mu mol/mu mol creatinine; P < 0.01). Limitations: 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 CADMA and is accompanied by oxidative stress. Am J Kidney Dis 51:184-191. (c) 2008 by the National Kidney Foundation, Inc
Udgivelsesdato: 2008/2
OriginalsprogEngelsk
TidsskriftAmerican Journal of Kidney Diseases
Vol/bind51
Udgave nummer2
Sider (fra-til)184-191
Antal sider7
ISSN0272-6386
DOI
StatusUdgivet - 2008

Bibliografisk note

Times Cited: 1ArticleEnglishWang, DGeorgetown Univ, Div Nephrol & Hypertens, Cardiovasc Kidney Hypertens Inst, 4000 Reservoir Rd NW, Washington, DC 20007 USACited References Count: 62285TRW B SAUNDERS CO-ELSEVIER INC1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USAPHILADELPHIA

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