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One of the kidney's major functions is to adjust the water and sodium balance in order to maintain a state of equilibrium. In the course of aging, even in the absence of renal pathology, changes are observed not only in renal macrostructure (reduction in kidney size, increase in the number of cysts), but also in microstructure (arteriosclerosis, glomerulosclerosis, fibrosis and tubular atrophy). All these changes can disrupt the homeostasis of water and sodium balances. The aim of this article is to review the physiology of water and sodium stores, and to assess the impact of aging on the regulatory loops of these different systems.

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Background: Herbal medicine Oryeongsan (ORS), also known as Wulingsan in Chinesehas been used for the treatment of impaired body fluid balance. However, the mechanisms involved are not clearly defined. The purpose of the present study was to identify the actions of ORS on the renal excretory function and blood pressure (BP) and to define the mechanisms involved in association with renin-angiotensin system (RAS) and natriuretic peptide system (NPS) in spontaneously hypertensive rats (SHR), an animal model of human essential hypertension. Methods: Changes in urine volume (UV), excretion of electrolytes including Na+ (urinary excretion of Na+ (UNaV)) were measured. RT-PCR was performed to trace the changes in expression of RAS, NPS and sodium (Na+)-hydrogen (H+) exchanger 3 (NHE3) in the renal cortex. Results: In the SHR treated with vehicle (SHR-V) group, UV and UNaV were suppressed and the Na+ balance was maintained at the higher levels leading to an increase in BP compared to WKY-V group. These were accompanied by an increase in NHE3 expression with an accentuation of angiotensin I converting enzyme-angiotensin II type 1 (ACE-AT1) receptor and concurrent suppression of angiotensin II type 2 (AT2) receptor/ACE2-Mas receptor expression in the renal cortex. Chronic treatment with ORS increased UV and UNaV, and decreased the Na+ and water balance with a decrease in BP in the ORS-treated SHR-ORS group compared to SHR-V. These were accompanied by a decrease in NHE3 expression with a suppression of ACE-AT1 receptor and concurrent accentuation of AT2/ACE2-Mas receptor. Conclusion: The present study shows that ORS reduced BP with a decrease in Na+ and water retention by a suppression of NHE3 expression via modulation of RAS and NPS in SHR. The present study provides pharmacological rationale for the treatment of hypertension with ORS in SHR.

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Consumption of salt (NaCl) and potassium (K+) has been completely modified, switching from a rich-K+/low-NaCl diet in the hunter-gatherer population to the opposite in the modern, westernized population. The ability to conserve K+ is crucial to maintain the plasma K+ concentration in a physiological range when dietary K+ intake is decreased. Moreover, a chronic reduction in the K+ intake is correlated with an increased blood pressure, an effect worsened by a high-Na+ diet. The renal adaptation to a low-K+ diet in order to maintain the plasma K+ level in the normal range is complex and interconnected with the mechanisms of the Na+ balance. In this short review, we will recapitulate the general mechanisms allowing the plasma K+ value to remain in the normal range, when there is a necessity to retain K+ (response to low-K+ diet and adaptation to gestation), by focusing on the processes occurring in the most distal part of the nephron. We will particularly outline the mechanisms of K+ reabsorption and discuss the consequences of its absence on the Na+ transport systems and the regulation of the extracellular compartment volume and blood pressure.

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INTRODUCTION: Adherence to a low-sodium (Na) diet is crucial in patients under hemodialysis, as it improves cardiovascular outcomes and reduces thirst and interdialytic weight gain. Recommended salt intake is lower than 5 g/day. The new 6008 CAREsystem monitors incorporate a Na module that offers the advantage of estimating patients' salt intake. The objective of this study was to evaluate the effect of dietary Na restriction for 1 week, monitored with the Na biosensor. METHODS: A prospective study was conducted in 48 patients who maintained their usual dialysis parameters and were dialyzed with a 6008 CAREsystem monitor with activation of the Na module. Total Na balance, pre-/post-dialysis weight, serum Na (sNa), changes in pre- to post-dialysis sNa (ΔsNa), diffusive balance, and systolic and diastolic blood pressure were compared twice, once after 1 week of patients' usual Na diet and again after another week with more restricted Na intake. RESULTS: Restricted Na intake increased the percentage of patients on a low-Na diet (<85 Na mmol/day) from 8% to 44%. Average daily Na intake decreased from 149 ± 54 to 95 ± 49 mmol, and interdialytic weight gain was reduced by 460 ± 484 g per session. More restricted Na intake also decreased pre-dialysis sNa and increased both intradialytic diffusive balance and ΔsNa. In hypertensive patients, reducing daily Na by more than 3 g Na/day lowered their systolic blood pressure. CONCLUSIONS: The new Na module allowed objective monitoring of Na intake, which in turn could permit more precise personalized dietary recommendations in patients under hemodialysis.

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BACKGROUND: Our previous studies showed that renal medullary sphingosine-1-phosphate receptor 1 (S1PR1) mediated sodium excretion, high salt intake increased S1PR1 level, deoxycorticosterone acetate (DOCA) blocked high salt-induced S1PR1 in the renal medulla, and that conditional knockout of S1PR1 in the collecting duct aggravated DOCA-salt hypertension. The present study tested the hypothesis that overexpression of S1PR1 transgene in the renal medulla attenuates the sodium retention and hypertension in DOCA-salt mouse model. METHODS: Male C57BL/6J mice received renal medullary transfection of control or S1PR1-expressing plasmids and then DOCA-salt treatment. Renal sodium excretion and arterial pressure were compared between control and S1PR1-overexpressed mice in response to high salt loading or pressure natriuresis. RESULTS: S1PR1-transfected mice showed significantly enhanced urinary sodium excretion in response to acute sodium loading (0.93 ± 0.27 in control vs. 4.72 ± 1.12 µmol/min/gKW in S1PR1-overexpressed mice, P < 0.05) and the pressure natriuresis (3.58 ± 1.77 vs. 9.52 ± 1.38, P < 0.05), less positive sodium balance in response to chronic high-salt intake (3.05 ± 0.39 vs. 1.65 ± 0.39 mmol/72 hr, P < 0.05), and consequently, the attenuation of DOCA-salt hypertension (134.2 ± 6.79 vs. 109.8 ± 3.54 mm Hg, P < 0.05). The αENaC protein amount in the renal medulla was not changed, however, the ßENaC was significantly decreased and the γENaC was significantly increased in S1PR1-overexpressed mice. The immunostaining showed apical membrane translocation of γENaC, while no change of αENaC and ßENaC in control mice, and that the apical membrane translocation of γENaC was blocked in S1PR1-treasffected mice. CONCLUSIONS: These results suggested that activation of S1PR1 in the renal medulla attenuates DOCA-induced sodium retention and salt-sensitive hypertension associated with inhibition of ENaC.

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BACKGROUND: Sodium (Na) balance is unexplored in dialyzed children. We assessed a simplified sodium balance (sNaB) and its correlates in pediatric patients receiving maintenance dialysis. METHODS: Patients < 18 years old on hemodialysis (HD) or peritoneal dialysis (PD) in six European Pediatric Dialysis Working Group centers were recruited. sNaB was calculated from enteral Na, obtained by a 3-day diet diary, Na intake from medications, and 24-h urinary Na (uNa). Primary outcomes were systolic blood pressure and diastolic blood pressure standard deviation scores (SBP and DBP SDS), obtained by 24-h ambulatory blood pressure monitoring or office BP according to age, and interdialytic weight gain (IDWG). RESULTS: Forty-one patients (31 HD), with a median age of 13.3 (IQR 5.2) years, were enrolled. Twelve patients (29.3%) received Na-containing drugs, accounting for 0.6 (0.7) mEq/kg/day. Median total Na intake was 1.5 (1.1) mEq/kg/day, corresponding to 60.6% of the maximum recommended daily intake for healthy children. Median uNa and sNaB were 0.6 (1.8) mEq/kg/day and 0.9 (1.7) mEq/kg/day, respectively. The strongest independent predictor of sNaB in the cohort was urine output. In patients receiving HD, sNaB correlated with IDWG, pre-HD DBP, and first-hour refill index, a volume index based on blood volume monitoring. sNaB was the strongest predictor of IDWG in multiple regression analysis (ß = 0.63; p = 0.005). Neither SBP SDS nor DBP SDS correlated with sNaB. CONCLUSIONS: Na intake is higher than uNa in children on dialysis, and medications may be an important source of Na. sNaB is best predicted by urine output in the population, and it is a significant independent predictor of IDWG in children on HD. A higher resolution version of the Graphical abstract is available as Supplementary information.

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NEW FINDINGS: What is the central question of this study? Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce cardiovascular risk in patients with both diabetic and non-diabetic kidney disease: can SGLT2 inhibition improve renal pressure natriuresis (PN), an important mechanism for long-term blood pressure control, which is impaired in type 1 diabetes mellitus (T1DM)? What is the main finding and its importance? The SGLT2 inhibitor dapagliflozin did not enhance the acute in vivo PN response in either healthy or T1DM Sprague-Dawley rats. The data suggest that the mechanism underpinning the clinical benefits of SGLT2 inhibitors on health is unlikely to be due to an enhanced natriuretic response to increased blood pressure. ABSTRACT: Type 1 diabetes mellitus (T1DM) leads to serious complications including premature cardiovascular and kidney disease. Hypertension contributes importantly to these adverse outcomes. The renal pressure natriuresis (PN) response, a key regulator of blood pressure (BP), is impaired in rats with T1DM as tubular sodium reabsorption fails to down-regulate with increasing BP. We hypothesised that sodium-glucose cotransporter 2 (SGLT2) inhibitors, which reduce cardiovascular risk in kidney disease, would augment the PN response in T1DM rats. Non-diabetic or T1DM (35-50 mg/kg streptozotocin i.p.) adult male Sprague-Dawley rats were anaesthetised (thiopental 50 mg/kg i.p.) and randomised to receive either dapagliflozin (1 mg/kg i.v.) or vehicle. Baseline sodium excretion was measured and then BP was increased by sequential arterial ligations to induce the PN response. In non-diabetic animals, the natriuretic and diuretic responses to increasing BP were not augmented by dapagliflozin. Dapagliflozin induced glycosuria, but this was not influenced by BP. In T1DM rats the PN response was impaired. Dapagliflozin again increased urinary glucose excretion but did not enhance PN. Inhibition of SGLT2 does not enhance the PN response in rats, either with or without T1DM. SGLT2 makes only a minor contribution to tubular sodium reabsorption and does not contribute to the impaired PN response in T1DM.

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About 5% of patients with heart failure (HF) reach the end-stage of disease, becoming refractory to therapy. The clinical course of end-stage HF is characterized by repeated hospitalizations, severe symptoms, and poor quality of life. Peritoneal ultrafiltration (PUF), removing water and sodium (Na+), can benefit patients with end-stage HF. However, effects on fluid and electrolyte removal have not been fully characterized. In this pilot study in patients with chronic HF and moderate chronic renal failure, we evaluated the effects of water and sodium removal through PUF on ventricular remodeling, re-hospitalization, and quality of life. Patients with end-stage HF (NYHA class IV, ≥3 HF hospitalization/year despite optimal therapy), not eligible for heart transplantation underwent peritoneal catheter positioning and began a single-day exchange with icodextrin at night (n=6), or 1-2 daily exchanges with hypertonic solution (3.86%) for 2 hours with 1.5-2 L fill volume (n=3). At baseline, average ultrafiltration was 500±200 ml with icodextrin, and 700±100 ml with hypertonic solution. Peritoneal excretion of Na+ was greater with icodextrin (68±4 mEq/exchange) compared to hypertonic solution (45±19 mEq/exchange). After a median 12-month follow-up, rehospitalizations decreased, while NYHA class and quality of life (by Minnesota Living with HF questionnaire), improved. In end-stage HF patients, PUF reduced re-hospitalization and improved quality of life. It can be an additional treatment to control volume and sodium balance.

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Background: The potassium ion (K+) plays an important role in maintaining plant growth and development, while excess potassium in the soil can cause stress to plants. The understanding of the molecular mechanism of plant's response to high KCl stress is still limited. Methods: At the seed stage, wild type (WT) and SENSITIVE TO SALT1 (SES1) mutants were exposed to different concentrations of potassium treatments. Tolerance was assayed as we compared their performances under stress using seedling establishment rate and root length. Na+content, K+content, and K+/Na+ ratio were determined using a flame atomic absorption spectrometer. In addition, the expressions of KCl-responding genes and ER stress-related genes were also detected and analyzed using qRT-PCR. Results: SES1 mutants exhibited seedling establishment defects under high potassium concentration conditions and exogenous calcium partially restored the hypersensitivity phenotype of ses1 mutants. The expression of some K+ transporter/channel genes were higher in ses1-2, and the ratio of potassium to sodium (K+/Na+) in ses1-2 roots decreased after KCl treatment compared with WT. Further analysis showed that the ER stress marker genes were dramatically induced by high K+ treatment and much higher expression levels were detected in ses1-2, indicating ses1-2 suffers a more serious ER stress than WT, and ER stress may influence the seedling establishment of ses1-2 under high KCl conditions. Conclusion: These results strongly indicate that SES1 is a potassium tolerance relevant molecule that may be related to maintaining the seedling K+/Na+ balance under high potassium conditions during seedling establishment and post-germination growth. Our results will provide a basis for further studies on the biological roles of SES1 in modulating potassium uptake, transport, and adaptation to stress conditions.

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The different formulae for resuscitation therapy after thermal damage recommend 0.5-0.6 mmol sodium for each % TBSA burned, suggesting fluid requirements from 2-4 ml/kg/% burn because of sodium loss in burned and unburned tissues. There is a gap especially in the recommendations regarding dysnatremia in the burn population. Many studies have focused on calculating amount of resuscitation fluids, avoiding the situation of "fluid creep", and not on calculating sodium remaining in the body after resuscitation. The goal of this observational study was to provide data for sodium disturbances in the shock period after burns. Our study underscores the challenge of understanding whether there is a relationship between amount of crystalloid fluids given during resuscitation and meeting sodium needs. We set out to examine sodium balance (sodium deficit, received, excreted, and retained) after burns. The area under the ROC curve was performed by analyzing fluid and sodium load. Moreover, we conducted linear regression to analyze if there was a correlation between sodium retained and sodium excreted. Sodium deficit persisted until the second 24h despite resuscitation. Resuscitation was performed using Parkland formula, but urine output (UO) values were higher than expected. The threshold for fluid administration (ml/kg/%) or fluid load in the first 24h and sodium load (mmol/kg/%) for positive state (sodium received >0.5-0.6 mmol/kg/%) was 3.7 ml/kg/%. With linear regression, it was evident that sodium excreted was responsible for sodium retained, indicating a moderate correlation in the first 24h and a strong correlation in the second 24h. Resuscitation with LR did not correct hypoosmolality hyponatremia, which persisted even after the first 24h, especially in patients with burns >60%. If more than 3.7 ml/kg/% of LR is given, a sodium load higher than the normal level will be introduced, leading to increased urinary output, elevated sodium excretion, and non-correction of plasma sodium at the end of resuscitation. What is important for colleagues in clinical practice is that the focus of burn resuscitation should be expanded with data regarding sodium balance and the impact of dysnatremias in morbidity and mortality.

Les différentes formules de remplissage initial après brûlure recommandent l'apport de 0,5 à 0,6 mmol de Na pour chaque pour cent de surface brûlé avec un volume de 2 à 4 mL/kg/% (en attirant l'attention sur le risque de sur-remplissage), en raison des pertes sodées tant en zone brûlée qu'en zone saine. Les dysnatrémies, fréquentes chez les brûlés, peuvent s'expliquer par le peu de cas fait au contenu sodique total après le remplissage initial. Le but de cette étude observationnelle était de recueillir des données concernant les déséquilibres sodés pendant la période du choc initial. Elle souligne la nécessité de comprendre s'il existe une relation ente le volume perfusé et les apports sodés nécessaires. Nous avons calculé le bilan sodé (Na perdu, apporté, excrété, retenu) après une brûlure. L'aire sous la courbe ROC a été réalisée en analysant les apports liquidien et sodé. De plus, nous avons effectué une régression linéaire à la recherche d'une corrélation entre Na excrété et Na retenu. Le déficit en sodium persiste à h48, malgré le remplissage, utilisant la formule de Parkland, constatant que les diurèses étaient supérieures à celles attendues. Le seuil de volume perfusé dans les 24 premières heures permettant l'apport de 0,5 à 0,6 mmol/kg/% de Na était de 3,7 mL/kg/%. En régression linéaire, la corrélation entre Na retenu et Na secrété est modérée pendant les premières 24 h, forte le jour suivant. Le remplissage au Ringer-lactate ne corrigeait ni l'hypoosmolalité ni l'hyponatrémie, qui persistaient après h24, en particulier chez les brûlés >60 %. Au delà de 3,7 mL/kg de RL pendant les 24 premières heures, une surcharge sodée est réalisée, entraînant une augmentation de diurèse et natriurèse, la natrémie n'étant pas corrigée en fin de remplissage. Il faut retenir pour la pratique clinique que l'attention doit être portée sur l'équilibre sodé. L'impact des dysnatrémies sur morbidité et mortalité devrait être étudié.

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PURPOSE: We aimed to provide an extended analysis of the physiological handling of of the sodium burden induced by maintenance fluids. MATERIALS AND METHODS: We revisited two studies that demonstrated, in healthy volunteers and in surgical patients, that maintenance fluids with 154 mmol/L of sodium lead to a more positive fluid balance than a regimen containing 54 mmol/L. We report different unpublished data on the renal handling of the imposed sodium burdens with specific attention to the resulting fluid and sodium balances. RESULTS: The kidneys adapt to the sodium-rich fluids not only by altering sodium excretion, but also by retaining extra free water by concentrating urine. Realigning urinary sodium excretion with an increased administration takes around one day in health and much longer in the clinical setting. This difference may be explained by the presence of hypovolemia-induced aldosterone secretion in the latter group. Non-osmotic storage of sodium limits an unrestrained fluid retention even when very high amounts of sodium are administered but fluid accumulation will inevitably be further prolonged. CONCLUSIONS: Sodium administration induced by sodium-rich maintenance fluids leads, especially in the clinical setting, to prolonged fluid retention when compared with a regimen that resembles a healthy dietary sodium intake, even when kidney function is normal.

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The original studies demonstrating the efficacy of oral glucose-electrolytes solutions in reducing or eliminating the need for intravenous therapy to correct dehydration caused by acute watery diarrheas (AWD) were focused chiefly on cholera patients. Later research adapted the oral therapy (ORT) methodology for treatment of non-cholera AWDs including for pediatric patients. These adaptations included the 2:1 regimen using 2 parts of the original WHO oral rehydration solution (ORS) formulation followed by 1 part additional plain water, and a "low sodium" packet formulation with similar average electrolyte and glucose concentrations when dissolved in the recommended volume of water. The programmatic desire for a single ORS packet formulation has led to controversy over use of the "low sodium" formulations to treat cholera patients. This is the subject of the current review, with the conclusion that use of the low-sodium ORS to treat cholera patients leads to negative sodium balance, leading to hyponatremia and, in severe cases, particularly in pediatric cholera, to seizures and other complications of sodium depletion. Therefore it is recommended that two separate ORS packet formulations be used, one for cholera therapy and the other for non-cholera pediatric AWD.

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(Pro)renin receptor (PRR), a 350-amino acid receptor initially thought of as a receptor for the binding of renin and prorenin, is multifunctional. In addition to its role in the renin-angiotensin system (RAS), PRR transduces several intracellular signaling molecules and is a component of the vacuolar H+-ATPase that participates in autophagy. PRR is found in the kidney and particularly in great abundance in the cortical collecting duct. In the kidney, PRR participates in water and salt balance, acid-base balance, and autophagy and plays a role in development and progression of hypertension, diabetic retinopathy, and kidney fibrosis. This review highlights the role of PRR in the development and function of the kidney, namely, the macula densa, podocyte, proximal and distal convoluted tubule, and the principal cells of the collecting duct, and focuses on PRR function in body fluid volume homeostasis, blood pressure regulation, and acid-base balance. This review also explores new advances in the molecular mechanism involving PRR in normal renal health and pathophysiological states.

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BACKGROUND: The worldwide spread of SARS-CoV-2 has infected millions of people leading to over 0.3 million mortalities. The disruption of sodium homeostasis, tends to be a common occurrence in patients with COVID-19. METHODS AND RESULTS: A total of 1,254 COVID-19 patients comprising 124 (9.9%) hyponatremic patients (under 135 mmol/L) and 30 (2.4%) hypernatremic patients (over 145 mmol/L) from three hospitals in Hubei, China, were enrolled in the study. The relationships between sodium balance disorders in COVID-19 patients, its clinical features, implications, and the underlying causes were presented. Hyponatremia patients were observed to be elderly, had more comorbidities, with severe pneumonic chest radiographic findings. They were also more likely to have a fever, nausea, higher leukocyte and neutrophils count, and a high sensitivity C-reactive protein (HS-CRP). Compared to normonatremia patients, renal insufficiency was common in both hyponatremia and hypernatremia patients. In addition, hyponatremia patients required extensive treatment with oxygen, antibiotics, and corticosteroids. The only significant differences between the hypernatremia and normonatremia patients were laboratory findings and clinical complications, and patients with hypernatremia were more likely to use traditional Chinese medicine for treatment compared to normonatremia patients. This study indicates that severity of the disease, the length of stay in the hospital of surviving patients, and mortality were higher among COVID-19 patients with sodium balance disorders. CONCLUSION: Sodium balance disorder, particularly hyponatremia, is a common condition among hospitalized patients with COVID-19 in Hubei, China, and it is associated with a higher risk of severe illness and increased in-hospital mortality.

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Increases in the volume of the interstitial space are readily recognized clinically as interstitial edema formation in the loose connective tissue of skin, mucosa, and lung. However, the contents and the hydrostatic pressure of this interstitial fluid can be very difficult to determine even in experimental settings. These difficulties have long obscured what we are beginning to appreciate is a dynamic milieu that is subject to both intrinsic and extrinsic regulation. This review examines current concepts regarding regulation of interstitial volume, pressure, and flow and utilizes that background to address three major topics of interest that impact IV fluid administration. The first of these started with the discovery that excess dietary salt can be stored non-osmotically in the interstitial space with minimal impact on vascular volume and pressures. This led to the hypothesis that, along with the kidney, the interstitial space plays an active role in the long-term regulation of blood pressure. Second, it now appears that hypovolemic shock leads to systemic inflammatory response syndrome principally through the entry of digestive enzymes into the intestinal interstitial space and the subsequent progression of enzymes and inflammatory agents through the mesenteric lymphatic system to the general circulation. Lastly, current evidence strongly supports the non-intuitive view that the primary factor leading to inflammatory edema formation is a decrease in interstitial hydrostatic pressure that dramatically increases microvascular filtration.

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BACKGROUND: Fluid overload is frequent among hemodialysis (HD) patients. Dialysis therapy itself may favor sodium imbalance from sodium dialysate prescription. As on-line hemodiafiltration (OL-HDF) requires large amounts of dialysate infusion, this technique can expose to fluid accumulation in case of a positive sodium gradient between dialysate and plasma. To evaluate this risk, we have analyzed and compared the fluid status of patients treated with HD or OL-HDF in French NephroCare centers. METHOD: This is a cross-sectional and retrospective analysis of prevalent dialysis patients. Data were extracted from the EUCLID5 data base. Patients were split in 2 groups (HD and OL-HDF) and compared as whole group or matched patients for fluid status criteria including predialysis relative fluid overload (RelFO%) status from the BCM®. RESULTS: 2242 patients (age 71 years; female: 39%; vintage: 38 months; Charlson index: 6) were studied. 58% of the cohort were prescribed post-dilution OL-HDF. Comparing the HD and OL-HDF groups, there was no difference between HD and OL-HDF patients regarding the predialysis systolic BP, the interdialytic weight gain, the dialysate-plasma sodium gradient, and the predialysis RelFO%. The stepwise logistic regression did not find dialysis modality (HD or OL-HDF) associated with fluid overload or high predialysis systolic blood pressure. In OL-HDF patients, monthly average convective or weekly infusion volumes per session were not related with the presence of fluid overload. CONCLUSIONS: In this cross-sectional study we did not find association between the use of post-dilution OL-HDF and markers of fluid volume excess. Aligned dialysis fluid sodium concentrations to patient predialysis plasma sodium and regular monitoring of fluid volume status by bioimpedance spectroscopy may have been helpful to manage adequately the fluid status in both OL-HDF and HD patients.

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Restoring and controlling fluid volume homeostasis is still a challenge in contemporary end-stage kidney disease patients treated by intermittent hemodialysis (HD) or hemodiafiltration (HDF). This primary target is achieved by ultrafiltration (dry weight probing) and control of intradialytic sodium transfer (dialysate-plasma Na gradient). The latter task is mostly ignored in clinical practice by applying a dialysate sodium prescription uniform for all patients of the dialysis center but unaligned to individual plasma sodium levels. Depending on the patient's natremia, a positive gradient gives rise to intradialytic diffusive sodium load and postdialytic thirst. On the contrary, a negative gradient may cause unwanted diffusive sodium removal and intradialytic symptoms. To overcome these challenges, a new conductivity-based electrolyte balancing algorithm embedded in a hemodialysis machine with the aim to achieve "zero diffusive sodium balance" in HD and online HDF treatments was tested in the form of a prospective clinical trial. The study comprised two phases: a first phase with a conventional fixed-sodium dialysate (standard care phase), followed by a phase with the electrolyte balancing control (EBC) module activated (controlled care phase). The results show a reduction in the variability of the intradialytic plasma sodium concentration shift, but it is overlain by a small but statistically significant increase in the mean plasma sodium levels. However, no clinical manifestations were observed. This sodium load can be explained by the design of the algorithm based on dialysate conductivity instead of sodium concentration. Furthermore, the increase in plasma sodium can be corrected by taking into account the potassium shift during the treatment. This study showed that the EBC module incorporated in the HD machine is able to automatically individualize the dialysate sodium to the patient's plasma sodium without measuring or calculating predialytic plasma levels from previous laboratory tests. This tool has the potential to facilitate fluid management, to control diffusive sodium flux, and to improve intradialytic tolerance in daily clinical practice.

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Hyperosmotic challenges trigger a hypertensive response and natriuresis mediated by central and peripheral sensors. Here, we evaluated the importance of the carotid bodies for the hypertensive and natriuretic responses to acute and sub-chronic NaCl load in conscious rats. Male Wistar rats (250-330 g) submitted to bilateral carotid body removal (CBX) or sham surgery were used. One day after the surgery, the changes in arterial blood pressure (n = 6-7/group) and renal sodium excretion (n = 10/group) to intravenous infusion of 3 M NaCl (1.8 mL/kg b.w. during 1 min) were evaluated in non-anesthetized rats. Another cohort of sham (n = 8) and CBX rats (n = 6) had access to 0.3 M NaCl as the only source of fluid to drink for 7 days while ingestion and renal excretion were monitored daily. The sodium balance was calculated as the difference between sodium infused/ingested and excreted. CBX reduced the hypertensive (8 ± 2 mmHg, vs. sham rats: 19 ± 2 mmHg; p < 0.05) and natriuretic responses (1.33 ± 0.13 mmol/90 min, vs. sham: 1.81 ± 0.11 mmol/90 min; p < 0.05) to acute intravenous infusion of 3 M NaCl, leading to an increase of sodium balance (0.38 ± 0.11 mmol/90 min, vs. sham: -0.06 ± 0.10 mmol/90 min; p < 0.05). In CBX rats, sub-chronic NaCl load with 0.3 M NaCl to drink for 7 days increased sodium balance (18.13 ± 4.45 mmol, vs. sham: 5.58 ± 1.71 mmol; p < 0.05) and plasma sodium concentration (164 ± 5 mmol/L, vs. sham: 140 ± 7 mmol/L; p < 0.05), without changing arterial pressure (121 ± 9 mmHg, vs. sham: 116 ± 2 mmHg). These results suggest that carotid bodies are important for the maintenance of the hypertensive response to acute hypertonic challenges and for sodium excretion to both acute and chronic NaCl load.