0
selected
-
1.
[New aspects of the pathomechanism of salt-sensitive hypertension].
Sulyok, E
Orvosi hetilap. 2019;(2):43-49
Abstract
This article shortly outlines the evolution of hypertonia from risk factors to end-organ damage. The pathogenetic role of salt intake is underlined and in the light of recent clinical and experimental observations, the importance of renal and extrarenal mechanism in the development of salt-sensitive hypertension is analysed. The generally accepted concept that the inefficient renal sodium excretion and the subsequent expansion of the extracellular space is the major factor in blood pressure elevation is challenged. Evidences have been provided that the retained sodium dissociates from the volume of extracellular space and, also from the blood pressure. It has been shown that the negatively charged macromolecules in the subcutaneous interstitium bind sodium ions in osmotically inactive form and store sodium reversibly. The local tissue hypertonicity induces monocytes/macrophages invasion and activation that causes increased expression of tonicity-responsive enhancer binding protein (TonEBP) and the secretion of vascular endothelial growth factor C that result in enhanced lymphangiogenesis. The expanded lymphatic system drains the excess sodium and volume back to the circulation. The reduction of buffer function of this system may contribute to the development or to worsening of hypertension. Similar buffer and barrier functions are attributed to the glycocalyx that covers the luminal surface of vascular endothelium. It is also recognised that the high sodium intake alone is an important pathogenetic factor in end-organ damage independent of hypertension. This may be accounted for by the induction and activation of Th17 cells as well as by the increased production of several pro-inflammatory and pro-fibrotic cytokines. Orv Hetil. 2019; 160(2): 43-49.
-
2.
[Salt sensitivity and hypertension].
Chatelanat, O, Pechère-Bertschi, A, Ponte, B
Revue medicale suisse. 2019;(662):1625-1628
Abstract
The salt sensitivity of the blood pressure (SSBP) is defined as a rise or fall in blood pressure induced by a change in sodium intake. There is an interindividual variation and no strong diagnostic criteria exist to date. The SSBP may lead to underestimation of the beneficial effect of sodium restriction in some patients in meta-analyzes. High sodium intake in salt sensitive patients results in an increase in the prevalence of hypertension and target organ damage. The etiology seems to be a failure of one or more natriuretic mechanisms. Some environmental, genetic and epidemiological factors increase its susceptibility. Per se, SSBP cannot be treated, but its identification may help in preventing hypertension and adapt the treatment in some populations.
-
3.
Body Fluid-Independent Effects of Dietary Salt Consumption in Chronic Kidney Disease.
Oppelaar, JJ, Vogt, L
Nutrients. 2019;(11)
Abstract
The average dietary salt (i.e., sodium chloride) intake in Western society is about 10 g per day. This greatly exceeds the lifestyle recommendations by the WHO to limit dietary salt intake to 5 g. There is robust evidence that excess salt intake is associated with deleterious effects including hypertension, kidney damage and adverse cardiovascular health. In patients with chronic kidney disease, moderate reduction of dietary salt intake has important renoprotective effects and positively influences the efficacy of common pharmacological treatment regimens. During the past several years, it has become clear that besides influencing body fluid volume high salt also induces tissue remodelling and activates immune cell homeostasis. The exact pathophysiological pathway in which these salt-induced fluid-independent effects contribute to CKD is not fully elucidated, nonetheless it is clear that inflammation and the development of fibrosis play a major role in the pathogenic mechanisms of renal diseases. This review focuses on body fluid-independent effects of salt contributing to CKD pathogenesis and cardiovascular health. Additionally, the question whether better understanding of these pathophysiological pathways, related to high salt consumption, might identify new potential treatment options will be discussed.
-
4.
[Validity and limitations of methods to measure the intake and elimination of salt].
Jiménez Rodríguez, A, Palomo Cobos, L, Novalbos Ruiz, JP, Rodríguez Martín, A
Atencion primaria. 2019;(10):645-653
-
-
Free full text
-
Abstract
High blood pressure (HBP) is the main modifiable cardiovascular risk factor. HBP can be related to high salt intake. To measure intake, not all feeding surveys are comparable and valid. The reference procedure for assessing salt intake consists of measuring the urinary excretion of sodium in urine collected during 24hours, although alternative methods have been proposed, such as the collection of punctual and timed urine samples. In this review, we analyze which instruments allow the assessment of salt intake and which of them have provided greater validity and reliability through studies of concordance with the elimination of sodium in urine. Current food consumption surveys are inadequate because of their wide variability and relatively low correlation with the elimination of sodium in 24-hour urine. Its main limitation is the need for validation in different population groups. In primary care, salt intake should be assessed by using frequency-of-consumption questionnaires that collect foods with a high salt content, the consumption of preprepared dishes and questions that quantify the addition of salt in the preparation of food or at the table. For the validation of these questionnaires, the standard gold elimination of 24-hour urine sodium adjusted according to creatinine clearance should be used.
-
5.
New advances in renal mechanisms of high fructose-induced salt-sensitive hypertension.
Xu, CM, Yang, TX
Sheng li xue bao : [Acta physiologica Sinica]. 2018;(6):581-590
Abstract
Fructose intake has increased dramatically over the past century and the upward trend has continued until recently. Increasing evidence suggests that the excessive intake of fructose induces salt-sensitive hypertension. While the underlying mechanism is complex, the kidney likely plays a major role. This review will highlight recent advances in the renal mechanisms of fructose-induced salt-sensitive hypertension, including (pro)renin receptor-dependent activation of intrarenal renin-angiotensin system, increased nephron Na+ transport activity via sodium/hydrogen exchanger 3 and Na/K/2Cl cotransporter, increased renal uric acid production, decreased renal nitric oxide production, and increased renal reactive oxygen species production, and suggest actions based on these mechanisms that have therapeutic implications.
-
6.
Dietary Salt Restriction in Chronic Kidney Disease: A Meta-Analysis of Randomized Clinical Trials.
Garofalo, C, Borrelli, S, Provenzano, M, De Stefano, T, Vita, C, Chiodini, P, Minutolo, R, De Nicola, L, Conte, G
Nutrients. 2018;(6)
Abstract
BACKGROUND A clear evidence on the benefits of reducing salt in people with chronic kidney disease (CKD) is still lacking. Salt restriction in CKD may allow better control of blood pressure (BP) as shown in a previous systematic review while the effect on proteinuria reduction remains poorly investigated. METHODS We performed a meta-analysis of randomized controlled trials (RCTs) evaluating the effects of low versus high salt intake in adult patients with non-dialysis CKD on change in BP, proteinuria and albuminuria. RESULTS Eleven RCTs were selected and included information about 738 CKD patients (Stage 1⁻4); urinary sodium excretion was 104 mEq/day (95%CI, 76⁻131) and 179 mEq/day (95%CI, 165⁻193) in low- and high-sodium intake subgroups, respectively, with a mean difference of −80 mEq/day (95%CI from −107 to −53; p <0.001). Overall, mean differences in clinic and ambulatory systolic BP were −4.9 mmHg (95%CI from −6.8 to −3.1, p <0.001) and −5.9 mmHg (95%CI from −9.5 to −2.3, p <0.001), respectively, while clinic and ambulatory diastolic BP were −2.3 mmHg (95%CI from −3.5 to −1.2, p <0.001) and −3.0 mmHg (95%CI from −4.3 to −1.7; p <0.001), respectively. Mean differences in proteinuria and albuminuria were −0.39 g/day (95%CI from −0.55 to −0.22, p <0.001) and −0.05 g/day (95%CI from −0.09 to −0.01, p = 0.013). CONCLUSION Moderate salt restriction significantly reduces BP and proteinuria/albuminuria in patients with CKD (Stage 1⁻4).
-
7.
[Sodium, hypertension, chronic kidney diseases, and public health].
Keller, N, Krummel, T, Hannedouche, T
Nephrologie & therapeutique. 2018;:S93-S98
Abstract
Salt consumption has substantially increased these last years in our modern societies and far exceeds our needs. It has a great impact on cardiovascular and renal disease and represents a major issue in public health. The present work is a review of observational and interventional studies exploring the relationship between salt consumption, high-blood pressure and cardiovascular morbimortality in the general population but also in chronic kidney diseases.
-
8.
Population dietary salt reduction and the risk of cardiovascular disease. A scientific statement from the European Salt Action Network.
Cappuccio, FP, Beer, M, Strazzullo, P, ,
Nutrition, metabolism, and cardiovascular diseases : NMCD. 2018;(2):107-114
Abstract
The publication in the last few years of a number of prospective observational studies suggesting a J-shaped association between levels of salt (sodium) consumption and cardiovascular outcomes has opened a debate on the pertinence of population-wide salt reduction policies to reduce cardiovascular disease burden, and some have even questioned the global World Health Organization guidelines, that recommend a 30% reduction in salt consumption by 2025, aiming at an ideal target of no more than 5 g of salt consumption per day. In September 2018 the European Salt Action Network (E.S.A.N.), after appraising the quality of publications questioning the appropriateness of population salt reduction, discussed the scientific evidence and identified the pitfalls of recent data. The new evidence was deemed inadequate and, in places, biased by flawed methodology. These were identified in the biased assessment of sodium intake from spot urine and the use of the Kawasaki formula, the biased assessment of the sodium-outcome relationships in prospective observational studies using spot urine samples, the impact of reverse causality in such studies, the inadequate analytical approaches to data analysis, the lack of biological plausibility and the lack of precision in assessing long-term salt consumption, as recently demonstrated in studies using more stringent quality features in their study designs. On the basis of such appraisal, the E.S.A.N. agreed a statement confirming the support to the implementation of national and regional programmes of moderate reduction in salt intake, as recommended by the World Health Organization.
-
9.
Recognition and Management of Pediatric Salt Toxicity.
Blohm, E, Goldberg, A, Salerno, A, Jenny, C, Boyer, E, Babu, K
Pediatric emergency care. 2018;(11):820-824
Abstract
OBJECTIVES Immediate recognition of salt toxicity and aggressive resuscitative measures are critical in the treatment of this lethal poisoning. Despite heroic measures, pediatric deaths due to salt toxicity still occur from irreversible neurological damage. The objective of this article is to review the relevant literature and offer a therapeutic algorithm for the management of pediatric patients presenting with salt toxicity. METHODS A literature search for cases of salt toxicity was conducted. Articles in English that were available electronically through PubMed and Google Scholar were reviewed. RESULTS Nineteen cases and case series of salt toxicity were located using our search strategy. Salt poisoning has a distinct pathophysiology compared with hypernatremia, most notable for the lack of formation of idiogenic osmoles. CONCLUSIONS The approach to treatment differs between salt toxicity and hypernatremia, focusing on rapid correction of serum osmolality rather than gradual normalization of serum sodium concentrations. Consultation of nephrology and child protection services are strongly recommended in the comprehensive treatment approach.
-
10.
Conflicting Evidence on Health Effects Associated with Salt Reduction Calls for a Redesign of the Salt Dietary Guidelines.
Graudal, N, Jürgens, G
Progress in cardiovascular diseases. 2018;(1):20-26
Abstract
Ninety-five percent of the World's populations have a mean salt intake between 6 and 12 g, which is much lower than the tolerated daily level of up to 55 g/d. In spite of this, the recommended upper level by many health institutions is as low as 5.8 g/day. When reviewing the evidence for an upper level of 5.8 g/day, it becomes apparent that neither the supporting studies selected by the health institutions, nor randomized controlled trials and prospective observational studies disregarded by the health institutions, document that a salt intake below this 5.8 g, has beneficial health effects. Although there is an association between salt intake and blood pressure, both in randomized controlled trials and in observational studies, this association is weak, especially in non-obese individuals with normal blood pressure. Furthermore a salt intake below 5.8 g is associated with the activation of the renin-angiotensin-aldosteron system, an increase in plasma lipids and increased mortality. A redesign of the salt dietary guidelines, therefore, seems to be needed.