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Nutritional and pharmacological therapies represent the basis for non-dialysis management of CKD patients. Both kinds of treatments have specific and unchangeable features and, in certain cases, they also have a synergic action. For instance, dietary sodium restriction enhances the anti-proteinuric and anti-hypertensive effects of RAAS inhibitors, low protein intake reduces insulin resistance and enhances responsiveness to epoetin therapy, and phosphate restriction cooperates with phosphate binders to reduce the net phosphate intake and its consequences on mineral metabolism. It can also be speculated that a reduction in either protein or salt intake can potentially amplify the anti-proteinuric and reno-protective effects of SGLT2 inhibitors. Therefore, the synergic use of nutritional therapy and medications optimizes CKD treatment. Quality of care management is improved and becomes more effective when compared to either treatment alone, with lower costs and fewer risks of unwanted side effects. This narrative review summarizes the established evidence of the synergistic action carried out by the combination of nutritional and pharmacological treatments, underlying how they are not alternative but complementary in CKD patient care.

Background: Idiopathic hyperaldosteronism (IHA) is one of the most common types of primary aldosteronism (PA), an important cause of hypertension. Although high dietary sodium is a major risk factor for hypertension, there is no consensus on the recommended dietary sodium intake for IHA., Objective: This study investigated the effect of a low-sodium diet on hemodynamic variables and relevant disease biomarkers in IHA patients, with the aim of providing a useful reference for clinical treatment., Methods: Fifty IHA patients were evenly randomized into two groups and provided, after a 7-day run-in period (100 mmol/d sodium), either a low-sodium diet (50 mmol/d sodium) or a normal sodium diet (100 mmol/d sodium) for an additional 7 days. After the 14-day intervention (conducted without potassium supplementation), changes in blood pressure (BP) and serum potassium were evaluated in both groups., Results: After the dietary intervention, the low sodium group exhibited, compared to the normal sodium group, decreased BP (SBP: 121.8 ± 12.8 vs . 129.9 ± 12.1 mmHg, p < 0.05; DBP: 82.6 ± 7.6 vs . 86.4 ± 8.2 mmHg, p < 0.05; MAP: 95.7 ± 8.8 vs . 100.9 ± 8.4 mmHg, p < 0.05) and increased serum potassium levels (3.38 ± 0.33 vs . 3.07 ± 0.27 mmol/L, p < 0.001). The low sodium group showed also better control of both BP and serum potassium: BP <140/90 mmHg in 70.0% of total patients (76.0% vs . 64.0%, in the low and normal sodium groups, respectively; p > 0.05), BP <130/85 mmHg in 38.0% of total patients (56.0% vs . 20.0%, p < 0.05), BP <120/80 mmHg in 28.0% of total patients (44.0% vs . 12.0%, p < 0.05); serum potassium ≥3.5 mmol/L in 22.0% of total patients (32.0% vs . 12.0% in the low and normal sodium groups, respectively; p = 0.088). There were differences between the controlled BP group (<120/80 mmHg) and the non-controlled BP group (≥120/80 mmHg) in gender, BP at baseline, and type of diet (low vs . normal sodium). Female gender and low-sodium diet were protective factors for BP control., Conclusions: A low-sodium diet is effective in lowering BP and elevating serum potassium in IHA patients. Female patients on a low-sodium diet are more likely to achieve BP control (<120/80 mmHg). We advocate a dietary sodium intake of 50 mmol/d for IHA patients., Clinical Trial Registration: https://clinicaltrials.gov, Identifier NCT05649631., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Zhou, Jiang, Zhang, Su, Jiang, Zhou, Zhong, Wu and Wang.)

The global burden of chronic kidney disease (CKD) has increased significantly over the past few decades. This reflects the rising prevalence of type 2 diabetes mellitus (T2DM) and hypertension, two leading causes of CKD. Hypertension, which can also be a complication of CKD, accelerates renal disease progression and augments cardiovascular risk, especially in individuals with diabetic kidney disease. Hence, blood pressure (BP) reduction is a vital component of CKD management. Sodium-glucose co-transporter 2 (SGLT2) inhibitors are a relatively novel class of medications developed to treat T2DM by inducing glycosuria and hence, lowering glycaemia. Additionally, SGLT2 inhibitors are antihypertensive, renoprotective and cardioprotective, even in individuals without T2DM, making them effective therapeutic agents for CKD. Another therapy that has proven to be antihypertensive, renoprotective and cardioprotective is dietary sodium restriction. This review evaluates the potential combined benefits of SGLT2 inhibition and dietary sodium restriction on the BP and renal parameters of individuals with CKD., (© 2022 The Authors. Internal Medicine Journal published by John Wiley & Sons Australia, Ltd on behalf of Royal Australasian College of Physicians.)

Nonpharmacological treatment is still an important supplement to the pharmacological treatment of hypertension. Thereby, either an elevated blood pressure can be lowered further or, alternatively, the use of antihypertensive drugs can be reduced. In the context of nonpharmacological treatment of hypertension, sodium restriction plays an important role. Sodium intake can either be reduced by lowering excessive dietary salt consumption or by the use of table salts with reduced sodium content. Lower dietary sodium consumption lowers blood pressure. This was controversial for a long time; however, now more and more observational and interventional studies have confirmed this fact. Nevertheless, some studies have shown an association of low salt consumption with increased mortality. This observation is explained by the so-called reverse epidemiology. This means that diseases with increased mortality, such as consuming diseases or severe heart diseases are associated with lowered food intake and as a consequence, with lower sodium intake. In addition to sodium restriction, the use of so-called salt substitutes with lower sodium content is also effective in lowering blood pressure. In most of the salt substitutes examined so far sodium chloride is partly replaced by potassium chloride. Numerous investigations show that these salt substitutes lower blood pressure. From a statistical point of view side effects such as hyperkalemia are very rare; however, hyperkalemia is potentially life-threatening. Therefore, the broader use of these salt substitutes is principally helpful but these salts should only be used after medical consultation. Especially renal insufficiency and the use of certain drugs, such as potassium-sparing diuretics and blockers of the renin-angiotensin system increase the risk of hyperkalemia., (© 2022. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.)

Purpose of Review: High blood pressure (BP) is the world's leading risk factor for cardiovascular disease (CVD) and death. This review highlights findings during the past 18 months that apply to the management of high BP in adults in the context of the 2017 American College of Cardiology/American Heart Association (AHA) BP guideline., Recent Findings: A comprehensive meta-analysis of clinical trials that employed a novel statistical method identified a substantially linear relationship between dietary sodium intake and BP, strongly supporting the AHA daily dietary sodium intake recommendation of less than 1500 mg/day but suggesting that any reduction in sodium intake is likely to be beneficial. Among adults with hypertension, use of a salt substitute (containing reduced sodium and enhanced potassium) led to striking reductions in CVD outcomes. Young adults with stage 1 hypertension and a low 10-year atherosclerotic CVD risk score should be started on a 6-month course of vigorous lifestyle modification; if their BP treatment goal is not achieved, a first-line antihypertensive agent should be added to the lifestyle modification intervention. In patients with stage 4 renal disease, the thiazide-like diuretic chlorthalidone (as add-on therapy) lowered BP markedly compared with placebo. Nonsteroidal mineralocorticoid receptor antagonists (MRAs) represent a new class of MRA that has been shown to lower BP and provide significant CVD protection. In Chinese adults aged 60-80 years at baseline, intensive BP control with a SBP target of 110-129 compared with 130-149 mmHg reduced CVD events with minimal side effects., Summary: Recent findings have advanced our knowledge of hypertension management, clarifying, amplifying and supporting the 2017 ACC/AHA BP guideline recommendations., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Gitelman's (GS) and Bartter's (BS) syndromes are rare, inherited autosomal recessive tubulopathies characterized by hypokalemia, metabolic alkalosis, renal sodium, chloride, and potassium and magnesium-wasting. While the treatment based on potassium, sodium, chloride, and magnesium supplementation in addition to other pharmacologic options are widely established, recommendations about the dietary approach to GS and BS still remain generic. In this review we focus on the dietary strategies to increase sodium, potassium, and magnesium intake in GS and BS patients. Potassium and magnesium-rich foods and supplements are considered together with those that may reduce through different mechanisms the potassium and magnesium plasma level. Magnesium supplementation is often poorly tolerated, causing abdominal pain and diarrhea in most patients. New formulations using liposome and, in particular, sucrosomial technology have been recently proposed for magnesium supplementation in order to increase magnesium supplement tolerability and intestinal absorption. The dietary approach to GS and BS may be very important in the therapeutic approach to these syndromes. Due to the relevance of the dietary approach to these syndromes, a nutritional counseling should always be recommended and the nutritionist should join nephrologists in the follow-up of GS and BS patient care.

Sodium intake theoretically has dual effects on both non-dialysis chronic kidney disease (CKD) patients and dialysis patients. One negatively affects mortality by increasing proteinuria and blood pressure. The other positively affects mortality by ameliorating nutritional status through appetite induced by salt intake and the amount of food itself, which is proportional to the amount of salt under the same salty taste. Sodium restriction with enough water intake easily causes hyponatremia in CKD and dialysis patients. Moreover, the balance of these dual effects in dialysis patients is likely different from their balance in non-dialysis CKD patients because dialysis patients lose kidney function. Sodium intake is strongly related to water intake via the thirst center. Therefore, sodium intake is strongly related to extracellular fluid volume, blood pressure, appetite, nutritional status, and mortality. To decrease mortality in both non-dialysis and dialysis CKD patients, sodium restriction is an essential and important factor that can be changed by the patients themselves. However, under sodium restriction, it is important to maintain the balance of negative and positive effects from sodium intake not only in dialysis and non-dialysis CKD patients but also in the general population.

Micronutrient deficiencies are widespread and disproportionately affect women and children in low- and middle-income countries (LMIC). Among various interventions, food fortification and supplementation with micronutrients have been proven to be cost-effective. The aim of the present paper is to review existing literature to assess risks of excessive intake in LMIC to then highlight programmatic changes required to maximise benefits of micronutrient interventions while minimising risks of adverse effects. While very few LMIC have national food consumption surveys that can inform fortification programmes, many more are implementing mandatory fortification programmes. The risks of inadequate micronutrient intakes were common, but risks of excessive intakes were also present for iodine, vitamin A, folic acid and iron. Excessive salt consumption, high concentrations of iodine in ground-water and excessive levels of iodisation were linked with excessive iodine intake. For vitamin A, overlapping interventions were the main risk for excessive intake; whereas for iron, contamination with iron from soil and screw-wares of millers and high iron concentration in drinking-water increased the risk of excessive intake, which could be further exacerbated with fortification. Before implementing micronutrient interventions, adherence to the basic principles of documenting evidence confirming that the deficiency in question exists and that fortification will correct this deficiency is needed. This can be supported with dietary intake assessments and biochemical screening that help diagnose nutrient deficiencies. Targeting micronutrient interventions, although programmatically challenging, should be considered whenever possible. Moreover, closer monitoring of appropriate fortification of foods and overlapping interventions is needed.

It is not unusual for those participating in ultra-endurance (> 4 hr) events to develop varying degrees of either hypohydration or hyperhydration. Yet, it is important for ultra-endurance athletes to avoid the performance limiting and potentially fatal consequences of these conditions. During short periods of exercise (< 1 hr), trivial effects on the relationship between body mass change and hydration status result from body mass loss due to oxidation of endogenous fuel stores, and water supporting the intravascular volume being generated from endogenous fuel oxidation and released with glycogen oxidation. However, these effects have meaningful implications during prolonged exercise. In fact, body mass loses well over 2% may be required during some ultra-endurance activities to avoid hyperhydration. Therefore, the typical hydration guidelines to avoid more than 2% body mass loss do not apply in ultra-endurance activities and can potentially result in hyperhydration. Fortunately, achieving the balance of proper hydration during ultra-endurance activities need not be complicated and has been well demonstrated to generally be achieved by simply drinking to thirst and avoiding excessive sodium supplementation with intention of replacing all sodium losses during the exercise.

High-salt intake is a major risk factor for developing hypertension in type 2 diabetes mellitus, but its effects on glucose homeostasis are controversial. We previously found that high-salt intake induces severe hypertension in WBN/Kob diabetic fatty (WBKDF) rats. In the present study, we examined the effects of a high-salt intake on glucose homeostasis in WBKDF rats. Male WBKDF rats and age-matched Wistar rats at 6 weeks of age were each divided into two groups and fed either a normal-sodium (NS, 0.26%) diet or high-sodium (HS, 8%) diet for 7 weeks. Systolic blood pressure and urine volume were increased in WBKDF-HS and Wistar-HS. Body weight gain and food consumption were comparable between NS and HS in both strains. Plasma and urine glucose levels were significantly increased in WBKDF-NS but not in WBKDF-HS. HOMA-IR in WBKDF-HS was significantly lower compared with that in WBKDF-NS. The high plasma adiponectin level in WBKDF-NS compared with that in Wistar-NS was further enhanced in WBKDF-HS. Glycogen deposits and fat droplets in the livers of WBKDF-HS were reduced compared with those of WBKDF-NS. The present study demonstrated that HS intake ameliorated hyperglycemia and insulin resistance in WBKDF rats, which may be due to increased plasma levels of adiponectin.

Introduction: Exertional hyponatremia (EH) during prolonged exercise involves all avenues of fluid-electrolyte gain and loss. Although previous research implicates retention of excess fluid, EH may involve either loss, gain, or no change of body mass. Thus, the etiology, predisposing factors, and recommendations for prevention are vague-except for advice to avoid excessive drinking., Purpose: This retrospective field study presents case reports of two unacquainted recreational cyclists (LC, 31y and AM, 39 years) who began exercise with normal serum electrolytes but finished a summer 164-km ride (ambient, 34±5°C) with a serum [Na+] of 130 mmol/L., Methods: To clarify the etiology of EH, their pre- and post-exercise measurements were compared to a control group (CON) of 31 normonatremic cyclists (mean ± SD; 37±6 years; 141±3 mmol Na+/L)., Results: Anthropomorphic characteristics, exercise time, and post-exercise ratings of thermal sensation, perceived exertion and muscle cramp were similar for LC, AM and CON. These two hyponatremic cyclists consumed a large and similar volume of fluid (191 and 189 ml/kg), experienced an 11 mmol/L decrease of serum [Na+], reported low thirst sensations; however, LC gained 3.1 kg (+4.3% of body mass) during 8.9 hr of exercise and AM maintained body mass (+0.1kg, +0.1%, 10.6h). In the entire cohort (n = 33), post-event serum [Na+] was strongly correlated with total fluid intake (R 2 = 0.45, p < .0001), and correlated moderately with dietary sodium intake (R 2 =0.28, p = .004) and body mass change (R 2 = 0.22, p = .02). Linear regression analyses predicted the threshold of EH onset (<135 mmol Na+/L) as 168 ml fluid/kg., Conclusions: The wide range of serum [Na+] changes (+6 to -11 mmol/L) led us to recommend an individualized rehydration plan to athletes because the interactions of factors were complex and idiosyncratic.

Computed tomography (CT) is a widely used imaging modality. Although hyponatremia after CT imaging is rare, its effects can be devastating. Hyperosmolar radiocontrast acts as effective osmoles and causes fluid migration from intracellular into extracellular compartment. Dilutional hyponatremia will ensue if translocation of fluid is in excess of diuresis. This case report detailed an unusual case of acute symptomatic hyponatremia after CT renal protocol and the treatments given after its recognition.

Aim: Managing neonatal Bartter syndrome by achieving adequate weight gain is challenging. We assessed the correlation between weight gain in neonatal Bartter syndrome and the introduction of fluid and sodium supplementations and indomethacin during the first 4 weeks of life., Methods: Daily fluid and electrolytes requirements were analysed using linear regression and Spearman correlation coefficients. The weight gain coefficient was calculated as daily weight gain after physiological neonatal weight loss., Results: We studied seven infants. The highest weight gain coefficients occurred between weeks two and four in the five neonates who either received prompt amounts of fluid (maximum 810 mL/kg/day) and sodium (maximum 70 mmol/kg/day) or were treated with indomethacin. For the two patients with the highest weight gain coefficient, water and sodium supplementations were decreased in weeks two to four leading to a significant negative Spearman correlation between weight gain and fluid supplements (r = -0.55 and -0.68) and weight gain and sodium supplementations (r = -0.96 and -0.72). The two patients with the lowest weight gain coefficient had positive Spearman correlation coefficients between weight gain and fluid and sodium supplementations., Conclusion: Infants with neonatal Bartter syndrome required rapid and enormous fluid and sodium supplementations or the early introduction of indomethacin treatment to achieve adequate weight gain during the early postnatal period., (©2015 Foundation Acta Paediatrica. Published by John Wiley & Sons Ltd.)

Background: Jellyfish envenomations are common amongst temperate coastal regions and vary in severity depending on the species. Stings result in a variety of symptoms and signs, including pain, dermatological reactions and, in some species, Irukandji syndrome (including abdominal/back/chest pain, tachycardia, hypertension, sweating, piloerection, agitation and sometimes cardiac complications). Many treatments have been suggested for the symptoms and signs of jellyfish stings. However, it is unclear which interventions are most effective., Objectives: To determine the benefits and harms associated with the use of any intervention, in both adults and children, for the treatment of jellyfish stings, as assessed from randomised trials., Search Methods: We searched the following electronic databases in October 2012 and again in October 2013: the Cochrane Central Register of Controlled Trials (CENTRAL;The Cochrane Library, Issue 9, 2013); MEDLINE via Ovid SP (1948 to 22 October 2013); EMBASE via Ovid SP (1980 to 21 October 2013); and Web of Science (all databases; 1899 to 21 October 2013). We also searched reference lists from eligible studies and guidelines, conference proceedings and the World Health Organization (WHO) International Clinical Trials Registry Platform (ICTRP) and contacted content experts to identify trials., Selection Criteria: We included randomised controlled trials that compared any intervention(s) to active and/or non-active controls for the treatment of symptoms and signs of jellyfish sting envenomation. No language, publication date or publication status restrictions were applied., Data Collection and Analysis: Two review authors independently conducted study selection and data extraction and assessed risk of bias using a standardised form. Disagreements were resolved by consensus with a third review author when necessary., Main Results: We included seven trials with a total of 435 participants. Three trials focused on Physalia (Bluebottle) jellyfish, one trial on Carukia jellyfish and three on Carybdea alata (Hawaiian box) jellyfish. Two ongoing trials were identified.Six of the seven trials were judged as having high risk of bias. Blinding was not feasible in four of the included trials because of the nature of the interventions. A wide range of interventions were assessed across trials, and a wide range of outcomes were measured. We reported results from the two trials for which data were available and reported the effects of interventions according to our definition of primary or secondary outcomes.Hot water immersion was superior to ice packs in achieving clinically significant (at least 50%) pain relief at 10 minutes (one trial, 96 participants, risk ratio (RR) 1.66, 95% confidence interval (CI) 1.01 to 2.72; low-quality evidence) and 20 minutes (one trial, 88 participants, RR 2.66, 95% CI 1.71 to 4.15; low-quality evidence). No statistically significant differences between hot water immersion and ice packs were demonstrated for dermatological outcomes.Treatment with vinegar or Adolph's meat tenderizer compared with hot water made skin appear worse (one trial, 25 participants, RR 0.31, 95% CI 0.14 to 0.72; low-quality evidence).Adverse events due to treatment were not reported in any trial., Authors' Conclusions: This review located a small number of trials that assessed a variety of different interventions applied in different ways and in different settings. Although heat appears to be an effective treatment for Physalia (Bluebottle) stings, this evidence is based on a single trial of low-quality evidence. It is still unclear what type of application, temperature, duration of treatment and type of water (salt or fresh) constitute the most effective treatment. In addition, these results may not apply to other species of jellyfish with different envenomation characteristics. Future research should further assess the most effective interventions using standardised research methodology.

Background: A growing body of evidence suggests that the fluid accumulation plays a key role in the pathophysiology of heart failure (HF) and that the inflammatory and neurohormonal activation contribute strongly to the progression of this disorder., Methods and Results: The study evaluated the long-term effects of 2 different sodium diets on cytokines neurohormones, body hydration and clinical outcome in compensated HF outpatients (New York Heart Association Class II). A total of 173 patients (105 males, mean age 72.5+/-7) recently hospitalized for worsening advanced HF and discharged in normal hydration and in clinical compensation were randomized in 2 groups (double blind). In Group 1, 86 patients received a moderate restriction in sodium (120mmol to 2.8g/day) plus oral furosemide (125 to 250mg bid); in Group 2, 87 patients: received a low-sodium diet (80mmol to 1.8g/day) plus oral furosemide (125 to 250mg bid). Both groups were followed for 12 months and the treatment was associated with a drink intake of 1000mL daily. Neurohormonal (brain natriuretic peptide, aldosterone, plasma rennin activity) and cytokines values (tumor necrosis factor-alpha, interleukin-6) were significantly reduced with a significant increase of the anti-inflammatory cytokine interleukin-10 at 12 months in normal, P < .0001) than low-sodium group. The low-sodium diet showed a significant activation of neurohormones and cytokines and worsening the body hydration, whereas moderate sodium restriction maintained dry weigh and improved outcome in the long term., Conclusions: Our results appear to suggest a surprising efficacy of a new strategy to improve the chronic diuretic response by increasing Na intake and limiting fluid intake. This counterintuitive approach underlines the need for a better understanding of factors that regulate sodium and water handling in chronic congestive HF. A larger sample of patients and further studies are required to evaluate whether this is due to the high dose of diuretic used or the low-sodium diet.

Idiopathic hypercalciuria (IH) is a common metabolic disorder in children and is associated with the development of renal calculi, nephrocalcinosis, hematuria and osteopenia. The effect of various dietary modifications and available pharmacologic therapies on reducing urinary calcium excretion and/or urinary supersaturation is discussed in this article. The importance of a multidisciplinary approach involving the patient, their families, and health-care professionals is also addressed.

Background: Tubulointerstitial damage plays an important role in chronic kidney disease (CKD) with proteinuria. Urinary kidney injury molecule 1 (KIM-1) reflects tubular KIM-1 and is considered a sensitive biomarker for early tubular damage. We hypothesized that a decrease in proteinuria by using therapeutic interventions is associated with decreased urinary KIM-1 levels., Study Design: Post hoc analysis of a randomized, double-blind, placebo-controlled, crossover trial., Setting & Participants: 34 proteinuric patients without diabetes from our outpatient renal clinic., Intervention: Stepwise 6-week interventions of losartan, sodium restriction (low-sodium [LS] diet), their combination, losartan plus hydrochlorothiazide (HCT), and the latter plus an LS diet., Outcomes & Measurements: Urinary excretion of KIM-1, total protein, and N-acetyl-beta-d-glucosaminidase (NAG) as a positive control for tubular injury., Results: Mean baseline urine protein level was 3.8 +/- 0.4 (SE) g/d, and KIM-1 level was 1,706 +/- 498 ng/d (increased compared with healthy controls; 74 ng/d). KIM-1 level was decreased by using placebo/LS (1,201 +/- 388 ng/d; P = 0.04), losartan/high sodium (1,184 +/- 296 ng/d; P = 0.09), losartan/LS (921 +/- 176 ng/d; P = 0.008), losartan/high sodium plus HCT (862 +/- 151 ng/d; P = 0.008) and losartan/LS plus HCT (743 +/- 170 ng/d; P = 0.001). The decrease in urinary KIM-1 levels paralleled the decrease in proteinuria (R = 0.523; P < 0.001), but not blood pressure or creatinine clearance. 16 patients reached target proteinuria with protein less than 1 g/d, whereas KIM-1 levels normalized in only 2 patients. Urinary NAG level was increased at baseline and significantly decreased during the treatment periods of combined losartan plus HCT only. The decrease in urinary NAG levels was not closely related to proteinuria., Limitations: Post hoc analysis., Conclusions: Urinary KIM-1 level was increased in patients with nondiabetic CKD with proteinuria and decreased in parallel with proteinuria by using losartan, sodium restriction, their combination, losartan plus HCT, and the latter plus sodium restriction. These results are consistent with the hypothesis of amelioration of proteinuria-induced tubular damage. Long-term studies are warranted to evaluate whether targeting treatment on KIM-1 can improve outcomes in patients with CKD with proteinuria.

A 58-year-old man went to his physician with complaints of midepigastric pain, flatulence, belching, and shortness of breath. During a physical examination, the patient was in no acute distress. The patient underwent an ultrasound examination, which revealed cholelithiasis, a laparoscopic cholecystectomy, which revealed chronic gallbladder disease, and esophagogastroduodenoscopy, which revealed gastritis, a hiatal hernia, and a phytobezoar. To treat the bezoar, the patient was given Adolph's Meat Tenderizer 1 teaspoonful in 8 oz of water before each meal for 7 days. This product contains papain, a proteolytic enzyme, that is thought to cleave protein linkages within bezoars. The patient's symptoms resolved with no adverse events reported, and follow-up endoscopy revealed resolution of the phytobezoar. Although a few other agents are used to treat phytobezoars, little clinical data exist on their safety and effectiveness. Adolph's Meat Tenderizer appears to be a safe and effective treatment for patients with a phytobezoar.

Iodine deficiency disorders were widely prevalent in Indian subcontinent before the successful salt iodisation. There has been a remarkable decline in goitre prevalence and improvement of functional thyroid status and normalisation of iodine nutrition status in the community. Goitre endemicity of varying degree persists among school children even a decade after successful salt iodisation in India. Some other factors like high thiocyanate exposure or auto-immune thyroid disease could be responsible for such a phenomenon.

Background: Antiproteinuric treatment by ACE inhibition (ACEi) provides renoprotection. However, resistance to antiproteinuric intervention occurs frequently, resulting in progressive renal damage. The extent of renal damage prior to treatment with ACEi reversely correlates with the antiproteinuric effects of ACEi in established adriamycin nephrosis. Sodium restriction enhances the response to ACEi, but whether it can overcome the negative predictive value of preceding renal damage on the therapeutic response is unknown. We studied the impact of preceding renal damage on the efficacy of ACEi in adriamycin nephrosis on different oral sodium loads., Methods: Male Wistar rats were randomly assigned to a low (LS), normal (NS) or high (HS) sodium diet, initiated 1 week before adriamycin induction. At week 6, proteinuria was stabilized (195 +/- 172 mg/24 h), a renal biopsy was performed for analysis of preceding damage and rats were instituted on lisinopril for 6 weeks until sacrifice at week 12., Results: ACEi reduced proteinuria in LS and NS animals. On univariate analysis, the antiproteinuric response was significantly predicted by preceding renal damage (focal glomerulosclerosis, interstitial macrophages and interstitial alpha-smooth muscle cell actin expression). On multivariate analysis, both sodium intake and preceding renal damage independently predicted residual proteinuria during ACEi (R2 model: 80% and 75% for data after 3 and 6 weeks of therapy, respectively)., Conclusion: Our data confirm the predictive value of pretreatment renal damage for the antiproteinuric response to ACEi, despite the fact that the renal damage prior to the ACEi was very mild. The impact of pretreatment damage on the therapeutic response, however, was overcome by low sodium. Thus, the impact of pretreatment damage does not warrant therapeutic nihilism, but rather optimization of therapy response by dietary sodium restriction. Further studies are needed to elucidate whether this also applies to more severe damage, and whether combining ACEi with low sodium diet can improve long-term renal outcome in human., (Copyright 2006 S. Karger AG, Basel.)

Neurally mediated reflex syncope (sometimes referred to as neurocardiogenic syncope), encompasses a group of disorders of which the best known and most frequently occurring forms are the vasovagal (or common) faint, and carotid sinus syndrome. Postmicturition syncope, defecation syncope, cough syncope, and other situational reflex faints are also included among these conditions. With the exception of carotid sinus syndrome in which cardiac pacing is effective, treatment of most neurally mediated reflex faints is shifting from reliance on various drugs to greater emphasis on education and nonpharmacologic therapy. Initial management should include counseling of patients regarding recognition of early warning symptoms, and avoidance of precipitating factors. Volume expansion with salt tablets or electrolyte-containing beverages and patient education on how to perform isometric arm contractions and/or leg crossing in order to abort impending syncope are also important. Thereafter, tilt-training has demonstrated benefit in several clinical studies. When symptoms remain despite the above-noted interventions, pharmacologic therapy with midodrine or a nonselective b-blocker can be considered. In the case of most neurally mediated reflex faints, permanent cardiac pacing should be reserved only for those older patients with significant bradycardia or asystole at time of syncope when all other interventions have failed.

Bed rest (BR) induces significant urinary and blood electrolyte changes, but little is known about the effect of fluid and salt supplements (FSS) on catabolism, hydration and electrolytes. The aim was to measure the effect of FSS on catabolism, body hydration and electrolytes during BR. Studies were done during 7 days of a pre-bed rest period and during 30 days of a rigorous bed rest period. Thirty male athletes aged, 24.6 +/- 7.6 years were chosen as subjects. They were divided into three groups: unsupplemented ambulatory control subjects (UACS), unsupplemented bed rested subjects (UBRS) and supplemented bed rested subjects (SBRS). The UBRS and SBRS groups were kept under a rigorous bed rest regime for 30 days. The SBRS daily took 30 ml water per kg body weight and 0.1 sodium chloride per kg bodyweight. Plasma sodium (Na), potassium (K), calcium (Ca) and magnesium (Mg) levels, urinary Na, K, Ca and Mg excretion, plasma osmolality, plasma protein level, whole blood hemoglobin (Hb) and hematocrit (Hct) level increased significantly (p < or = 0.05), while plasma volume (PV), body weight, body fat, peak oxygen uptake, food and fluid intake decreased significantly (p < or = 0.05) in the UBRS group when compared with the SBRS and UACS groups. In contrast, plasma and urinary electrolytes, osmolality, protein level, whole blood Hct and Hb level decreased significantly (p < or = 0.05), while PV, fluid intake, body weight and peak oxygen uptake increased significantly (p < or = 0.05) in the SBRS group when compared with the UBRS group. The measured parameters did not change significantly in the UACS group when compared with their baseline control values. The data indicate that FSS stabilizes electrolytes and body hydration during BR, while BR alone induces significant changes in electrolytes and body hydration. We conclude that FSS may be used to prevent catabolism and normalize body hydration status and electrolyte values during BR., (c2002 Published by Elsevier Science Ltd.)

We report the case of a 14-year-old boy with instantaneous orthostatic hypotension (INOH) with symptoms of orthostatic intolerance. We investigated the effect of high sodium intake on hemodynamics and circulatory responses to orthostatic stress using Portapres. Moreover, a multifrequency bioelectrical impedance method was used to confirm increased plasma volume. Although we began treatment with an alpha-adrenoceptor agonist after his admission into our hospital, the effect was not sufficient. We, therefore, began a regimen of high sodium intake (NaCl 3 g two times a day per os in addition to regular diet, NaCl 5-6 g /day) to increase plasma volume. As a result, 48 hours after sodium intake, orthostatic tolerance was markedly improved with a concomitant increase in blood pressure in the orthostatic test. By measuring the patient's body water before and after the high sodium intake, we were able to document the increase in plasma volume. We conclude that high sodium intake is an effective treatment for orthostatic hypotension in combination with vasoactive drugs.

Background and Aim: Recent clinical studies have demonstrated that plant sterols moderately lower serum cholesterol levels in patients with mild hypercholesterolemia. Furthermore, there is evidence suggesting that mineral nutrients, such as calcium and magnesium, may also decrease serum cholesterol concentrations. In this study, we tested the hypothesis that supplementation with mineral nutrients may enhance the cholesterol-lowering effect of plant sterols in obese Zucker rats. Furthermore, we compared the lipid-lowering effects of monovalent sodium and potassium cations with those of divalent calcium and magnesium cations., Methods and Results: A Western-type high-fat/high-cholesterol diet increased serum cholesterol by 175% and liver cholesterol by 65% in comparison with a low-fat/low-cholesterol control diet. On the contrary, the high-fat/high-cholesterol diet decreased intestinal cholesterol absorption, as assessed by means of serum campesterol-, sitosterol-, and sitostanol-to-cholesterol ratios, thus indicating that it was under negative feedback regulation. Supplementation of the high-fat/high-cholesterol diet with plant sterols or mineral nutrients partially prevented the diet-induced increased in serum cholesterol and, when given concurrently, their cholesterol-lowering effect was enhanced. Their combination also effectively prevented the diet-induced increase in liver cholesterol concentration, and had beneficial effects on liver and myocardial hypertrophy, and the development of obesity. These beneficial effects were at least partially mediated by an enhanced blockade of intestinal cholesterol absorption. Interestingly, only divalent cations enhanced the cholesterol-lowering effect of plant sterols, thus supporting the idea that the lipid-lowering effect of divalent cations is related to the formation of insoluble and inabsorbable calcium and magnesium chelates with fatty acids., Conclusions: Our findings indicate that the cholesterol-lowering effect of plant sterols is enhanced by the co-administration of divalent calcium and magnesium cations but not by monovalent sodium and potassium cations.

It is well known that fluid and electrolyte balance are critical to optimal exercise performance and, moreover, health maintenance. Most research conducted on extreme sporting endeavour (>3 hours) is based on case studies and studies involving small numbers of individuals. Ultra-endurance sportsmen and women typically do not meet their fluid needs during exercise. However, successful athletes exercising over several consecutive days come close to meeting fluid needs. It is important to try to account for all factors influencing bodyweight changes, in addition to fluid loss, and all sources of water input. Increasing ambient temperature and humidity can increase the rate of sweating by up to approximately 1 L/h. Depending on individual variation, exercise type and particularly intensity, sweat rates can vary from extremely low values to more than 3 L/h. Over-hydration, although not frequently observed, can also present problems, as can inappropriate fluid composition. Over-hydrating or meeting fluid needs during very long-lasting exercise in the heat with low or negligible sodium intake can result in reduced performance and, not infrequently, hyponatraemia. Thus, with large rates of fluid ingestion, even measured just to meet fluid needs, sodium intake is vital and an increased beverage concentration [30 to 50 mmol/L (1.7 to 2.9 g NaCl/L) may be beneficial. If insufficient fluids are taken during exercise, sodium is necessary in the recovery period to reduce the urinary output and increase the rate of restoration of fluid balance. Carbohydrate inclusion in a beverage can affect the net rate of water assimilation and is also important to supplement endogenous reserves as a substrate for exercising muscles during ultra-endurance activity. To enhance water absorption, glucose and/or glucose-containing carbohydrates (e.g. sucrose, maltose) at concentrations of 3 to 5% weight/volume are recommended. Carbohydrate concentrations above this may be advantageous in terms of glucose oxidation and maintaining exercise intensity, but will be of no added advantage and, if hyperosmotic, will actually reduce the net rate of water absorption. The rate of fluid loss may exceed the capacity of the gastrointestinal tract to assimilate fluids. Gastric emptying, in particular, may be below the rate of fluid loss, and therefore, individual tolerance may dictate the maximum rate of fluid intake. There is large individual variation in gastric emptying rate and tolerance to larger volumes. Training to drink during exercise is recommended and may enhance tolerance.

Cardiovascular adaptations observed during exposure to microgravity results in impairment of baroreflex activity partially as a result of fluid and electrolyte shifts. The head-down tilt rat model mimics some of the physiological observations that have been made in astronauts. We examined the effects of salt-loading on baroreflex activity after 7 day simulated microgravity (30 degrees tail-suspension) and the subsequent 6 hr post-suspension in Sprague-Dawley (SD) rats, using low salt (0.3% NaCl) and high salt (8% NaCl) diets. In suspended animals on a low salt diet, the baroreflex response curve was shifted to the left, while the heart rate (HR) range and MAP50 values were reduced compared to their parallel tethered, non-suspended controls. For non-suspended animals, salt-loading shifted the curve to the right with a reduced HR range. In salt-loaded, suspended animals, the curve and its parameters resemble those of non-suspended animals on a low salt diet. In summary, these data have demonstrated that a short-term (seven days) simulated weightlessness may elicit cardiovascular deconditioning in rats after release from the simulation manifested as an altered responsiveness in baroreceptor-heart rate reflex and a lowered blood pressure while the rats are tethered and horizontal. Our results also suggest the counteracting effect of salt loading on cardiovascular deconditioning.

Objective: Recently, we found that sodium restriction restored the circadian rhythm of blood pressure from non-dippers to dippers in patients with a sodium-sensitive type of essential hypertension. In the present study, we investigated the effects of sodium restriction on the circadian blood pressure rhythm in patients with primary aldosteronism, a typical sodium-sensitive form of secondary hypertension., Design and Methods: We performed 24 h blood pressure monitoring in eight patients with primary aldosteronism due to unilateral adenoma (Conn's syndrome) during normal-sodium (7-12 g/day of NaCl) and low-sodium (1-3 g/day) diets, and after adrenalectomy., Results: Sodium restriction lowered the 24 h mean arterial pressure from 116+/-14 to 109+/-12 mmHg (P< 0.01). During a normal-sodium diet, there was no change in systolic, diastolic and mean arterial pressures during the night-time compared with the daytime. In contrast, during a low-sodium diet, all night-time pressure values were significantly lower than those in the daytime. After adrenalectomy, the night-time pressures in patients on a normal-sodium diet were lower than those of the daytime. The nocturnal mean arterial pressure fall was increased by sodium restriction and adrenalectomy., Conclusions: These results indicate that the circadian rhythm of blood pressure was disturbed in patients with primary aldosteronism who maintained a relatively high sodium intake. Both adrenalectomy and sodium restriction restored a nocturnal dip in blood pressure in primary aldosteronism. Therefore, sodium restriction affects the circadian blood pressure rhythm in sodium-sensitive types of hypertension, not only in primary hypertension, but also in secondary hypertension.

The management of unexplained syncope begins with the patient's history and physical examination, which are oriented to help separate benign from serious causes. Malignant etiologies are more likely to occur with exertional syncope. Cardiac causes should be considered, particularly cardiomyopathy, postoperative congenital heart disease, right ventricular dysplasia, anomalous coronary artery, pulmonary artery hypertension, myocarditis, long QT syndrome, and Wolff-Parkinson-White syndrome. Neurological and metabolic disorders may underlie a syncope episode. After malignant causes of syncope have been excluded and the diagnosis of neurocardiac syncope has been established, treatment strategies include behavior modification, salt and increased fluids, and pharmacological agents. Efficacious agents include beta-blockers, dysopyramide, fludrocortisones, and alpha agents. Yet, behavior modification alone may be as effective as salt or pharmacological therapy. Because the natural history of neurocardiac syncope in children is spontaneous resolution, it is appropriate to try the simple measures before introducing drug therapy.

Low sodium intake is the most widely used nonpharmacological approach to the treatment of hypertension. Although nonpharmacological treatment is by definition regarded as safe, the suggestion has been made that low sodium intake is not totally devoid of inconveniences, and animal data have shown it to be accompanied by an impairment of reflex blood pressure control and homeostasis. However, no data exist on this issue in humans. In mild essential hypertensive patients (age, 34.1+/-3.3 years [mean+/-SEM]), we measured beat-to-beat arterial blood pressure (finger photoplethysmographic device), heart rate (electrocardiogram), and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor stimulation and deactivation, induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Measurements were performed at the end of three dietary periods, ie, after 8 days of regular sodium intake (210 mmol NaCl/d), low sodium intake (20 mmol NaCl/d) with unchanged potassium intake, and again regular sodium intake. Compared with the initial regular sodium diet, low sodium intake reduced urinary sodium excretion, whereas urinary potassium excretion was unchanged. Systolic blood pressure was significantly (P<.05), although slightly, reduced, whereas diastolic blood pressure was unaffected. Muscle sympathetic nerve activity was increased by 23.1+/-5.2% (P<.05). The increase was accompanied by a clear-cut impairment of the baroreceptor ability to modulate muscle sympathetic nerve activity, ie, by a 43.9+/-5.7% (P<.01) reduction in the sensitivity of the baroreceptor-muscle sympathetic nerve activity reflex compared with the control condition. Baroreceptor modulation of heart rate was also impaired, although to a smaller and less consistent extent. When regular sodium intake was restored, all the above-mentioned parameters and baroreflex responses returned to the values observed at the initial regular sodium diet. These data raise evidence that in humans sodium restriction may impair the arterial baroreflex. This may be responsible for the sympathetic activation occurring in this condition and for the impairment of blood pressure homeostasis.

Thirty-two patients with liver cirrhosis and ascites were treated by stepped care diuretic treatment as follows: step 1, placed on a 35 mEq sodium diet; step 2, given 400 mg/day of potassium canrenoate in addition to step 1 treatment; step 3, given 40-80 mg/day of furosemide in addition to step 2 treatment. Eleven out of 32 patients (34.4%, group 1) and 12 of 21 patients (57.1%, group 2) lost their ascites at step 1 and step 2, respectively. The remaining nine patients (group 3) required step 3 treatment. Basal urinary sodium excretion and creatinine clearance were significantly lower and beta 2-microglobulin was significantly higher in group 3 than those in groups 1 and 2. Elevation of basal plasma renin activity and norepinephrine was evident only in group 3. In group 1, urinary sodium excretion decreased after the treatment. In group 2, plasma alpha-atrial natriuretic polypeptide was lowered and plasma renin activity and norepinephrine were elevated after the treatment. These results suggest that basal renal function and plasma renin activity and norepinephrine levels are useful indices to predict the effect of ascites treatment and that responders to sodium restriction or potassium canrenoate may be in the state of vascular overflow, while non-responders to potassium canrenoate may be in the state of vascular underfilling. In summary, this stepped care treatment is safe without any side effects, although the diuretics themselves may lead to relative vascular underfilling.

Captopril, furosemide, and a sodium-restricted diet were administered to 6 normal dogs and 10 dogs with congestive heart failure. Serum electrolyte concentrations and renal function were monitored in both groups. In the normal dogs, no clinically meaningful changes in serum electrolyte, urea nitrogen, or creatinine concentrations developed during therapy with a sodium-restricted diet and 4 weeks each of furosemide alone, captopril alone, or furosemide plus captopril. Three of 6 normal dogs on furosemide and a sodium-restricted diet had at least one serum potassium concentration above the reference range during the 4 weeks of observation. One normal dog on captopril, furosemide, and a sodium-restricted diet developed azotemia, and 2 dogs had serum potassium concentrations above the reference range during the 4 weeks of observation. Ten dogs with congestive heart failure were treated with captopril, furosemide, a sodium-restricted diet, and digoxin. Etiopathogenesis of the heart failure included valvular insufficiency (n = 6), dilated cardiomyopathy (n = 3), and dilated cardiomyopathy and dirofilariasis (n = 1). Serum electrolyte concentrations and renal function were monitored for 5 consecutive weeks in 7 of the 10 dogs and for 17 weeks or longer in 6. Two dogs were euthanized after 4 weeks because of acute decompensation of heart failure, and one dog developed severe azotemia and uremia. Six of 10 dogs with congestive heart failure had at least one serum potassium concentration above the reference range sometime during the 5 weeks of observation, although the changes in the mean serum potassium concentrations were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

To assess the interaction of dietary sodium and the antihypertensive response to a calcium antagonist, spontaneously hypertensive rats (SHR) were given a diet of regular or increased (120 v 342 mumol Na+/g food) sodium intake from 4 until 16 weeks of age. Nifedipine was added at 10 weeks of age. This level of sodium intake did not enhance the development of hypertension in SHR. In rats with the regular sodium intake, nifedipine caused only a minor decrease in blood pressure. In contrast, with increased sodium intake nifedipine caused a marked antihypertensive response, preventing the rise in blood pressure occurring between 10 and 16 weeks of age. This enhanced response was associated with a diminished blood pressure fall from ganglionic blockade. These results indicate that modest increases in sodium intake enhance the blood pressure response to a calcium antagonist possibly by potentiating its inhibitory effects on sympathetic activity.

The increased frequency and duration of antifungal treatment with amphotericin B in immunocompromised patients has stimulated a great deal of research into the mechanisms of its nephrotoxic effects and treatment modalities designed to attenuate these effects. A review of amphotericin B-induced nephrotoxicity, the underlying pathophysiologic mechanisms, and the role of salt loading as a means of minimizing renal impairment are described. Both animal and human studies regarding the efficacy of sodium loading are presented as well as a case report describing the use of salt supplementation over a prolonged course of therapy.

Urinary uric acid excretion was assessed in 38 children to determine whether hyperuricuria was a risk factor in children with urolithiasis. Uric acid excretion (measured per deciliter glomerular filtration rate), and fractional excretion of uric acid were similar in 27 children with hypercalciuria and calcium oxalate urinary stones, in six children with idiopathic calcium oxalate urolithiasis, and in five with uric acid urolithiasis, of whom four were white boys and one was an Asian girl. One boy with a urate stone had cystinosis. Serum uric acid concentrations exceeded 6.0 mg/dl (360 mumol/L) in two children with hypercalciuria and in two patients with idiopathic calcium oxalate urolithiasis. None of the children with calcium urolithiasis had excessive urinary excretion of uric acid. In children with hypercalciuria, uric acid excretion did not change significantly when dietary sodium was increased from 1.0 to 5.0 gm/1.73 m2. We conclude that excessive urinary uric acid excretion is seldom an additional risk factor in children with calcium urolithiasis and that dietary sodium chloride does not have a strong influence on urinary excretion of uric acid in children with hypercalciuria.