Publication:
Sugar, salt, immunity and the cause of primary hypertension

dc.contributor.coauthorSanchez-Lozada, Laura G.
dc.contributor.coauthorMadero, Magdalena
dc.contributor.coauthorMazzali, Marilda
dc.contributor.coauthorFeig, Daniel, I
dc.contributor.coauthorNakagawa, Takahiko
dc.contributor.coauthorLanaspa, Miguel A.
dc.contributor.coauthorKuwabara, Masanari
dc.contributor.coauthorRodriguez-Iturbe, Bernardo
dc.contributor.coauthorJohnson, Richard J.
dc.contributor.departmentSchool of Medicine
dc.contributor.kuauthorKanbay, Mehmet
dc.contributor.schoolcollegeinstituteSCHOOL OF MEDICINE
dc.date.accessioned2025-01-19T10:31:57Z
dc.date.issued2023
dc.description.abstractDespite its discovery more than 150 years ago, the cause of primary hypertension remains unknown. Most studies suggest that hypertension involves genetic, congenital or acquired risk factors that result in a relative inability of the kidney to excrete salt (sodium chloride) in the kidneys. Here we review recent studies that suggest there may be two phases, with an initial phase driven by renal vasoconstriction that causes low-grade ischemia to the kidney, followed by the infiltration of immune cells that leads to a local autoimmune reaction that maintains the renal vasoconstriction. Evidence suggests that multiple mechanisms could trigger the initial renal vasoconstriction, but one way may involve fructose that is provided in the diet (such as from table sugar or high fructose corn syrup) or produced endogenously. The fructose metabolism increases intracellular uric acid, which recruits NADPH oxidase to the mitochondria while inhibiting AMP-activated protein kinase. A drop in intracellular ATP level occurs, triggering a survival response. Leptin levels rise, triggering activation of the sympathetic central nervous system, while vasopressin levels rise, causing vasoconstriction in its own right and stimulating aldosterone production via the vasopressin 1b receptor. Low-grade renal injury and autoimmune-mediated inflammation occur. High-salt diets can amplify this process by raising osmolality and triggering more fructose production. Thus, primary hypertension may result from the overactivation of a survival response triggered by fructose metabolism. Restricting salt and sugar and hydrating with ample water may be helpful in the prevention of primary hypertension. Lay Summary Here we discuss recent studies that suggest that fructose, present in added sugars, may have a role in primary hypertension. These studies help link the association of obesity and metabolic syndrome with high blood pressure, and the interaction of salt and sugar in causing high blood pressure.
dc.description.indexedbyWOS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.issue8
dc.description.openaccessgold
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuN/A
dc.description.volume16
dc.identifier.doi10.1093/ckj/sfad058
dc.identifier.eissn2048-8513
dc.identifier.issn2048-8505
dc.identifier.quartileQ1
dc.identifier.scopus2-s2.0-85187017965
dc.identifier.urihttps://doi.org/10.1093/ckj/sfad058
dc.identifier.urihttps://hdl.handle.net/20.500.14288/26332
dc.identifier.wos983934800001
dc.keywordsAutoimmune
dc.keywordsfructose
dc.keywordsHypertension
dc.keywordsLeptin
dc.keywordsUric acid
dc.keywordsVasopressin
dc.language.isoeng
dc.publisherOxford Univ Press
dc.relation.ispartofClinical Kidney Journal
dc.subjectMedicine
dc.titleSugar, salt, immunity and the cause of primary hypertension
dc.typeReview
dspace.entity.typePublication
local.contributor.kuauthorKanbay, Mehmet
local.publication.orgunit1SCHOOL OF MEDICINE
local.publication.orgunit2School of Medicine
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