The Predictive Value of Salt Sensitivity and Osmotic Fragility in the Development of Cerebral Small Vessel Disease.

Larisa A Dobrynina,Kamila V Shamtieva,Alla A Shabalina,Marina V Krotenkova,Alexander B Berdalin,Elena V Gnedovskaya

doi:10.3390/ijms21062036

Larisa A Dobrynina, Kamila V Shamtieva + Show 4 more

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https://doi.org/10.3390/ijms21062036

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Abstract

Increased salt intake in food probably affects the progression of cerebral small vessel disease (CSVD), which justifies the study of disturbances in sodium homeostasis associated with the development of CSVD. We aimed to clarify the role of salt sensitivity and osmotic fragility in the development of CSVD. Erythrocyte salt sensitivity was measured using the modified salt blood test, and osmotic fragility was measured using the classic osmotic fragility test in 73 patients with CSVD (48 women; 60.1 ± 6.5 years) and 19 healthy volunteers (14 women; 56.9 ± 6.4 years). Salt sensitivity and osmotic fragility exhibited a predictive value in relation to CSVD. These parameters were associated with an increase in white matter hyperintensities (p = 0.019 and 0.004, respectively). Their simultaneous use increased their predictive ability for CSVD (p < 0.000001; AUC (95% CI), 0.824 (0.724–0.923)). The possibility of predicting CSVD using erythrocyte salt sensitivity and osmotic fragility indicates the value of the individual glycocalyx buffer capacity in relation to sodium and the activity of sodium channels in the development of CSVD. Increased salt sensitivity and osmotic fragility seem to be risk factors for CSVD.

Highlights

Cerebral small vessel disease (CSVD), which is associated with age and vascular risk factors, is the main cause of vascular cognitive impairment and mixed variants of Alzheimer’s disease and is a significant cause of stroke, disability and mortality [1]
There was a significant difference between the patients with CSVD and the subjects in the control group regarding the presence and severity of Arterial hypertension (AH) and diabetes mellitus (DM) type 2
To clarify the potential role of disturbances in sodium homeostasis in the development of CSVD, the mToodcifilaerdifysathltebplotoednttieasltro[1le6o,1f7d] iastnudrbtahneceossminostoicdifurmagihloitmy eteosta[s1i8s]inwtehreeduesveedlotpommenetaosuf CreSVthDe, ptahreameotdeirfsieodf ssaalltt sbelnosoidtivtietsyta[n1d6,1o7s]maontdic ftrhaegiolsitmyointicthferaegriylitthyrotceyste[s18o]f pwaetrienutssewditthoCmSVeaDsu. rTehethire spenarsaitmiveityerasnodf spaletcsifiecnistiytiivnitpyreadnidctoinsgmCotSiVc Dfraagnidlittyheinirtchoerreerlyathiornocwyittehs MofRpIastiigenstswweritehaClsSoVaDss.eTssheedir. sensTithiveityestasnudsesdpiencitfhicisitsytuidnyprreefldeiccttitnhge eCvSenVtDs thaantdoctchuerirwchoernredlaiettiaorny wsailthisMcoRnIsusmigends: wtherfiellainlsgo oafstsheessgeldy.cocalyx with sodium according to its buffer capacity and the movement of sodium mediated by endothelial sodium channels into the intercellular space, via the activity of sodium transporters, mainly Na+/K+-ATPase [9,10]

Summary

Introduction

Cerebral small vessel disease (CSVD), which is associated with age and vascular risk factors, is the main cause of vascular cognitive impairment and mixed variants of Alzheimer’s disease and is a significant cause of stroke, disability and mortality [1]. One of them may be the disturbance in sodium homeostasis, mainly considered as a phenomenon of salt sensitivity The latter implies an increase in blood pressure with excessive salt loading and a decrease in blood pressure at low salt diet in hypertensive and normotensive patients [4]. This assumption stems from the association between increased salt intake and hypertension-independent cardiovascular risk [5], the accelerated development of CSVD in stroke-prone spontaneously hypertensive rats [6] and increased areas of white matter hyperintensities (WMHs) [7,8] and other MRI signs of CSVD, such as lacunes and microbleeds, after adjustment for age and AH [8]

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