Pathogenesis of Higher Blood Pressure and Worse Renal Function in Salt-Sensitive Hypertension

Background: The underlying pathogenesis of patients with salt-sensitive hypertension expressing higher blood pressure and severer renal damage remains uncertain. Methods: We recruited 329 subjects, 131 in salt-sensitive (SS) group, 148 in nonsalt-sensitive (NSS) group, and 50 healthy people in norma...

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Main Authors: Yuguang Chu, Yan Zhou, Shihua Lu, Feng Lu, Yuanhui Hu
Format: Article
Language:English
Published: Karger Publishers 2021-04-01
Series:Kidney & Blood Pressure Research
Subjects:
Online Access:https://www.karger.com/Article/FullText/515088
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spelling doaj-c934962130954573ac68b87b126aec2d2021-04-29T14:25:42ZengKarger PublishersKidney & Blood Pressure Research1420-40961423-01432021-04-0146223624410.1159/000515088515088Pathogenesis of Higher Blood Pressure and Worse Renal Function in Salt-Sensitive HypertensionYuguang Chu0Yan Zhou1Shihua Lu2Feng Lu3Yuanhui Hu4Department of Cardiology, Guang’anmen Hospital, Chinese Academy of Traditional Chinese Medicine, Beijing, ChinaDepartment of Cardiology, Guang’anmen Hospital, Chinese Academy of Traditional Chinese Medicine, Beijing, ChinaDepartment of Cardiology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, ChinaDepartment of Cardiology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, ChinaDepartment of Cardiology, Guang’anmen Hospital, Chinese Academy of Traditional Chinese Medicine, Beijing, ChinaBackground: The underlying pathogenesis of patients with salt-sensitive hypertension expressing higher blood pressure and severer renal damage remains uncertain. Methods: We recruited 329 subjects, 131 in salt-sensitive (SS) group, 148 in nonsalt-sensitive (NSS) group, and 50 healthy people in normal group and tested their renal function, 24-h ambulatory blood pressure, and growth factor series. Results: The SS group showed worse renal function with lower estimated glomerular filtration rate and higher urinary microalbumin, α-microglobulin, urinary protein Cr ratio, and urinary immunoglobulin. Most indicators in 24-h ambulatory blood pressure of the SS group were significantly enhanced than the NSS group, indicating their higher blood pressure. The significantly elevated growth factors in the SS group were AR, BMP-5, EG-VEGF, GH, HGF, IGFBP-2, IGFBP-3, IGFBP-6, MCSFR, NT-4, PDGF-AA, SCF, SCFR, VEGFR2, VEGFR3, and VEGF-D, compared to other 2 groups or one of them. PI3K-AKT pathway was activated in the SS group. Conclusions: Differences in growth factors and pathways may account for the manifestations of the SS group. Activated PI3K-AKT pathway with higher IGFBP-3 and GH can lead to renal damage. Higher MCSFR in the SS group indicates that high blood pressure and severe kidney damage may be associated with the activation of the immune system. EG-VEGF, VEGFR2, VEGFR3, and VEGF-D can also explain the elevated blood pressure due to the dilated lymphatic system which drains excess sodium and water back into circulation. The SS group presented higher AR and HGF which may worsen renal function by regulating cell proliferation and tumor formation. However, due to the potential low awareness rate of hypertension at the very beginning, we cannot ensure the exact occurrence order of blood pressure, renal damage, and salt sensitivity. Therefore, further studies which can track data from the onset of hypertension are needed.https://www.karger.com/Article/FullText/515088salt-sensitive hypertensionambulatory blood pressuregrowth factorrenal damagepi3k-akt signaling pathway
collection DOAJ
language English
format Article
sources DOAJ
author Yuguang Chu
Yan Zhou
Shihua Lu
Feng Lu
Yuanhui Hu
spellingShingle Yuguang Chu
Yan Zhou
Shihua Lu
Feng Lu
Yuanhui Hu
Pathogenesis of Higher Blood Pressure and Worse Renal Function in Salt-Sensitive Hypertension
Kidney & Blood Pressure Research
salt-sensitive hypertension
ambulatory blood pressure
growth factor
renal damage
pi3k-akt signaling pathway
author_facet Yuguang Chu
Yan Zhou
Shihua Lu
Feng Lu
Yuanhui Hu
author_sort Yuguang Chu
title Pathogenesis of Higher Blood Pressure and Worse Renal Function in Salt-Sensitive Hypertension
title_short Pathogenesis of Higher Blood Pressure and Worse Renal Function in Salt-Sensitive Hypertension
title_full Pathogenesis of Higher Blood Pressure and Worse Renal Function in Salt-Sensitive Hypertension
title_fullStr Pathogenesis of Higher Blood Pressure and Worse Renal Function in Salt-Sensitive Hypertension
title_full_unstemmed Pathogenesis of Higher Blood Pressure and Worse Renal Function in Salt-Sensitive Hypertension
title_sort pathogenesis of higher blood pressure and worse renal function in salt-sensitive hypertension
publisher Karger Publishers
series Kidney & Blood Pressure Research
issn 1420-4096
1423-0143
publishDate 2021-04-01
description Background: The underlying pathogenesis of patients with salt-sensitive hypertension expressing higher blood pressure and severer renal damage remains uncertain. Methods: We recruited 329 subjects, 131 in salt-sensitive (SS) group, 148 in nonsalt-sensitive (NSS) group, and 50 healthy people in normal group and tested their renal function, 24-h ambulatory blood pressure, and growth factor series. Results: The SS group showed worse renal function with lower estimated glomerular filtration rate and higher urinary microalbumin, α-microglobulin, urinary protein Cr ratio, and urinary immunoglobulin. Most indicators in 24-h ambulatory blood pressure of the SS group were significantly enhanced than the NSS group, indicating their higher blood pressure. The significantly elevated growth factors in the SS group were AR, BMP-5, EG-VEGF, GH, HGF, IGFBP-2, IGFBP-3, IGFBP-6, MCSFR, NT-4, PDGF-AA, SCF, SCFR, VEGFR2, VEGFR3, and VEGF-D, compared to other 2 groups or one of them. PI3K-AKT pathway was activated in the SS group. Conclusions: Differences in growth factors and pathways may account for the manifestations of the SS group. Activated PI3K-AKT pathway with higher IGFBP-3 and GH can lead to renal damage. Higher MCSFR in the SS group indicates that high blood pressure and severe kidney damage may be associated with the activation of the immune system. EG-VEGF, VEGFR2, VEGFR3, and VEGF-D can also explain the elevated blood pressure due to the dilated lymphatic system which drains excess sodium and water back into circulation. The SS group presented higher AR and HGF which may worsen renal function by regulating cell proliferation and tumor formation. However, due to the potential low awareness rate of hypertension at the very beginning, we cannot ensure the exact occurrence order of blood pressure, renal damage, and salt sensitivity. Therefore, further studies which can track data from the onset of hypertension are needed.
topic salt-sensitive hypertension
ambulatory blood pressure
growth factor
renal damage
pi3k-akt signaling pathway
url https://www.karger.com/Article/FullText/515088
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