Systemic Succinate, Hypoxia-Inducible Factor-1 Alpha, and IL-1β Gene Expression in Autosomal Dominant Polycystic Kidney Disease with and without Hypertension.


Journal

Cardiorenal medicine
ISSN: 1664-5502
Titre abrégé: Cardiorenal Med
Pays: Switzerland
ID NLM: 101554863

Informations de publication

Date de publication:
2019
Historique:
received: 06 01 2019
accepted: 09 04 2019
pubmed: 19 7 2019
medline: 7 7 2020
entrez: 19 7 2019
Statut: ppublish

Résumé

Cyst pressure induces renin-angiotensin-aldosterone system activation and kidney hypoxia in autosomal dominant polycystic kidney disease (ADPKD). Lipopolysaccharide-induced Toll-like receptor activation causes metabolic disturbances that are triggered by increased succinate levels and hypoxia inducible factors, which results in inflammation via IL-1β activation. Since we aimed to investigate the role of both inflammation and hypoxia in the clinical course of ADPKD, via succinate levels from sera samples, HIF-1α gene expression from whole blood and urine samples and IL-1βgene expression from whole blood were measured. One hundred ADPKD patients and 100 matched healthy controls were enrolled to this cross-sectional study. Twenty-four-hour ambulatory blood pressure monitoring was conducted in all participants. Blood, serum, and urine samples were taken after 12-h fasting for the measurement of biochemical parameters and succinate levels. Whole blood and urine samples were used for HIF-1α and IL-1β geneexpression by using quantitative real-time PCR. There were significant differences in whole blood HIF-1α, IL-1β geneexpression, and serumsuccinate levels between the ADPKD patients and the control subjects. Whole blood HIF-1αgene expression, IL-1β geneexpression, and serumsuccinate levels were also significantly different in ADPKD patients with hypertension in comparison with normotensive ones (p < 0.05). Serum succinate levels and blood IL-1β geneexpression were increased in ADPKD patients with high levels of HIF-1α geneexpression (p = 0.018 and p = 0.029, respectively). Increased age,low eGFR, and HIF-1α and IL-1β geneexpressions were also independently associated with hypertension in ADPKD patients. Inflammation and hypoxia are both relevant factors that might be associated with hypertension in ADPKD.

Sections du résumé

BACKGROUND AND OBJECTIVES
Cyst pressure induces renin-angiotensin-aldosterone system activation and kidney hypoxia in autosomal dominant polycystic kidney disease (ADPKD). Lipopolysaccharide-induced Toll-like receptor activation causes metabolic disturbances that are triggered by increased succinate levels and hypoxia inducible factors, which results in inflammation via IL-1β activation. Since we aimed to investigate the role of both inflammation and hypoxia in the clinical course of ADPKD, via succinate levels from sera samples, HIF-1α gene expression from whole blood and urine samples and IL-1βgene expression from whole blood were measured.
METHODS
One hundred ADPKD patients and 100 matched healthy controls were enrolled to this cross-sectional study. Twenty-four-hour ambulatory blood pressure monitoring was conducted in all participants. Blood, serum, and urine samples were taken after 12-h fasting for the measurement of biochemical parameters and succinate levels. Whole blood and urine samples were used for HIF-1α and IL-1β geneexpression by using quantitative real-time PCR.
RESULTS
There were significant differences in whole blood HIF-1α, IL-1β geneexpression, and serumsuccinate levels between the ADPKD patients and the control subjects. Whole blood HIF-1αgene expression, IL-1β geneexpression, and serumsuccinate levels were also significantly different in ADPKD patients with hypertension in comparison with normotensive ones (p < 0.05). Serum succinate levels and blood IL-1β geneexpression were increased in ADPKD patients with high levels of HIF-1α geneexpression (p = 0.018 and p = 0.029, respectively).
CONCLUSIONS
Increased age,low eGFR, and HIF-1α and IL-1β geneexpressions were also independently associated with hypertension in ADPKD patients. Inflammation and hypoxia are both relevant factors that might be associated with hypertension in ADPKD.

Identifiants

pubmed: 31319406
pii: 000500478
doi: 10.1159/000500478
doi:

Substances chimiques

HIF1A protein, human 0
Hypoxia-Inducible Factor 1, alpha Subunit 0
IL1B protein, human 0
Interleukin-1beta 0
RNA, Messenger 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

370-381

Informations de copyright

© 2019 S. Karger AG, Basel.

Auteurs

Ismail Kocyigit (I)

Department of Nephrology, Erciyes University Medical Faculty, Kayseri, Turkey, iikocyigit@gmail.com.

Serpil Taheri (S)

Department of Medical Biology, Erciyes University Medical Faculty, Kayseri, Turkey.

Eray Eroglu (E)

Department of Nephrology, Erciyes University Medical Faculty, Kayseri, Turkey.

Elif Funda Sener (EF)

Department of Medical Biology, Erciyes University Medical Faculty, Kayseri, Turkey.

Gokmen Zararsız (G)

Department of Biostatistics, Erciyes University Medical Faculty, Kayseri, Turkey.

Ilknur Uzun (I)

Department of Internal Medicine, Erciyes University Medical Faculty, Kayseri, Turkey.

Esra Tufan (E)

Betul-Ziya Eren Genome and Stem Cell Center, Erciyes University Medical Faculty, Kayseri, Turkey.

Ecmel Mehmetbeyoglu (E)

Betul-Ziya Eren Genome and Stem Cell Center, Erciyes University Medical Faculty, Kayseri, Turkey.

Kezban Korkmaz Bayramov (K)

Betul-Ziya Eren Genome and Stem Cell Center, Erciyes University Medical Faculty, Kayseri, Turkey.

Murat Hayri Sipahioglu (MH)

Department of Nephrology, Erciyes University Medical Faculty, Kayseri, Turkey.

Yusuf Ozkul (Y)

Department of Genetics, Erciyes University Medical Faculty, Kayseri, Turkey.

Bulent Tokgoz (B)

Department of Nephrology, Erciyes University Medical Faculty, Kayseri, Turkey.

Oktay Oymak (O)

Department of Nephrology, Erciyes University Medical Faculty, Kayseri, Turkey.

Jonas Axelsson (J)

Transplant Immunology Division, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.
Department of Clinical Immunology, Karolinska University Hospital, Stockholm, Sweden.
Clinical Research Center, Lund University, Lund, Sweden.

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Classifications MeSH