High Salt Intake Research Articles

Awareness, behavior, and determinants of dietary salt intake in adults: results from the National NCD Monitoring Survey, India

A diet high in sodium contributes to a significant proportion of Disability Adjusted Life Years (DALYs) due to cardiovascular diseases. This paper describes the awareness, behaviour and determinants related to dietary salt intake in an adult population of 18–69 years that were assessed as part of the National NCD Monitoring Survey (NNMS) in India. A sub-sample of 3000 adults selected through simple random sampling from 150 nationally representative Primary Sampling Units (PSUs) was included. Data regarding awareness and behaviour related to dietary salt intake were collected. Urinary sodium excretion in spot urine samples was estimated and used to calculate dietary salt intake. The dietary salt intake’s sociodemographic, behavioural and metabolic determinants were also analysed. Less than one-third of the adults of both genders in all age groups in rural and urban areas were aware that daily high salt intake could affect health. The estimated mean daily salt intake was 8.0 g (8.9 g/day for men and 7.1 g/day for women). The salt intake was significantly higher in men [Adjusted OR = 17.66 (5.24–59.46)], rural areas [Adjusted OR = 6.14 (1.83–20.60)], overweight and obese respondents [Adjusted OR = 17.62 (3.17–98.07)]. The perception of the harmful effects of high salt intake and practices to limit salt intake was low in the study population. The mean daily salt intake was higher than the WHO recommendation of up to 5 g daily. The mean dietary salt intake is high in the Indian population, which calls for planning and implementing control of dietary salt consumption measures.

Salt Sensitivity: Causes, Consequences, and Recent Advances.

Salt (sodium chloride) is an essential nutrient required to maintain physiological functions. However, for most people, daily salt intake far exceeds their physiological need and is habitually greater than recommended upper thresholds. Excess salt intake leads to elevation in blood pressure which drives cardiovascular morbidity and mortality. Indeed, excessive salt intake is estimated to be responsible for ≈5 million deaths per year globally. For approximately one-third of otherwise healthy individuals (and >50% of those with hypertension), the effect of salt intake on blood pressure elevation is exaggerated; such people are categorized as salt sensitive and salt sensitivity of blood pressure is considered an independent risk factor for cardiovascular disease and death. The prevalence of salt sensitivity is higher in women than in men and, in both, increases with age. This narrative review considers the foundational concepts of salt sensitivity and the underlying effector systems that cause salt sensitivity. We also consider recent updates in preclinical and clinical research that are revealing new modifying factors that determine the blood pressure response to high salt intake.

Developing a social mobilisation intervention for salt reduction: participatory action research in Bombali district, Sierra Leone

BackgroundHigh salt intake is a major risk factor for hypertension, which in turn contributes to cardiovascular diseases, the major cause of death from non communicable diseases (NCDs). Research is limited on social mobilisation interventions to tackle NCDs, including in fragile health settings such as Sierra Leone.MethodsParticipatory action research methods were used to develop a social mobilisation intervention for salt reduction in Bombali District, Sierra Leone. A team of 20 local stakeholders were recruited to develop and deliver the intervention. Stakeholder workshop reports and interviews were used to record outcomes, enablers, and barriers to the intervention. Focus group discussions were used to observe knowledge, attitudes, and behaviours of community members pre- and post- the intervention.ResultsStakeholders showed enthusiasm and were well engaged in the social mobilisation process around salt reduction. They developed radio jingles, radio show talks, organised community awareness raising meetings, school sensitisation outreaches, and door to door engagements. Stakeholders reported benefiting personally through developing their own skills and confidence in communication and felt positive about their role in educating their community. The interventions led to reported increased awareness of risks of high salt intake and NCDs, resulting in a reduction of salt use in the community, leading to perceived health gains. However, salt reduction was also met with some resistance due to social factors. Local community structures were also reactivated to work on the interventions and connect the community to the local health facility, which saw an increase in patients having their blood pressure checked. The comparison villages also experienced an increase in awareness and perceived reductions in salt intake behaviours. This was as messages had cascaded via the radio and initial focus group discussions. The social mobilisation stakeholders also agreed on future activities that could continue at no or low cost.ConclusionSocial mobilisation interventions can provide low-cost strategies to tackle NCDs in fragile settings such as Sierra Leone through the utilisation of community structures. However, more research is required to ascertain the key enablers for replicability and if such successes can be sustained over a longer follow up period.

High-Salt-Diet (HSD) aggravates the progression of Inflammatory Bowel Disease (IBD) via regulating epithelial necroptosis

Due to its unclear etiology, there is no specific medicine to cure the recurrent and incurable inflammatory bowel disease (IBD). Unhealthy dietary habits unconsciously contributed to the progression of IBD, for example a High-Salt-Diet (HSD) is the most neglected and frequently adopted habit. However, the molecular mechanism of how HSD aggravates the progression of IBD has yet to remain uncovered. Herein, we focus on the hypothesis that necroptosis pathway may be involved in the process of IBD exacerbated by HSD. To this end, different gene expression (DEGs) profiles of human epithelia under hypertonic culture conditions were applied to screen candidate pathways. What’s more, gene expression manipulation, immune microenvironment detection, RIPK3/MLKL gene knockout (KO), and wild-type (WT) mice were carried out to research the promotion of IBD progression under treatments of high salt intake. Based on our present results, gene expression profiles in human normal colon epithelia cell NCM460 were significantly changed under salt- or sucrose-induced hypertonic culture conditions. RIPK3 was significantly up-regulated under both conditions. Furthermore, mice colon epithelia cell CT26 growth was inhibited in a time- and dose-dependent manner by extra NaCl incubation. Autophagy, and Necroptosis pathways were activated and enhanced by LPS pretreatment. HSD significantly exacerbated DSS-induced IBD symptoms in vivo in a dose-dependent manner. Moreover, RIPK3-/- and MLKL-/- mice presented severe IBD symptoms in vivo. Overall, the results demonstrated that HSD aggravated the IBD progression via necroptosis activation, providing novel strategies and promising targets for the clinical treatment of IBD.

Sodium as an Important Regulator of Immunometabolism.

Salt sensitivity concerns blood pressure alterations after a change in salt intake (sodium chloride). The heart is a pump, and vessels are tubes; sodium can affect both. A high salt intake increases cardiac output, promotes vascular dysfunction and capillary rarefaction, and chronically leads to increased systemic vascular resistance. More recent findings suggest that sodium also acts as an important second messenger regulating energy metabolism and cellular functions. Besides endothelial cells and fibroblasts, sodium also affects innate and adaptive immunometabolism, immune cell function, and influences certain microbes and microbiota-derived metabolites. We propose the idea that the definition of salt sensitivity should be expanded beyond high blood pressure to cellular and molecular salt sensitivity.

Prevalence and determinants of resistant hypertension in the delta region of Egypt: A prospective observational study.

Hypertension (HTN) is a leading cause of morbidity and mortality affecting about 30%-40% of the adult population in developed countries. Fewer data were published about the prevalence, sociodemographics, and clinical characteristics of the resistant hypertensive population in Egypt. Hence, our aim is to focus the attention on these determinantsespecially in the delta region of Egypt. Data belonging to patients visiting our HTN clinic in the Cardiovascular Department, Tanta University Hospital, Gharbeyah Governorate, Egypt, were collected over 12 months, between January 1, 2022, and 31 December 31, 2022, and then carefully analyzed. We found that the prevalence of resistant hypertension (RHTN) in the delta region of Egypt was 18%. We noted more RHTN cases in older age, that is, mean ± Std. was 51.5 ± 13.24 and 62.1 ± 7.56 for non-RHTN and RHTN, respectively. Also, the prevalence was higher in women representing about 54.4% of cases. Sixty-two percentof the patients with RH were obese (mean ± Std. of body mass indexwas 30.7 ± 5.36 in HTNand 47.7 ± 30.3 in RHTNgroups with p value <0.001). We found a significant relationship between chronic kidney disease, diabetes, and RHTN. Control of HTN among the Egyptian population in the delta region was unsatisfactory and higher than rates published globally. RH was more obvious in women, elderly, obese population, and diabetic and chronic kidney disease patients. Excessive use of nonsteroidal anti-inflammatory drugs, smoking, and high salt intake were clearly observed.

Abstract 036: The Single-cell Gene Expression Landscape Of The Hypothalamus During The Development Of Hypertension In Three Major Models

The hypothalamus plays a key role in blood pressure regulation through coordinating and integrating signals in the central nervous system. However, it’s remains underexplored how the cell signaling network in the hypothalamus changes during the progression of hypertension, the key regulators involved, and whether shared or distinct pathophysiological mechanisms underlie the development of hypertension triggered by various genetic susceptibility or environmental factors. To address these questions, we applied the single-nucleus RNA sequencing technology to analyze hypothalamus samples from three well-established models of hypertension with distinct pathogenesis - mice treated with Ang II, the Dahl salt-sensitive rat, and the spontaneous hypertensive rat - along with their respective controls. Data were obtained from 238,445 nuclei from 24 samples under 12 experimental conditions. By characterizing the cellular composition under different disease conditions, we discovered an elevated glia-to-neuron ratio in Ang II-induced hypertension, with increases of 3.1-fold in astrocytes, 4.0-fold in microglia, and 3.4-fold in oligodendrocytes. Moreover, astrocytes underwent a transition from the resting state to a reactive mode associated with neuroinflammation and stronger neuron adhesion. Additionally, multiple neuronal signal communication pathways were overactivated in response to Ang II, including neurexin-neuroligin signaling, nitric oxide-guanylate cyclase pathway, and glutamate and its receptors. In the salt-sensitive hypertension, a 2.3-fold expansion of pro-inflammatory microglia via Cd74 activation was observed after a short-term high-sodium diet, which leveled off thereafter. With a prolonged high-salt intake, there was a 1.7-fold increase in the proportion of Plagl1+ GABA-ergic neurons. In 26 weeks old spontaneously hypertensive rats, a distinctive 1.4-fold increase in the proportion of Slit3+ Glu-ergic neurons was observed, setting them apart from WKY rats. These findings provide new insights into how the hypothalamus may be involved in the development of hypertension under different disease conditions.

Association of sodium intake with diabetes in adults without hypertension: evidence from the National Health and Nutrition Examination Survey 2009-2018.

Sodium is essential for human health, however the prevalence of various diseases is associated with excessive sodium intake, particularly cardiovascular disorders. However, in most countries, salt intake is much higher than the World Health Organization recommends. Several studies in recent years have revealed that high salt intake is associated with diabetes in the general population, but the association is uncertain in people who do not have hypertension. In this study, we aimed to find out whether high sodium intake increases the risk of diabetes in this particular population. Data were extracted from the National Health and Nutrition Examination Survey (NHANES; 2009-2018). Participants included adults aged over 20 years old who have undergone the diabetes questionnaire, and the hypertension population was excluded. In order to adjust the confounders, multivariate analysis models were built. Finally, subgroup analysis were conducted to investigate the association between sodium intake and diabetes separately. In the present study, 7,907 participants are included (3,920 female and 3,987 male), and 512 (6.48%) individuals reported diabetes. The median sodium intake of the participants was 3,341 mg/d (IQR: 2498, 4,364 mg/d). A linear association between sodium intake and the prevalence of diabetes was found (p = 0.003). According to the multivariate analysis models, the odds ratio of diabetes for every 1,000 mg sodium intake increment is 1.20 (OR: 1.20, 95% CI 1.07-1.35). The highest sodium intake quartile was 1.80-fold more likely to have diabetes than the lowest quartile (OR: 1.80, 95% CI 1.17-2.76). Our results suggest that higher sodium intake is associated with an increased risk of diabetes in the population without hypertension, and for every 1,000 mg sodium intake increment, the risk of diabetes increased by 1.20-fold. To sum up, we have provided the clue to the etiology of diabetes and further prospective research is needed to contribute recommendations for the primary prevention of diabetes in the US.

Hordeum vulgare ethanolic extract mitigates high salt-induced cerebellum damage via attenuation of oxidative stress, neuroinflammation, and neurochemical alterations in hypertensive rats

High salt intake increases inflammatory and oxidative stress responses and causes an imbalance of neurotransmitters involved in the pathogenesis of hypertension that is related to the onset of cerebral injury. Using natural compounds that target oxidative stress and neuroinflammation pathways remains a promising approach for treating neurological diseases. Barley (Hordeum vulgare L.) seeds are rich in protein, fiber, minerals, and phenolic compounds, that exhibit potent neuroprotective effects in various neurodegenerative diseases. Therefore, this work aimed to investigate the efficacy of barley ethanolic extract against a high salt diet (HSD)-induced cerebellum injury in hypertensive rats. Forty-eight Wistar rats were divided into six groups. Group (I) was the control. The second group, the HSD group, was fed a diet containing 8% NaCl. Groups II and III were fed an HSD and simultaneously treated with either amlodipine (1 mg /kg b.wt p.o) or barley extract (1000 mg /kg b.wt p.o) for five weeks. Groups IV and V were fed HSD for five weeks, then administered with either amlodipine or barley extract for another five weeks. The results revealed that barley treatment significantly reduced blood pressure and effectively reduced oxidative stress and inflammation in rat's cerebellum as indicated by higher GSH and nitric oxide levels and lower malondialdehyde, TNF-α, and IL-1ß levels. Additionally, barley restored the balance of neurotransmitters and improved cellular energy performance in the cerebellum of HSD-fed rats. These findings suggest that barley supplementation exerted protective effects against high salt-induced hypertension by an antioxidant, anti-inflammatory, and vasodilating effects and restoring neurochemical alterations.Graphical abstract

Social determinants of health and cardiometabolic risk factors in Nepal: A scoping review

AimsCardiometabolic risk factors are modifiable contributors to cardiometabolic disease and adverse outcomes. Cardiometabolic risk factors are emerging health concerns among adults in low and middle-income countries. The role of social determinants of health on cardiometa gaps. Data synthesisA comprehensive search was conducted in multiple databases: PubMed (MEDLINE), Web of Science (Clarivate), and CINAHL (EBSCO). Joanna Briggs Institute's (JBI) Scoping Review methodology and PRISMA extension for scoping reviews-SCRA guided this review. Forty-four cross-sectional studies published between 2010 and 2022 were eligible for this review. Men were more likely to have hypertension, while women were more likely to have obesity and abdominal obesity. Participants from marginalized caste/ethnicity, urban regions, and those with lower education, and greater wealth index had a greater likelihood of hypertension, dyslipidemia, and hyperglycemia; however, differences across these sociodemographic subgroups are narrowing. Smoking, harmful alcohol use, high salt intake, low fruit and vegetable intake, and sedentary lifestyles were associated with one or more cardiometabolic risk factors. Finally, one cardiometabolic risk factor increased the risk of others. ConclusionsFindings reflect that Nepal is at the intersection of rapid urbanization, nutritional transition, and socioeconomic shift. Future studies should take a multilevel approach to investigate the role of social determinants in increasing the cardiometabolic risk burden in Nepal.

Influence of Salt Intake on Segmental Lesions of Patients with Ischaemic Heart Disease in Sri Lanka: A Cross-sectional Study

Background: Sodium assists in maintaining body fluid balance. Excess sodium intake increases the risk of ischaemic heart disease (IHD) adding to global and local mortality due to non-communicable diseases. Aim: To determine the salt intake levels of patients having coronary artery bypass grafting (CABG) and to explain the relationship between salt consumption and atheroma development. This study used an adapted cross-sectional design with 233 patients admitted to Sri Jayewardenepura General Hospital with acute heart diseases. Method: Demographic and lifestyle-related data, medical history and food intake data were collected. Salt intake was calculated based on the consumption of salt used per month at household level, salt added to food – including in restaurants. Salt content was determined using web-based applications and food tables. Multivariate logistic regression was used to identify variables significantly associated with IHD. Results: In this study, the daily intake of sodium per person was 6,176 mg. This was much higher than WHO’s recommended level of 2,000 mg/day, demonstrating a significant relationship between segmental lesions and sodium intake (p&lt;0.01). The multivariate binary logistic model demonstrated that high salt intake (OR 8.54; 95% CI [4.545–16.734]) and the presence of diabetes (OR 2.23; 95% CI [1.206–4.238]), contributed to the high number of segmental lesions (p&lt;0.01). Conclusion: A high daily intake of sodium increases the risk of atheroma formation in more coronary segments, regardless of age, sex, several known disease conditions and risk factors.

Effectiveness of a Health Education Program in Hypertensive Patients with Dyslipidemia and/or Microalbuminuria: A Quasi-Experimental Study in Vinh Long Province, Vietnam.

Hypertension, a major health concern, is associated with significant mortality and disease burden worldwide, including Vietnam. Comprehensive interventions targeting medication, lifestyle modifications, dyslipidemia (DLP), and microalbuminuria (MAU) are vital for effective hypertension management and reducing the risk of cardiovascular disease complications (CDV). While medication interventions have proven efficacy, the evidence regarding the effectiveness of community-based health education interventions in managing DLP and MAU is limited. Therefore, this study aims to evaluate the effectiveness of community health education interventions in reducing hypertension risk factors and achieving hypertension management objectives, as well as managing DLP and MAU among hypertension patients. A quasi-experimental study was conducted on 330 hypertensive patients with dyslipidemia (DLP) and/or microalbuminuria (MAU) who were divided into a control group (n = 164) and an intervention group (n = 166). The control group received standard national hypertension management, while the intervention group received additional intensive health education provided by trained volunteers. The effectiveness of the intervention was assessed by comparing outcomes such as lifestyle factors, BMI control, treatment adherence, hypertension control, and DLP and MAU status between the two groups before and after a two-year intervention period. The health education intervention resulted in significant reductions in dietary risk factors, specifically in fruit and vegetable consumption (p < 0.001). There was a lower prevalence of high salt intake in the intervention group compared to the control group (p = 0.002), while no significant differences were observed in other dietary factors. Smoking habits and low physical activity significantly decreased in the intervention group, with a notable disparity in physical activity proportions (p < 0.001). Both groups showed significant improvements in achieving hypertension management targets, with the intervention group demonstrating superior outcomes. The intervention was effective in reducing the prevalence of risk factors, particularly treatment non-adherence, blood pressure control, and low physical activity. Additionally, the intervention group had a higher likelihood of achieving DLP and MAU control compared to the control group. This study underscored the additional positive impact of incorporating health education by non-professional educators in achieving favorable outcomes, including better control of BMI, blood pressure, medication adherence, and management of dyslipidemia (DLP) and microalbuminuria (MAU). Further research is warranted to fully explore the potential of health education in primary healthcare settings and maximize its effectiveness.

Reno- and cardioprotective molecular mechanisms of SGLT2 inhibitors beyond glycemic control - from bedside to bench.

Large placebo-controlled clinical trials have shown that sodium-glucose cotransporter-2 inhibitors (SGLT2i) delay the deterioration of renal function and reduce cardiovascular events in a glucose-independent manner, thereby ultimately reducing mortality in patients with chronic kidney disease (CKD) and/or heart failure. These exiting clinical data stimulated preclinical studies aiming to understand the observed clinical effects. In animal models, it was shown that the beneficial effect of SGLT2i on the tubuloglomerular feedback (TGF) improves glomerular pressure and reduces tubular workload by improving renal haemodynamics, which appears to be dependent on salt intake. High salt intake might blunt the SGLT2i effects on the TGF. Beyond the salt-dependent effects of SGLT2i on renal haemodynamics, the beneficial effects of SGLT2i on CKD progression are at least partly mediated by targeting TGF-β1 and or STAT3 and or AMPK signaling pathways affecting macrophage differentiation and polarization as well as inhibiting the activation of inflammatory factors within macrophages. As macrophages are also important cells mediating atherosclerosis and myocardial remodeling after injury, the inhibitory effects of SGLT2i on macrophage differentiation and inflammatory responses may also play a role in stabilizing atherosclerotic plaques and ameliorating myocardial inflammation and fibrosis. Recent studies suggest that SGLT2i may also act directly on the Na+/H+ exchanger and Late-INa in cardiomyocytes thus reducing Na+ and Ca2+ overload-mediated myocardial damage, but studies in this area are limited. In addition, the renal-cardioprotective mechanisms of SGLT2i include systemic effects on the sympathetic nervous system, blood volume, salt excretion and energy metabolic patterns.

T helper cell polarity determines salt sensitivity and hypertension development.

High-salt intake is known to induce pathogenic T helper (Th) 17 cells and hypertension, but contrary to what is known, causes hypertension only in salt-sensitive (SS) individuals. Thus, we hypothesized that Th cell polarity determines salt sensitivity and hypertension development. Cultured splenic T cells from Dahl SS and salt-resistant (SR) rats subjected to hypertonic salt solutions were evaluated via ELISA, flow cytometry, immunocytochemistry and RT-qPCR. Seven-week-old SS and SR rats were fed a chow (CD) or high-salt diet (HSD) for 4 weeks, with weekly measurements of systolic blood pressure. The relaxation response of the aorta rings to the cumulative addition of acetylcholine was measured ex vivo. In these experimental animals, the Th cell polarity (Th17 and T regulatory [Treg]), the expression of Th17- or Treg-related genes, and the enrichment of the transcription factors RORγt and FOXP3 on the target gene promoter regions were determined via flow cytometry, RT-qPCR, and chromatin immunoprecipitation. Hypertonic salt solution induced Th17 and Treg cell differentiation in cultured splenic T cells isolated from SS and SR rats, respectively. HSD induced hypertension, endothelial dysfunction and proinflammatory Th17 cell differentiation only in SS rats. The enrichment of RORγt on the promoter regions of Il17a and Il23r increased their expression only in SS rats. Regardless of HSD, SR rats remained normotensive with Treg polarity, causing high Treg-related gene expressions (Il10, Cd25 and Foxp3). This study demonstrated that Th cell polarity determines salt sensitivity and drives hypertension development. SR rats were protected from HSD-associated hypertension via anti-inflammatory Treg polarity.

Generalization of contextual fear is sex-specifically affected by high salt intake.

A hallmark symptom of many anxiety disorders, and multiple neuropsychiatric disorders more broadly, is generalization of fearful responses to non-fearful stimuli. Anxiety disorders are often comorbid with cardiovascular diseases. One established, and modifiable, risk factor for cardiovascular diseases is salt intake. Yet, investigations into how excess salt consumption affects anxiety-relevant behaviors remains little explored. Moreover, no studies have yet assessed how high salt intake influences generalization of fear. Here, we used adult C57BL/6J mice of both sexes to evaluate the influence of two or six weeks of high salt consumption (4.0% NaCl), compared to controls (0.4% NaCl), on contextual fear acquisition, expression, and generalization. Further, we measured osmotic and physiological stress by quantifying serum osmolality and corticosterone levels, respectively. Consuming excess salt did not influence contextual fear acquisition nor discrimination between the context used for training and a novel, neutral context when training occurred 48 prior to testing. However, when a four week delay between training and testing was employed to induce natural fear generalization processes, we found that high salt intake selectively increases contextual fear generalization in females, but the same diet reduces contextual fear generalization in males. These sex-specific effects were independent of any changes in serum osmolality nor corticosterone levels, suggesting the behavioral shifts are a consequence of more subtle, neurophysiologic changes. This is the first evidence of salt consumption influencing contextual fear generalization, and adds information about sex-specific effects of salt that are largely missing from current literature.

The Relationship Between Knowledge and Long Suffering from Hypertension with Low-Salt Diet Control for Hypertension Patients at the Antang Makassar Health Centre

Hypertension at a young age should not be underestimated because of its increasing prevalence so it is necessary to do prevention early, especially related to low-salt diet control. Public knowledge about a low-salt diet to lower blood pressure is still minimal even though a low-salt diet is very necessary because high salt intake can be detrimental to health, especially in the cardiovascular system. Purpose: The purpose of this study was to know the relationship between knowledge and duration of suffering from hypertension with low-salt diet control in patients with hypertension in the Working Area of Antang Health Center Makassar City. This study used quantitative research methods with a cross sectional study research design. Sampling using purposive sampling with the number of samples obtained as many as 50 respondents. Data were collected using knowledge, long suffering, and low-salt diet control questionnaires. Data analysis using SPSS 24 with chi square statistical test found a relationship between knowledge of low-salt diet control with a value of ρ=0.001&lt;α=0.05, and no relationship between the length of suffering from hypertension to low-salt diet control with a value of ρ=0.000&lt;α=0.48. The conclusion in this study is that there is a relationship between knowledge and low-salt diet control in hypertensive patients and there is no relationship between long suffering from hypertension and low-salt diet control at Antang Health Center Makassar City. It is expected that people with hypertension can control a low-salt diet as one way to prevent an increase in blood pressure. For nurses, it is expected to provide information or health education about low-salt diet control in people with hypertension. Keywords: Hypertension, Knowledge, long suffering from hypertension, Low Salt Diet Control

A Mechanistic Insight into Beneficial Effects of Polyphenols in the Prevention and Treatment of Nephrolithiasis: Evidence from Recent In Vitro Studies

Nephrolithiasis is a pathological condition characterized by the formation of solid crystals in the kidneys or other parts of urinary tract. Kidney stones are a serious public health issue and financial burden for health care system, as well as a painful and uncomfortable condition for patients, resulting in renal tissue injury in severe cases. Dietary habits, low fluid and high salt intake predominantly, contribute to the development of kidney stones. Current research suggests that polyphenols have a protective effect in the pathogenesis of kidney stones. Polyphenols are a group of naturally occurring compounds found in plant-based foods such as fruits, vegetables, tea, and coffee. In this review, we explore mechanisms underlying the beneficial effects of polyphenols, such as oxidative stress reduction and modulation of inflammatory pathways, in various in vitro models of nephrolithiasis. Additionally, certain polyphenols, such as catechins found in green tea, have been shown to inhibit the formation and growth of kidney stones in animal studies. This review highlights the antioxidant and anti-inflammatory effects, as well as the inhibition of crystal formation, as results of polyphenol treatment in vitro. Further research is required to determine the specific effects of polyphenols on kidney stone formation in humans; however, current knowledge implicates that incorporating a variety of polyphenol-rich foods into the diet may be a beneficial strategy for individuals at risk of developing nephrolithiasis.

Excessive sodium chloride ingestion promotes inflammation and kidney fibrosis in aging mice.

In aging kidneys, a decline of function resulting from extracellular matrix (ECM) deposition and organ fibrosis is regarded as "physiological." Whether a direct link between high salt intake and fibrosis in aging kidney exists autonomously from arterial hypertension is unclear. This study explores kidney intrinsic changes (inflammation, ECM derangement) induced by a high-salt diet (HSD) in a murine model lacking arterial hypertension. The contribution of cold shock Y-box binding protein (YB-1) as a key orchestrator of organ fibrosis to the observed differences is determined by comparison with a knockout strain (Ybx1ΔRosaERT+TX). Comparisons of tissue from mice fed with normal-salt diet (NSD, standard chow) or high-salt diet (HSD, 4% NaCl in chow; 1% NaCl in water) for up to 16 mo revealed that with HSD tubular cell numbers decrease and tubulointerstitial scarring [periodic acid-Schiff (PAS), Masson's trichrome, Sirius red staining] prevails. In Ybx1ΔRosaERT+TX animals tubular cell damage, a loss of cell contacts with profound tubulointerstitial alterations, and tubular cell senescence was seen. A distinct tubulointerstitial distribution of fibrinogen, collagen type VI, and tenascin-C was detected under HSD, transcriptome analyses determined patterns of matrisome regulation. Temporal increase of immune cell infiltration was seen under HSD of wild type, but not Ybx1ΔRosaERT+TX animals. In vitro Ybx1ΔRosaERT+TX bone marrow-derived macrophages exhibited a defect in polarization (IL-4/IL-13) and abrogated response to sodium chloride. Taken together, HSD promotes progressive kidney fibrosis with premature cell aging, ECM deposition, and immune cell recruitment that is exacerbated in Ybx1ΔRosaERT+TX animals.NEW & NOTEWORTHY Short-term experimental studies link excessive sodium ingestion with extracellular matrix accumulation and inflammatory cell recruitment, yet long-term data are scarce. Our findings with a high-salt diet over 16 mo in aging mice pinpoints to a decisive tipping point after 12 mo with tubular stress response, skewed matrisome transcriptome, and immune cell infiltration. Cell senescence was aggravated in knockout animals for cold shock Y-box binding protein (YB-1), suggesting a novel protective protein function.

Effects of a high salt diet on blood pressure dipping and the implications on hypertension.

High blood pressure, also known as hypertension, is a major risk factor for cardiovascular disease. Salt intake has been shown to have a significant impact on BP, but the mechanisms by which it influences the blood pressure dipping pattern, and 24-h blood pressure remains controversial. This literature review aims to both summarize the current evidence on high salt diet induced hypertension and discuss the epidemiological aspects including socioeconomic issues in the United States and abroad. Our review indicates that a high salt diet is associated with a blunted nocturnal blood pressure dipping pattern, which is characterized by a reduced decrease in blood pressure during the nighttime hours. The mechanisms by which high salt intake affects blood pressure dipping patterns are not fully understood, but it is suggested that it may be related to changes in the sympathetic nervous system. Further, we looked at the association between major blood pressure and circadian rhythm regulatory centers in the brain, including the paraventricular nucleus (PVN), suprachiasmatic nucleus (SCN) and nucleus tractus solitarius (nTS). We also discuss the underlying social and economic issues in the United States and around the world. In conclusion, the evidence suggests that a high salt diet is associated with a blunted, non-dipping, or reverse dipping blood pressure pattern, which has been shown to increase the risk of cardiovascular disease. Further research is needed to better understand the underlying mechanisms by which high salt intake influences changes within the central nervous system.

Intestinal Cckbr-specific knockout mouse as a novel model of salt-sensitive hypertension via sodium over-absorption.

To investigate the value of CCKBRfl/fl villin-Cre mice as a mouse model of salt-sensitive hypertension (SSH). In the first part, 2-month-old CCKBRfl/fl villin-Cre mice (CKO) and control CCKBRfl/fl mice (WT) were fed with normal diet (0.4% NaCl) or high salt diet (4% NaCl), separately for 6 weeks. In the rescue study, one week of hydrochlorothiazide or saline injection were treated with the CKO mice fed high salt diet. The blood pressure, biochemical indexes, and the expression of small intestinal sodium transporters (NHE3, NKCC1, eNaC) was detected. The organ injury markers (MMP2/MMP9) and the histopathological changes of kidneys were observed, whereas the changes of duodenal sodium absorption were detected by small intestinal perfusion in vivo. The CCKBRfl/fl villin-Cre mice with high salt intake exhibited high blood pressure, increased duodenal sodium absorption and urinary sodium excretion, and with renal injury. The protein expression of NHE3, NKCC1 and eNaC were also significant increase in the intestine of CKO-HS mice. Treatment with hydrochlorothiazide remarkably attenuated the elevated blood pressure by high salt absorption in the CCKBRfl/fl villin-Cre mice, but no significant histopathological changes were observed. These results support a crucial role of intestinal Cckbr deficiency on SSH development and the diuretic antihypertension effect in CCKBRfl/fl villin-Cre mice. The CCKBRfl/fl villin-Cre mice with the high salt intake may serve as a stable model of salt-sensitive hypertensive induced by sodium overloading.