The Effect of Urine pH and Urinary Uric Acid Levels on the Development of Contrast Nephropathy.


Journal

Kidney & blood pressure research
ISSN: 1423-0143
Titre abrégé: Kidney Blood Press Res
Pays: Switzerland
ID NLM: 9610505

Informations de publication

Date de publication:
2020
Historique:
received: 04 09 2019
accepted: 01 11 2019
pubmed: 23 12 2019
medline: 8 10 2020
entrez: 23 12 2019
Statut: ppublish

Résumé

Hyperuricemia may cause acute kidney injury by activating inflammatory, pro-oxidative and vasoconstrictive pathways. In addition, radiocontrast causes an acute uricosuria, potentially leading to crystal formation. We therefore aimed to investigate the effect of urine acidity and urine uric acid level on the development of contrast-induced nephropathy (CIN) in patients undergoing elective coronary angiography. We enrolled 175 patients who underwent elective coronary angiography. CIN was defined as a >25% increase in the serum creatinine levels relative to basal values 48-72 h after contrast use. Prior to coronary angiography and 48-72 h later, serum uric acid, urea, creatinine, bicarbonate levels, and spot uric acid to creatinine ratio (UACR) were measured. Of the 175 subjects included, 29 (16.6%) developed CIN. Those who developed CIN had a higher prevalence of diabetes, higher UACR (0.60 vs. 0.44, p = 0.014), higher contrast volume, and lower serum sodium level. With univariate analysis of a logistic regression model, the risk of CIN was found to be associated with diabetes (p = 0.0016, OR = 3.8 [95% CI: 1.7-8.7]), urine UACR (p = 0.0027, OR = 9.6 [95% CI: 2.2-42.2]), serum sodium (p = 0.0079, OR = 0.8 [95% CI: 0.77-0.96]), and contrast volume (p = 0.0385, OR = 1.8 [95% CI: 1.03-3.09]). In a multiple logistic regression model with stepwise method of selection, diabetes (p = 0.0120, OR = 3.2 [95% CI: 1.3-8.1]) and UACR (p = 0.0163, OR = 6.9 [95% CI: 1.4-33.4]) were the 2 risk factors finally identified. We have demonstrated that higher urine UACR is associated with the development of CIN in patients undergoing elective coronary angiography.

Sections du résumé

BACKGROUND BACKGROUND
Hyperuricemia may cause acute kidney injury by activating inflammatory, pro-oxidative and vasoconstrictive pathways. In addition, radiocontrast causes an acute uricosuria, potentially leading to crystal formation. We therefore aimed to investigate the effect of urine acidity and urine uric acid level on the development of contrast-induced nephropathy (CIN) in patients undergoing elective coronary angiography.
METHODS METHODS
We enrolled 175 patients who underwent elective coronary angiography. CIN was defined as a >25% increase in the serum creatinine levels relative to basal values 48-72 h after contrast use. Prior to coronary angiography and 48-72 h later, serum uric acid, urea, creatinine, bicarbonate levels, and spot uric acid to creatinine ratio (UACR) were measured.
RESULTS RESULTS
Of the 175 subjects included, 29 (16.6%) developed CIN. Those who developed CIN had a higher prevalence of diabetes, higher UACR (0.60 vs. 0.44, p = 0.014), higher contrast volume, and lower serum sodium level. With univariate analysis of a logistic regression model, the risk of CIN was found to be associated with diabetes (p = 0.0016, OR = 3.8 [95% CI: 1.7-8.7]), urine UACR (p = 0.0027, OR = 9.6 [95% CI: 2.2-42.2]), serum sodium (p = 0.0079, OR = 0.8 [95% CI: 0.77-0.96]), and contrast volume (p = 0.0385, OR = 1.8 [95% CI: 1.03-3.09]). In a multiple logistic regression model with stepwise method of selection, diabetes (p = 0.0120, OR = 3.2 [95% CI: 1.3-8.1]) and UACR (p = 0.0163, OR = 6.9 [95% CI: 1.4-33.4]) were the 2 risk factors finally identified.
CONCLUSIONS CONCLUSIONS
We have demonstrated that higher urine UACR is associated with the development of CIN in patients undergoing elective coronary angiography.

Identifiants

pubmed: 31865342
pii: 000504547
doi: 10.1159/000504547
doi:

Substances chimiques

Contrast Media 0
Uric Acid 268B43MJ25

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

131-141

Informations de copyright

© 2019 The Author(s) Published by S. Karger AG, Basel.

Auteurs

Gamze Aslan (G)

Department of Cardiology, Koc University Hospital, Istanbul, Turkey, gamzeaslan@e-mail.com.tr.

Baris Afsar (B)

Division of Nephrology, Department of Internal Medicine, Suleyman Demirel University School of Medicine, Isparta, Turkey.

Alan A Sag (AA)

Division of Vascular and Interventional Radiology, Department of Radiology, Duke University Medical Center, Durham, North Carolina, USA.

Volkan Camkiran (V)

Department of Cardiology, Koc University Hospital, Istanbul, Turkey.

Nihan Erden (N)

Department of Medicine, Koc University School of Medicine, Istanbul, Turkey.

Sezen Yilmaz (S)

Department of Medicine, Koc University School of Medicine, Istanbul, Turkey.

Dimitrie Siriopol (D)

Department of Nephrology, University of Medicine and Pharmacy "Gr. T. Popa", Iasi, Romania.

Said Incir (S)

Department of Biochemistry, Koc University School of Medicine, Istanbul, Turkey.

Zhiying You (Z)

Division of Renal Diseases and Hypertension, School of Medicine, University of Colorado Denver, Aurora, Colorado, USA.

Miguel L Garcia (ML)

Division of Renal Diseases and Hypertension, School of Medicine, University of Colorado Denver, Aurora, Colorado, USA.

Adrian Covic (A)

Department of Nephrology, University of Medicine and Pharmacy "Gr. T. Popa", Iasi, Romania.

David Z I Cherney (DZI)

Division of Nephrology, University Health Network, University of Toronto, Toronto, Ontario, Canada.

Richard J Johnson (RJ)

Division of Renal Diseases and Hypertension, School of Medicine, University of Colorado Denver, Aurora, Colorado, USA.

Mehmet Kanbay (M)

Division of Nephrology, Department of Medicine, Koc University School of Medicine, Istanbul, Turkey.

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