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A gastrointestinal–renal natriuretic signaling axis has been proposed to regulate sodium excretion in response to acute sodium ingestion. Such an axis is thought to be regulated by a gastrointestinal sodium sensor coupled to the activation/release of a natriuretic signal and could have important clinical and scientific implications. Here we systematically tested for this putative axis and the potential involvement of the gastrointestinal-derived natriuretic prohormones prouroguanylin and proguanylin in 15 healthy volunteers. There was no difference in sodium excretion following equivalent oral or intravenous sodium loads during either high- or low-sodium diets. Furthermore, serum concentrations of prouroguanylin and proguanylin did not increase, did not differ following oral or intravenous sodium, and did not correlate with sodium excretion. Thus, our results do not support an acute gastrointestinal–renal natriuretic axis or a central role for prouroguanylin or proguanylin in humans. If such an axis does exist, it is not characterized by a significant difference in the pattern of sodium excretion following either an oral or intravenous sodium load.

The objective of the study was to determine if balanced electrolyte solution (BES) prevents hyperchloremic metabolic acidosis in patients with diabetic ketoacidosis (DKA). This is a prospective, randomized, double-blind study. A convenience sample of DKA patients aged 18 to 65 years with serum bicarbonate less than or equal to 15 and anion gap greater than or equal to 16 was enrolled at “Louisiana State University Health Sciences Center-Shreveport\" an capitalize Emergency Department over a 24-month period (2006-2008). Patients were randomized to standardized resuscitation with normal saline (NS) or BES (Plasma-Lyte A pH 7.4; Baxter International, Deerfield, IL). Every 2 hours, serum chloride and bicarbonate were measured until the patient's anion gap decreased to 12. An intention-to-treat analysis was performed on patients who met inclusion criteria and received at least 4 hours of study fluid. Chloride and bicarbonate measurements from the BES and NS groups were compared using unpaired and paired Student t tests. Of 52 patients enrolled, 45 (22 in BES group and 23 in NS group) met inclusion criteria and received 4 hours of fluid. The mean postresuscitation chloride was 111 mmol/L (95% confidence interval [CI] = 110-112) in the NS group and 105 mmol/L (95% CI = 103-108) in the BES group ( P ≤ .001). The mean postresuscitation bicarbonate was 17 mmol/L (95% CI = 15-18) in the NS group and 20 mmol/L (95% CI = 18-21) in the BES group ( P = .020). Resuscitation of DKA patients with BES results in lower serum chloride and higher bicarbonate levels than patients receiving NS, consistent with prevention of hyperchloremic metabolic acidosis.

Background Acute kidney injury and hyperchloremia are commonly present in critically ill septic patients. Our study goal was to evaluate the association of hyperchloremia and acute kidney injury in severe sepsis and septic shock patients. Methods In this retrospective cohort study in a provincial tertiary care hospital, adult patients with severe sepsis or septic shock and serum chloride measurements were included. Serum chloride was measured on a daily basis for 48 hours. Primary outcome was development of acute kidney injury (AKI) and association of AKI and serum chloride parameters was analyzed. Results A total of 240 patients were included in the study, 98 patients (40.8 %) had hyperchloremia. The incidence of acute kidney injury (AKI) was significantly higher in the hyperchloremia group (85.7 % vs 47.9 %; p  < 0.001). Maximal chloride concentration in the first 48 hours ([Cl - ] max ) was significantly associated with AKI. In multivariate analysis, [Cl - ] max was independently associated with AKI [adjusted odds ratio (OR) for AKI = 1.28 (1.02–1.62); p  = 0.037]. The increase in serum chloride (Δ[Cl - ] = [Cl - ] max – initial chloride concentration) demonstrated a dose-dependent relationship with severity of AKI. The mean Δ[Cl - ] in patients without AKI was 2.1 mmol/L while in the patients with AKI stage 1, 2 and 3 the mean Δ[Cl - ] was 5.1, 5.9 and 6.7 mmol/L, respectively. A moderate increase in serum chloride (Δ[Cl - ] ≥ 5 mmol/L) was associated with AKI [OR = 5.70 (3.00–10.82); p  < 0.001], even in patients without hyperchloremia [OR = 8.25 (3.44–19.78); p  < 0.001]. Conclusions Hyperchloremia is common in severe sepsis and septic shock and independently associated with AKI. A moderate increase in serum chloride (Δ[Cl - ] ≥5 mmol/L) is associated with AKI even in patients without hyperchloremia.

The aetiology of minimal hepatic encephalopathy (mHE) remains unclear. It is generally accepted that hyperammonaemia plays a major role, however there are a multitude of metabolic perturbations present. To determine the contribution of hyperammonaemia to mHE symptom development, ten healthy males (Age:25 ± 5 yrs, BM:76.3 ± 7.1 kg, Height:178.6 ± 4.5 cm, mean ± SD) received two 4 h intravenous infusions of either a 2% ammonium chloride solution (AMM) or a placebo (PLA;0.9% sodium chloride) using a double blind cross-over design. Sensations of fatigue were measured at baseline, 2 and 4 h using the Multidimensional Fatigue Symptom Inventory-Short Form (MFSI-SF) questionnaire. Learning & memory, motor control and cognition were assessed using Rey’s Auditory Verbal Learning Test (AVL), Continuous Compensatory Tracking (COMPTRACK) Task and Inhibitory Control Test (ICT) respectively. Arterialised venous blood samples were collected every hour, and analysed for ammonia concentration. There was a significantly higher plasma ammonia concentration in the AMM trial than the PLA trial at every time point during the infusion, peaking at 2 h (57 ± 4 μmol/L PLA, 225 ± 14 μmol/L AMM; p  < 0.05). At 2 h there were significantly higher sensations of general fatigue ( Z  = −2.527, p  = 0.008, 2 tailed) and physical fatigue ( Z  = −2.156, p  = 0.027, 2 tailed), and lower sensations of vigour ( Z  = −2.456, p =  0.012, 2 tailed) for the AMM trial. There were no significant effects on the performance of the psychological tasks. These results demonstrate that hyperammonaemia in the absence of other complications induces significant sensations of fatigue but does not cause the typically observed performance impairment in individuals with mHE. Supporting the hypothesis for synergism between ammonia and other co-factors in mHE.

A device for measuring biological small volume liquid samples in real time is appealing. One way to achieve this is by using a microwave sensor based on reflection measurement. A prototype sensor was manufactured from low cost printed circuit board (PCB) combined with a microfluidic channel made of polymethylsiloxane (PDMS). Such a sensor was simulated, manufactured, and tested including a vacuum powered sample delivery system with robust fluidic ports. The sensor had a broad frequency band from 150 kHz to 6 GHz with three resonance frequencies applied in sensing. As a proof of concept, the sensor was able to detect a NaCl content of 125 to 155 mmol in water, which is the typical concentration in healthy human blood plasma.

Objective To assess the safety of low-dose vasopressin infusion in critically ill children requiring prolonged mechanical ventilation (MV) at risk of developing sedation/analgesia-related hypotension. Method Randomized pilot safety study in children expected to require MV for at least 3 days. Children received either vasopressin (0.0005 U/kg/min) or sodium chloride (0.9%) infusion for a period of 48 h. Haemodynamic variables, urine output and serum electrolytes were closely monitored and analyzed. Results Twelve children in each group had similar baseline characteristics. Vasopressin infusion was associated with an 8 mmol/L fall in serum sodium concentration ( p  < 0.01) and with higher incidence of hyponatraemia (8 vs. 66%, p  < 0.01). In normotensive children, low-dose vasopressin also induced a reversible decrease in urine output, and acutely increased blood pressure ( p  < 0.01). After stopping the vasopressin there was rebound hypotension ( p  < 0.01). Conclusion Low-dose vasopressin infusion in haemodynamically stable, but critically ill, children is associated with reduction in urine output and decreased serum sodium level, yielding a high incidence of hyponatraemia. We conclude that these effects limit further study of prophylactic vasopressin for sedation-related hypotension in a randomized controlled trial.

Background: Multiple micronutrient deficiencies are prevalent in India. Objective: The study aims to establish the efficacy of multi-micronutrient fortified salt in addressing multiple micronutrient deficiencies among children compared to nutrition education and no intervention in Tamilnadu. Methods: The study employed a community based randomized controlled trial designed to study the impact of multiple micronutrient salt (micronutrient group) in comparison with nutrition education (education group) and no intervention (control group) on haemoglobin, serum ferritin, soluble transferrin receptor, body iron stores, serum retinol and urinary iodine outcomes over a period of 8 months. The fortified salt contained iron, iodine, vitamin A, vitamin B12 and folic acid. All the children were dewormed at baseline and at the end of the study just before the biochemical measurements. Results: There was a significant improvement in most biochemical parameters studied in the micronutrient group when compared with the control group whereas this was not seen between the education and control. Over 8 months, in the micronutrient group, hemoglobin increased by 0.52 g/dL, retinol by 8.56 mug/dL, ferritin by 10.8 mug/L, body iron stores by 1.27 mg and the decrease in the prevalence of retinol deficiency was from 51.6% to 28.1%, anaemia from 46.0% to 32.6%, iron deficiency from 66.9% to 51.3% and iron deficiency anaemia from 35.2% to 31.0%, while the prevalence of all these deficiencies increased or the changes were not significant in the other two groups. Conclusions: Multiple micronutrient fortified salt was able to improve iron and vitamin A status, whereas this was not seen in the nutrition education group.

Sodium is an essential mineral and nutrient used in dietary practices across the world and is important to maintain proper blood volume and blood pressure. A high sodium diet is associated with increased expression of β—myosin heavy chain, decreased expression of α/β—myosin heavy chain, increased myocyte enhancer factor 2/nuclear factor of activated T cell transcriptional activity, and increased salt-inducible kinase 1 expression, which leads to alteration in myocardial mechanical performance. A high sodium diet is also associated with alterations in various proteins responsible for calcium homeostasis and myocardial contractility. Excessive sodium intake is associated with the development of a variety of comorbidities including hypertension, chronic kidney disease, stroke, and cardiovascular diseases. While the American College of Cardiology/American Heart Association/Heart Failure Society of America guidelines recommend limiting sodium intake to both prevent and manage heart failure, the evidence behind such recommendations is unclear. Our review article highlights evidence and underlying mechanisms favoring and contradicting limiting sodium intake in heart failure.

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

Introduction The prevalence of metabolic acidosis is high in patients with chronic kidney disease (CKD). For the diagnosis, a blood gas analysis is necessary, but not always available. The aim of the study was to evaluate the base excess (BE) of the sodium–chloride difference (BE Na–Cl  = Na + –Cl − —34 mmol/l) as a screening parameter for hyperchloremic metabolic acidosis. Methods and statistical analysis We retrospectively performed acid–base analyses of 168 non-dialysed patients with CKD according to the physiologic and to the Stewart’s approach. We performed linear regression analysis, Bland–Altman plot and receiver operating characteristics (ROC) analysis of BE Na–Cl  and BE to evaluate the accuracy of BE Na–Cl  predicting the BE. We further investigated possible confounding factors. Results The corrected R 2  for the correlation of BE Na–Cl  and BE was 0.60 (p < 0.001). The Bland–Altman plot showed a good overall agreement. The bias was negligible, but the 95%-limits of agreement showed a wide interval (10.4 mmol/l). For BE ≤ 2 mmol/l, the ROC analysis yielded an AUC of 0.89 and moderate sensitivity (0.75) and specificity (0.86) for the optimal BE Na–Cl  threshold (≤ 2 mmol/l). Subgroup analysis showed similar results. The main factor for the imprecision of BE Na–Cl  predicting the BE across all stages of CKD is the variability of the serum anion gap (SAG). Conclusions The BE Na–Cl  is not an adequate parameter for screening of hyperchloremic acidosis because of the high variability of the SAG. Only, if the BE Na–Cl  is ≤ 5 mmol/l, a hyperchloremic acidosis should be suspected. Therefore, a complete blood gas analysis is necessary for the correct diagnosis of acid–base disorders in patients with chronic kidney disease.