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

Dan Wang; S. Strandgaard; M.L. Borresen; Z.M. Luo; S.G. Connors; Q. Yan; C.S. Wilcox

doi:10.1053/j.ajkd.2007.09.020

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

Dan Wang, S. Strandgaard, M.L. Borresen, Z.M. Luo, S.G. Connors, Q. Yan, C.S. Wilcox

58 Citations (Scopus)

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. 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

Original language	English
Journal	American Journal of Kidney Diseases
Volume	51
Issue number	2
Pages (from-to)	184-191
Number of pages	7
ISSN	0272-6386
DOIs	https://doi.org/10.1053/j.ajkd.2007.09.020
Publication status	Published - 2008

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10.1053/j.ajkd.2007.09.020

Cite this

@article{a90e4b60f77a11ddbf70000ea68e967b,

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. 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",

author = "Dan Wang and S. Strandgaard and M.L. Borresen and Z.M. Luo and S.G. Connors and Q. Yan and C.S. Wilcox",

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",

year = "2008",

doi = "10.1053/j.ajkd.2007.09.020",

language = "English",

volume = "51",

pages = "184--191",

journal = "American Journal of Kidney Diseases",

issn = "0272-6386",

publisher = "W.B.Saunders Co.",

number = "2",

}

TY - JOUR

T1 - Asymmetric dimethylarginine and lipid peroxidation products in early autosomal dominant polycystic kidney disease

AU - Wang, Dan

AU - Strandgaard, S.

AU - Borresen, M.L.

AU - Luo, Z.M.

AU - Connors, S.G.

AU - Yan, Q.

AU - Wilcox, C.S.

N1 - 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

PY - 2008

Y1 - 2008

N2 - 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

AB - 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

U2 - 10.1053/j.ajkd.2007.09.020

DO - 10.1053/j.ajkd.2007.09.020

M3 - Journal article

C2 - 18215696

SN - 0272-6386

VL - 51

SP - 184

EP - 191

JO - American Journal of Kidney Diseases

JF - American Journal of Kidney Diseases

IS - 2

ER -