Variation in Sodium Intake and Intra-individual Change in Blood Pressure in Chronic Kidney Disease

Pathak, Chetna M.; Ix, Joachim H.; Anderson, Cheryl A.M.; Woodell, Tyler B.; Smits, Gerard; Persky, Martha S.; Block, Geoffrey A.; Rifkin, Dena E.

doi:10.1053/j.jrn.2017.07.002

Cited by 3 publications

(2 citation statements)

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“…Dietary salt intake can unmask a salt sensitivity blood pressure phenotype. While it is well established from clinical observations [48][49][50], and in some animal studies [51,52] that high dietary salt (above 5 g/day) contributes to BP elevations and salt-sensitive hypertension, the effect of high dietary salt on BP is heterogeneous. While not directly elevating BP in some individuals, it raises BP in others.…”

Section: Pressor Response To Salt Taste Sensitivity and Hypertensionmentioning

confidence: 99%

Salt Taste and Salt Sensitive Hypertension in HIV

2023

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Purpose of Review:To provide a summary of current literature and propose potential mechanistic models to help us understand the role of HIV infection/antiretroviral therapy (ART), salt taste sensitivity (STS), and salt sensitivity of blood pressure (SSBP) in hypertension development. Recent Findings:The epithelial sodium channel (ENaC) is the main protein/sodium channel for recognizing Na + in the tongue and mediates preference to low-medium salt concentrations in animals and humans. Considering the pressor response to oral salt in individuals with SSBP, poor STS may worsen blood pressure. Specific genetic variants in ENaC are linked to salt taste perception and hypertension. HIV infection, some ART, and specific antihypertensive drugs are associated with reduced STS and an increased liking for salty foods. Summary: Persons with HIV (PWH) on ART may have a decreased STS and are at a higher risk of developing saltsensitive hypertension. Inflammation mediated by dietary salt is one of the drivers of poor STS and saltsensitive hypertension among PWH.Keywords (separated by '-') Salt taste sensitivity -Salt sensitivity of blood pressure -HIV -Hypertension -ENaC Footnote InformationThis article is part of the Topical Collection on Inflammation and Cardiovascular Diseases

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Section: Pressor Response To Salt Taste Sensitivity and Hypertensionmentioning

confidence: 99%

Salt Taste and Salt Sensitive Hypertension in HIV

2023

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“…2,3 Furthermore, CKD can significantly affect life span/quality and places a heavy burden on health care systems, families, and society. 4 Therefore, it is urgent to develop new therapeutic drugs for the treatment of CKD.…”

Section: Introductionmentioning

confidence: 99%

Rhein Inhibits Proliferation, Extracellular Matrix Deposition, and Inflammation in Mesangial Cells via ROS/Akt Signaling Pathway

Xiong

et al. 2022

Natural Product Communications

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It has been reported that rhein, a Chinese herbal compound, has a potent anti-inflammatory effect on various diseases. However, it remains elusive whether rhein has a protective effect on chronic kidney disease (CKD) and what its underlying mechanism may be. In the present study, we evaluated whether rhein could prevent lipopolysaccharide (LPS)-induced proliferation, expression of extracellular matrix (ECM) proteins, and inflammation in rat mesangial cells (MCs), and whether these effects were mediated by reactive oxygen species (ROS) and Akt signaling. We also investigated the protective effect of rhein on renal function in a rat CKD model. Results showed that rhein significantly suppressed LPS-initiated proliferation in MCs in a cell counting kit-8 (CCK8) assay. Meanwhile, rhein significantly inhibited LPS-induced expression of ECM proteins and inflammation, as indicated by the decreased expression of fibronectin, α smooth muscle actin (α-SMA), tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), interleukin 6 (IL-6), and interferon γ (IFN-γ). Of note, rhein significantly enhanced LPS-induced production of reactive oxygen species (ROS) and inhibited LPS-induced Akt phosphorylation. Furthermore, the inhibitory effect of rhein on Akt phosphorylation was inhibited by H2O2 scavenger catalase. Importantly, the protective effect of rhein was almost totally lost in the presence of phosphatidylinositol 3-kinase (PI3K) protagonist insulin-like growth factor 1 (IGF-1). Finally, rhein significantly decreased 24 h urinary protein, serum creatinine (SCr), and blood urea nitrogen (BUN) in CKD rats. Collectively, these results suggested that rhein improved CKD through inhibition of proliferation, ECM synthesis, and inflammation via ROS/Akt signaling in MCs.

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