Sodium Chloride Supplementation Research Articles

Osmotic Demyelination Syndrome after Primary Hypoadrenocorticism Crisis Management

Background: Primary hypoadrenocorticism is a rare condition resulting from immune-mediated destruction of the adrenal cortices. It can also occur due to necrosis, neoplasms, infarctions and granulomas. The clinical and laboratory changes are due to deficient secretion of glucocorticoids and mineralocorticoids, which leads to electrolyte disorders associated with hyponatremia and hyperkalemia. These disorders can cause hypotension, hypovolemia and shock, putting a patient's life at risk if inadequate hydroelectrolytic supplementation and hormone replacement is provided. Nevertheless, rapid sodium chloride supplementation is contraindicated due to the risk of central pontine myelinolysis induction. The present study aims to describe a thalamic osmotic demyelination syndrome after management of a primary hypoadrenocorticism crisis in a 2-year-old, female West White Highland Terrier. Case: The patient had a presumptive diagnosis of hypoadrenocorticism already receiving oral prednisolone and gastrointestinal protectants in the last 2 days. After prednisolone dose reduction the dog presented a severe primary hypoadrenocorticism crisis treated with intravenous sodium chloride 0.9% solution along with supportive therapy. Four days after being discharged from the hospital, the patient showed severe neurological impairment and went back to the clinic where a neurological examination revealed mental depression, drowsiness, ambulatory tetraparesis and proprioceptive deficit of the 4 limbs, postural deficits, and cranial nerves with decreased response. Due to these clinical signs, a magnetic resonance imaging was performed. It showed 2 intra-axial circular lesions, symmetrically distributed in both thalamus sides, with approximately 0.8 cm in diameter each without any other anatomical changes on magnetic resonance imaging. The images were compatible with metabolic lesions, suggesting demyelination. Furthermore, liquor analysis did not show relevant abnormalities, except for a slight increase in density and pH at the upper limit of the reference range. After treatment, the patient had a good neurological evolution secondary to standard primary hypoadrenocorticism treatment, without sequelae. Discussion: In the present case report, primary hypoadrenocorticism gastrointestinal signs seemed to be triggered by a food indiscretion episode, not responsive to the symptomatic therapies employed. The patient´s breed and age (young West White Highland Terrier bitch) is in accordance with the demographic profile of patients affected by the disease, where young females are frequently more affected. Regarding the probable thalamic osmotic demyelination syndrome documented in this case, is important to notice that myelinolysis or demyelination is an exceedingly rare noninflammatory neurological disorder, initially called central pontine myelinolysis, which can occur after rapid correction of hyponatremia. It has already been observed in dogs after correction of hyponatremia of different origins, including hypoadrenocorticism and parasitic gastrointestinal disorders. Currently, the terms "osmotic myelinolysis" or “osmotic demyelination syndrome" are considered more suitable when compared to the term "central pontine myelinolysis" since it has been demonstrated in dogs and humans the occurrence of demyelination secondary to the rapid correction of hyponatremia in distinct regions of the central nervous system including pons, basal nuclei, striatum, thalamus, cortex, hippocampus and cerebellum. The present case report emphasizes the difficulties for hormonal confirmation of primary hypoadrenocorticism in a patient already on corticosteroid treatment, as well as proposes that the current term osmotic demyelination syndrome replace the term “central pontine myelinolysis” in veterinary literature related to the management of hypoadrenocorticism crisis.Keywords: Addison Syndrome, hyponatremia, osmotic myelinolysis, magnetic resonance imaging.

Effect of sodium bicarbonate supplementation on the renin-angiotensin system in patients with chronic kidney disease and acidosis: a randomized clinical trial

BackgroundAcidosis-induced kidney injury is mediated by the intrarenal renin-angiotensin system, for which urinary renin is a potential marker. Therefore, we hypothesized that sodium bicarbonate supplementation reduces urinary renin excretion in patients with chronic kidney disease (CKD) and metabolic acidosis.MethodsPatients with CKD stage G4 and plasma bicarbonate 15–24 mmol/l were randomized to receive sodium bicarbonate (3 × 1000 mg/day, ~ 0.5 mEq/kg), sodium chloride (2 × 1,00 mg/day), or no treatment for 4 weeks (n = 15/arm). The effects on urinary renin excretion (primary outcome), other plasma and urine parameters of the renin-angiotensin system, endothelin-1, and proteinuria were analyzed.ResultsForty-five patients were included (62 ± 15 years, eGFR 21 ± 5 ml/min/1.73m2, plasma bicarbonate 21.7 ± 3.3 mmol/l). Sodium bicarbonate supplementation increased plasma bicarbonate (20.8 to 23.8 mmol/l) and reduced urinary ammonium excretion (15 to 8 mmol/day, both P < 0.05). Furthermore, a trend towards lower plasma aldosterone (291 to 204 ng/L, P = 0.07) and potassium (5.1 to 4.8 mmol/l, P = 0.06) was observed in patients receiving sodium bicarbonate. Sodium bicarbonate did not significantly change the urinary excretion of renin, angiotensinogen, aldosterone, endothelin-1, albumin, or α1-microglobulin. Sodium chloride supplementation reduced plasma renin (166 to 122 ng/L), and increased the urinary excretions of angiotensinogen, albumin, and α1-microglobulin (all P < 0.05).ConclusionsDespite correction of acidosis and reduction in urinary ammonium excretion, sodium bicarbonate supplementation did not improve urinary markers of the renin-angiotensin system, endothelin-1, or proteinuria. Possible explanations include bicarbonate dose, short treatment time, or the inability of urinary renin to reflect intrarenal renin-angiotensin system activity.Graphic abstract

Sodium Status and Replacement in Children and Adults Living with Cystic Fibrosis: A Narrative Review

Patients with cystic fibrosis (CF) have a two- to four-fold higher sodium chloride sweat content compared with healthy controls. This high sweat salt loss increases the risk for electrolyte disturbances, associated with subacute or chronic complications. Sodium status therefore needs to be adequately monitored and salt intake adjusted to individual needs. The lack of current evidence to formulate specific recommendations and assess sodium status is reflected in a variability of recommendations in international guidelines. This narrative review presents an overview of the current evidence. Infants with CF in particular are at risk for severe sodium deficiency, potentially leading to metabolic alkalosis due to low intake and high sweat losses. More research on the assessment of sodium status and efficacy of sodium chloride supplements in the population of patients with CF, especially given the changing era of CF transmembrane conductance regulator modulatory treatment, is warranted.

The Impact of Oral Sodium Chloride Supplementation on Thrive and the Intestinal Microbiome in Neonates With Small Bowel Ostomies: A Prospective Cohort Study.

Background: Infants with ileostomies often suffer from sodium depletion, ultimately leading to a failure to thrive. Moreover, early-infantile microbial dysbiosis may potentially aggravate weight faltering. Given that sodium supplementation has been used to restore weight gain and feeding practices largely determine infantile microbiota, the current study investigated the effect of sodium chloride (NaCl) on weight gain and intestinal microbiome in infants with jejuno- and ileostomies.Methods: A prospective cohort study including 24 neonates with enterostomies compared 19 subjects receiving oral NaCl (5.85%) to five subjects without supplementation with respect to postoperative changes in thrive and the intestinal microbiome.Results: Infants receiving NaCl after enterostomy-surgery showed vastly improved weight gain and an increased abundance of Lactobacillus in fecal samples, as compared to subjects without oral supplement who displayed decreasing percentiles for weight and did not reveal a higher abundance of probiotic strains within the ostomy effluent. Contrarily, Klebsiella was equally enriched in supplemented infants, reflecting a higher susceptibility for infections in preterm neonates.Discussion: Our findings support oral NaCl supplementation as a mainstay of postoperative treatment in infants with small bowel ostomies who are predisposed to suffer from a sodium depletion-associated failure to thrive. Not only does NaCl promote weight gain by increasing glucose resorption, but it also appears to induce microbial restoration by enhancing the abundance of health-promoting probiotic bacteria. This finding has an even greater significance when facing an elevated Klebsiella/Bifidobacteria (K/B) ratio, believed to represent an early-life microbial biomarker for development of allergic disease.

Efficacy of Furosemide, Oral Sodium Chloride, and Fluid Restriction for Treatment of Syndrome of Inappropriate Antidiuresis (SIAD): An Open-label Randomized Controlled Study (The EFFUSE-FLUID Trial)

First-line therapy for syndrome of inappropriate antidiuresis (SIAD) is fluid restriction. Additional treatment for patients who do not respond to fluid restriction are water restriction with furosemide or water restriction with furosemide and salt supplementation. However, the efficacy of these treatments has never been tested in a randomized controlled study. The objective of this study was to investigate whether, combined with fluid restriction, furosemide with or without sodium chloride (NaCl) supplementation was more effective than fluid restriction alone in the treatment of hyponatremia in SIAD. Open-label randomized controlled study. Patients with serum sodium concentrations ([Na+])≤ 130mmol/L due to SIAD. Random assignment to 1 of 3 groups: fluid restriction alone (FR), fluid restriction and furosemide (FR+FM), or fluid restriction, furosemide, and NaCl (FR+FM+NaCl). Strictness of fluid restriction (<1,000 or<500mL/d) was guided by the urine to serum electrolyte ratio. Furosemide dosage was 20 to 40mg/d. NaCl supplements were 3g/d. All treatments were continued for 28 days. The primary outcome was change in [Na+] at days 4, 7, 14, and 28 after randomization. 92 patients were recruited (FR, n=31; FR+FM, n=30; FR+FM+NaCl, n=31). Baseline [Na+] was 125±4mmol/L, and there were no significantdifferences between groups. Mean [Na+] on day 4 in all treatment groups was significantly increased from baseline by 5mmol/L (P<0.001); however, the change in [Na+] was not significantly different across groups (P=0.7). There was no significant difference in percentage of patients ortime to reach [Na+]≥ 130 or≥135mmol/L across the 3 groups. Acute kidney injury and hypokalemia(potassium≤3.0mmol/L) were more common in patients receiving furosemide. Open-label treatment. In patients with SIAD, furosemide with NaCl supplement in combination with fluid restriction did not show benefits in correction of [Na+] compared with treatment with fluid restriction alone. Incidences of acute kidney injury and hypokalemia were increased in patients receiving furosemide. None. Registered at the Thai Clinical Trial Registry with study number TCTR20170629004.

Biofilm Formation by Staphylococcus aureus Clinical Isolates is Differentially Affected by Glucose and Sodium Chloride Supplemented Culture Media.

Staphylococcus aureus (S. aureus) causes persistent biofilm-related infections. Biofilm formation by S. aureus is affected by the culture conditions and is associated with certain genotypic characteristics. Here, we show that glucose and sodium chloride (NaCl) supplementation of culture media, a common practice in studies of biofilms in vitro, influences both biofilm formation by 40 S. aureus clinical isolates (methicillin-resistant and methicillin-sensitive S. aureus) and causes variations in biofilm quantification. Methicillin-resistant strains formed more robust biofilms than methicillin-sensitive strains in tryptic soy broth (TSB). However, glucose supplementation in TSB greatly promoted and stabilized biofilm formation of all strains, while additional NaCl was less efficient in this respect and resulted in significant variation in biofilm measurements. In addition, we observed that the ST239-SCCmec (Staphylococcal Cassette Chromosome mec) type III lineage formed strong biofilms in TSB supplemented with glucose and NaCl. Links between biofilm formation and accessory gene regulator (agr) status, as assessed by δ-toxin production, and with mannitol fermentation were not found. Our results show that TSB supplemented with 1.0% glucose supports robust biofilm production and reproducible quantification of S. aureus biofilm formation in vitro, whereas additional NaCl results in major variations in measurements of biofilm formation.

Dietary Salt Intake Exaggerates Arterial Blood Pressure during Exercise in healthy Normotensive Adults

High dietary salt intake is associated with an increased risk for the development of hypertension, cardiovascular (CVD) and cerebrovascular disease. Additionally, exaggerated blood pressure during dynamic exercise is independently predictive of future CVD beyond resting blood pressure and other conventional risk factors. This is critical given that in animal models, dietary salt negatively augments blood pressure responses during static hind‐limb contractions, suggesting an increased risk of an adverse CVD event during exercise with high dietary salt. However, it currently remains unknown if high salt intake increases arterial blood pressure and impairs vascular function during voluntary dynamic exercise in healthy men and women. Based on previous preclinical reports, we hypothesized that high salt intake would decrease resting vascular endothelial function, increase arterial blood pressure during dynamic exercise and decrease functional sympatholysis. Thirteen healthy men and women underwent a randomized, double‐blind, placebo‐controlled trial for 7 days with either 15g/day sodium chloride supplement or cellulose. Beat‐by‐beat mean (MAP), systolic (SBP) and diastolic (DBP) were recorded throughout the trial on the non‐exercising limb. Forearm blood flow (FBF) was calculated via mean blood velocity derived from ultrasonography on the brachial artery of the exercising limb. All patients performed a flow‐mediated dilation (FMD) protocol followed by (20% maximal voluntary contraction) submaximal hand‐grip exercise for 7 min with lower‐body negative pressure initiated during min 5 – 7. FMD was significantly reduced during the HS condition (HS: 2.2±0.26e−5; Pl: 4.1±0.56e−5; p&lt;0.01). Compared to placebo, the absolute steady‐state exercise MAP and SBP were significantly higher during HS compared to the placebo condition (p&lt;0.05). However, functional sympatholysis was not different between conditions (p=0.07). In summary, the results of this study show the effects of HS intake on arterial blood pressure during handgrip exercise. These findings highlight that the augmented exercise blood pressures may be key mediator for the increased risk for adverse CVD outcomes associated with high dietary salt intake.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Effects of sodium chloride supplementation for Pacific white shrimp Penaeus vannamei diets, cultured in low salinity waters

The culture of Penaeus vannamei in low-salinity waters is a recent development in Brazilian Northeast. The purpose of this study was to investigate the effects of NaCl dietary supplementation on shrimp growth, survival, haemolymph osmolality and total hemocyte counts. In trial 1, earthen pond-reared shrimp ranging from 5 to 20 g were sampled at intervals for determination of haemolymph osmolality. Haemolymph osmolality was not influenced by the increased weight of shrimp. Juveniles shrimp (5-20 g) haemolymph osmolality were then evaluated 24 h after they had been transferred from pond water (0.5 ppt) to the seawater (35 ppt). Shrimp haemolymph osmolality increased with external salinity and ranged from 661.0 ± 25.2 mOsm/kg (D1) and 916.9 ± 40.1 mOsm/kg (D4). In trial 2, shrimp reared in low-salinity water (0.3-0.5 ppt) were distributed into five groups (control, D1, and treatments, D2, D3, D4 e D5) with four replicates. Diets consisted of the basal diet supplemented with 0 g/kg, 5 g/kg, 10 g/kg, 20 g/kg, and 40 g/kg of NaCl, respectively. After 22 days, differences in survival, final weight, specific growth rates (SGR) and absolute growth rate (AGR) among treatments were significant. However, there were no significant trends in haemolymph osmolality and shrimp total hemocyte counts within the five tested groups.

Effect of nonsteroidal anti-inflammatory drugs in children with Bartter syndrome.

Bartter syndrome (BS) is a salt-wasting tubulopathy with induced expression of cyclooxygenase-2 in the macula densa, leading to increased prostaglandin production and hyperreninemia. Nonsteroidal anti-inflammatory drugs (NSAIDs) are currently used in BS; however, there is limited information on the impact of NSAIDs at treatment initiation or the potential utility of plasma renin level to guide therapy in patients with BS. We included 19 patients with BS treated with NSAIDs between 1994 and 2016. We assessed serum levels of renin, aldosterone, electrolytes, calcium, phosphorus, vitamin D, and intact parathyroid hormone (iPTH) before and after treatment initiation. We also recorded modifications in sodium and potassium supplements and changes in urine calcium. Median age at diagnosis was 0.9months [IQR 0-6.9]. Seven patients had BS types 1 or 2, 12 had BS type 3 and two had no mutation identified. There was a trend towards a decrease in sodium chloride supplementation after initiation of NSAIDs. When defining response to treatment based on the normalization of plasma renin level, responders had a greater reduction in their electrolytes supplementation. NSAIDs treatment was associated with a reduction in urine calcium. Before treatment, half of the patients had elevated iPTH, but iPTH normalized following initiation of NSAIDs in all but one patient. This study confirms that NSAIDs reduce urine wasting of sodium and calcium in patients with BS. Monitoring serum renin levels may be useful to identify the lowest effective dose of NSAIDs that optimizes reduction of urine electrolyte losses.

P179 A retrospective audit of sodium chloride supplementation in infants with cystic fibrosis

P179 A retrospective audit of sodium chloride supplementation in infants with cystic fibrosis

Sodium Chloride Supplementation Is Not Routinely Performed in the Majority of German and Austrian Infants with Classic Salt-Wasting Congenital Adrenal Hyperplasia and Has No Effect on Linear Growth and Hydrocortisone or Fludrocortisone Dose

Introduction: Sodium chloride supplementation in salt-wasting congenital adrenal hyperplasia (CAH) is generally recommended in infants, but its implementation in routine care is very heterogeneous. Objective: To evaluate oral sodium chloride supplementation, growth, and hydrocortisone and fludrocortisone dose in infants with salt-wasting CAH due to 21-hydroxylase in 311 infants from the AQUAPE CAH database. Results: Of 358 patients with classic CAH born between 1999 and 2015, 311 patients had salt-wasting CAH (133 females, 178 males). Of these, 86 patients (27.7%) received oral sodium chloride supplementation in a mean dose of 0.9 ± 1.4 mmol/kg/day (excluding nutritional sodium content) during the first year of life. 225 patients (72.3%) were not treated with sodium chloride. The percentage of sodium chloride-supplemented patients rose from 15.2% in children born 1999–2004 to 37.5% in children born 2011–2015. Sodium chloride-supplemented and -unsupplemented infants did not significantly differ in hydrocortisone and fludrocortisone dose, target height-corrected height-SDS, and BMI-SDS during the first 2 years of life. Conclusion: In the AQUAPE CAH database, approximately one-third of infants with salt-wasting CAH receive sodium chloride supplementation. Sodium chloride supplementation is performed more frequently in recent years. However, salt supplementation had no influence on growth, daily fludrocortisone and hydrocortisone dose, and frequency of adrenal crisis.

Diagnosis and Management of Combined Central Diabetes Insipidus and Cerebral Salt Wasting Syndrome After Traumatic Brain Injury

Combined central diabetes insipidus and cerebral salt wasting syndrome after traumatic brain injury (TBI) is rare, is characterized by massive polyuria leading to severe water and electrolyte disturbances, and usually is associated with very high mortality mainly as a result of delayed diagnosis and improper management. We retrospectively reviewed the clinical presentation, management, and outcomes of 11 patients who developed combined central diabetes insipidus and cerebral salt wasting syndrome after traumatic brain injury to define distinctive features for timely diagnosis and proper management. The most typical clinical presentation was massive polyuria (10,000 mL/24 hours or >1000 mL/hour) refractory to vasopressin alone but responsive to vasopressin plus cortisone acetate. Other characteristic presentations included low central venous pressure, high brain natriuretic peptide precursor level without cardiac dysfunction, high 24-hour urine sodium excretion and hypovolemia, and much higher urine than serum osmolarity; normal serum sodium level and urine specific gravity can also be present. Timely and adequate infusion of sodium chloride was key in treatment. Of 11 patients, 5 had a good prognosis 3 months later (Extended Glasgow Outcome Scale score ≥6), 1 had an Extended Glasgow Outcome Scale score of 4, 2 died in the hospital of brain hernia, and 3 developed a vegetative state. For combined diabetes insipidus and cerebral salt wasting syndrome after traumatic brain injury, massive polyuria is a major typical presentation, and intensive monitoring of fluid and sodium status is key for timely diagnosis. To achieve a favorable outcome, proper sodium chloride supplementation and cortisone acetate and vasopressin coadministration are key.

Electrolyte supplementation during severe energy restriction increases exercise capacity in the heat

This study examined the effects of sodium chloride and potassium chloride supplementation during 48-h severe energy restriction on exercise capacity in the heat. Nine males completed three 48-h trials: adequate energy intake (100 % requirement), adequate electrolyte intake (CON); restricted energy intake (33 % requirement), adequate electrolyte intake (ER-E); and restricted energy intake (33 % requirement), restricted electrolyte intake (ER-P). At 48 h, cycling exercise capacity at 60 % VO2 peak was determined in the heat (35.2 °C; 61.5 % relative humidity). Body mass loss during the 48 h was greater during ER-P [2.16 (0.36) kg] than ER-E [1.43 (0.47) kg; P < 0.01] and CON [0.39 (0.68) kg; P < 0.001], as well as greater during ER-E than CON (P < 0.01). Plasma volume decreased during ER-P (P < 0.001), but not ER-E or CON. Exercise capacity was greater during CON [73.6 (13.5) min] and ER-E [67.0 (17.2) min] than ER-P [56.5 (13.1) min; P < 0.01], but was not different between CON and ER-E (P = 0.237). Heart rate during exercise was lower during CON and ER-E than ER-P (P < 0.05). These results demonstrate that supplementation of sodium chloride and potassium chloride during energy restriction attenuated the reduction in exercise capacity that occurred with energy restriction alone. Supplementation maintained plasma volume at pre-trial levels and consequently prevented the increased heart rate observed with energy restriction alone. These results suggest that water and electrolyte imbalances associated with dietary energy and electrolyte restriction might contribute to reduced exercise capacity in the heat.

Role of sph2 Gene Regulation in Hemolytic and Sphingomyelinase Activities Produced by Leptospira interrogans.

Pathogenic members of the genus Leptospira are the causative agents of leptospirosis, a neglected disease of public and veterinary health concern. Leptospirosis is a systemic disease that in its severest forms leads to renal insufficiency, hepatic dysfunction, and pulmonary failure. Many strains of Leptospira produce hemolytic and sphingomyelinase activities, and a number of candidate leptospiral hemolysins have been identified based on sequence similarity to well-characterized bacterial hemolysins. Five of the putative hemolysins are sphingomyelinase paralogs. Although recombinant forms of the sphingomyelinase Sph2 and other hemolysins lyse erythrocytes, none have been demonstrated to contribute to the hemolytic activity secreted by leptospiral cells. In this study, we examined the regulation of sph2 and its relationship to hemolytic and sphingomyelinase activities produced by several L. interrogans strains cultivated under the osmotic conditions found in the mammalian host. The sph2 gene was poorly expressed when the Fiocruz L1-130 (serovar Copenhageni), 56601 (sv. Lai), and L495 (sv. Manilae) strains were cultivated in the standard culture medium EMJH. Raising EMJH osmolarity to physiological levels with sodium chloride enhanced Sph2 production in all three strains. In addition, the Pomona subtype kennewicki strain LC82-25 produced substantially greater amounts of Sph2 during standard EMJH growth than the other strains, and sph2 expression increased further by addition of salt. When 10% rat serum was present in EMJH along with the sodium chloride supplement, Sph2 production increased further in all strains. Osmotic regulation and differences in basal Sph2 production in the Manilae L495 and Pomona strains correlated with the levels of secreted hemolysin and sphingomyelinase activities. Finally, a transposon insertion in sph2 dramatically reduced hemolytic and sphingomyelinase activities during incubation of L. interrogans at physiologic osmolarity. Complementation of the mutation with the sph2 gene partially restored production of hemolytic and sphingomyelinase activities. These results indicate that the sph2 gene product contributes to the hemolytic and sphingomyelinase activities secreted by L. interrogans and most likely dominates those functions under the culture condition tested.

Short-term dietary salt supplementation blunts telmisartan induced increases in plasma renin activity in hypertensive patients with type2 diabetes mellitus.

Current guidelines recommend low dietary salt intake (LDS) in patients with diabetes to reduce blood pressure (BP). However, low salt intake has been associated with higher mortality rates in people with diabetes. Our aim is to examine the effect of angiotensin II receptor blocker (ARB), telmisartan, with and without dietary sodium chloride (NaCl) supplementation, on BP [mean arterial pressure (MAP)], plasma renin activity (PRA), serum aldosterone level and estimated glomerular filtration rate (eGFR) in hypertensive patients with type2 diabetes. In a randomized, double-blind, placebo-controlled study (RCT), 28 patients with type2 diabetes, treated with telmisartan (40mg daily), received 2weeks of placebo or NaCl capsules (100mmol/24h). Following a 6-week washout, the protocol was repeated in reverse. Twenty-four-hour urinary sodium excretion (24hUNa), ambulatory BP (ABP) monitoring and blood tests were performed before and after each study phase. The telmisartan-associated increase in PRA was blunted by approximately 50% during salt supplementation compared with placebo; median PRA was 2.3μg/l/h with placebo compared with 1.7μg/l/h with salt (P<0.001). A trend towards blunting of ARB induced increases in serum aldosterone was also demonstrated. Salt supplementation significantly reduced the MAP lowering effects of telmisartan (P<0.05). The present study demonstrates that salt supplementation blunts the telmisartan induced increase in PRA in patients with type2 diabetes.

A Case of Difficult Management of Fluid-electrolyte Imbalance in Choroid Plexus Papilloma

A 22-month-old boy presented with nausea and gradual deterioration of gait disturbance. Computed tomography (CT) demonstrated an intraventricular mass lesion in the right lateral ventricle. He was referred to our department 3 weeks after onset. Acute hydrocephalus gradually proceeded 4 days after admission, and external ventricular drainage (EVD) was performed. EVD revealed cerebrospinal fluid (CSF) overproduction (800-1,500 mL/day) under constant pressure of 10 cm H2O above external auditory meatus. Magnetic resonance imaging showed a multi-lobular mass in the inferior horn of the right lateral ventricle. A choroid plexus tumor was suspected. The ratio of blood urea nitrogen:creatinine (BUN:Cre) remained between 30 and 40, and hemoglobin was between 14.0-17.0 mg/dL, suggesting marked dehydration. Serum sodium varied between 117 and 140 mmol/L, and serum potassium between 2.2 mmol/L and 6.9 mmol/L. The amount of EVD was unstable and fluid balance management was difficult. Hypotonic fluid with sodium chloride supplement was used to adjust the fluid and electrolyte imbalance. Surgical removal of the tumor was performed 6 days after EVD and tumor was grossly and totally removed. The high BUN:Cre ratio decreased to about 15 and hemoglobin recovered to 7.5-9.0 mg/dL after removal. Electrolytes returned to the normal range. Overproduction of CSF also markedly improved to < 300 mL/day. Histopathological examination diagnosed choroid plexus papilloma.We experienced a case of choroid plexus papilloma associated with fluid-electrolyte imbalance due to over-drainage after EVD, which could not be effectively controlled before tumor removal. Cautious fluid management and emergent surgical resection might be required to manage the overproduction of CSF and fluid-electrolyte imbalance.

Classic Bartter syndrome complicated with profound growth hormone deficiency

Case history A Japanese boy was born at 41 weeks of gestational age by spontaneous cephalic delivery, with birth weight 3,680g. Family history was remarkable for his elderly sister suffering from classic Bartter syndrome. He also was diagnosed as classic Bartter syndrome, based on the findings such as failure to thrive, metabolic alkalosis with hypokalemia, and the activated renin-aldosterone system. The diagnosis was later confirmed by CLCNKB gene analysis which revealed compound heterozygous mutations: deletion of the exon 1 3 (derived from his mother) and ΔL130 (derived from the father). Treatment with spironolactone, indomethacin, sodium chloride, and potassium supplementation was commenced at 8 months of age. However, his serum potassium level failed to normalize, and tended to be around 2 3mEq/L. He had mild intellectual impairment, and needed specialized education. When he was 11 years old, through the investigation for macrohematuria, renal stones with nephrocalcinosis were detected. This complication resolved following the amelioration of hypokalemia, which was achieved by vigorous potassium fortification. Because his growth rate was consistently subnormal and he was very short (-4.7SD), scrutiny for growth hormone (GH) secretion was conducted at his 14 years of age.

Is hyponatremia mistreated? – Challenging the current paradigm

BackgroundHyponatremia is a common but often mistreated clinical situation in the ICU. This often requires the physician to identify the underlying problem, adrenal insufficiency. However, by the textbook, the current treatment always involves sodium chloride supplementation to hyponatremic patients, either intravenous or oral intake. We hypothesize that the mechanism behind most hyponatremia is most likely to be the sodium and water redistribution from the serum to the cells or the interstitial spaces due to the insufficient cortical steroid, not the sodium deficiency. As we have no reason to believe the patients have lost that much sodium which caused hyponatremia. Therefore, giving this type of hyponatremic patients (adrenal insufficient) sodium chloride is always ineffective and sometimes catastrophic. MethodsWe discuss the possible mechanism for hyponatremia in critically ill/post surgery patients who are mostly likely to be adrenal insufficient rather than absolute sodium deficiency. In combination with many other common but unexplainable symptoms such as nausea, vomiting, obstinate diarrhea, hypotension and coma in the ICU, it is highly likely that hyponatremia is a condition which reflects the patients’ adrenal function. The evidence supporting our hypothesis is that, (1) the serum sodium level does not always respond well to sodium supplementation therapy; (2) those aforementioned symptoms alleviated simultaneously with the serum sodium level returned to normal after the hydrocortisone or prednisone was administered without any oral/intravenous sodium supplementation; (3) patient with an elevated serum/urine cortisol level suffers from aforementioned unexplainable symptoms does not warrant him being adrenal sufficient. If the patient also has hyponatremia, the diagnosis can be considered as “relative adrenal insufficiency” and the patient would respond well to hydrocortisone or prednisone therapy. ConclusionsWe hypothesize that hyponatremia without significant loss of sodium can be used as an indicator to monitor the patients’ adrenal function regardless of the serum/urine cortisol level. Furthermore, we propose a novel approach toward hyponatremia treatment in critically ill patients would be hydrocortisone or prednisone therapy depending on the circumstances.

Pseudohypoaldosteronism type 1: Management issues

We report a newborn girl with life-threatening hyperkalemia and salt wasting crisis due to severe autosomal recessive multiple target organ dysfunction pseudohypoaldosteronism type 1 (MTOD PHA1). She was aggressively managed with intravenous fluids, potassium-lowering agents, high-dose sodium chloride supplementation and peritoneal dialysis. Genetic analysis revealed a homozygous mutation of the α- ENaC (epithelial Na(+) channel) gene. She had a stormy clinical course with refractory hyperkalemia and prolonged hospitalization. Eventually, she succumbed to pneumonia and septicemia at 4 months of age. This is probably the first case of PHA1 confirmed by genetic analysis from India.

Growth condition optimization for docosahexaenoic acid (DHA) production by Moritella marina MP-1

The marine organism Moritella marina MP-1 produces the polyunsaturated fatty acid docosahexaenoic acid (DHA). While the basic metabolic pathway for DHA production in this organism has been identified, the impact of growth conditions on DHA production is largely unknown. This study examines the effect of supplemental carbon, nitrogen and salts, growth temperature and media composition and pH on DHA and biomass production and the fatty acid profile. The addition of supplemental nitrogen significantly increased the overall DHA titer via an increase in biomass production. Supplemental glucose or glycerol increased biomass production, but decreased the amount of DHA per biomass, resulting in no net change in the DHA titer. Acidification of the baseline media pH to 6.0 increased DHA per biomass. Changes in growth temperature or provision of supplemental sodium or magnesium chloride did not increase DHA titer. This organism was also shown to grow on defined minimal media. For both media types, glycerol enabled more DHA production per biomass than glucose. Combination of these growth findings into marine broth supplemented with glycerol, yeast extract, and tryptone at pH 6.0 resulted in a final titer of 82±5 mg/L, a nearly eightfold increase relative to the titer of 11±1 mg/L seen in the unsupplemented marine broth. The relative distribution of other fatty acids was relatively robust to growth condition, but the presence of glycerol resulted in a significant increase in myristic acid (C14:0) and decrease in palmitic acid (C16:0). In summary, DHA production by M. marina MP-1 can be increased more than fivefold by changing the growth media. Metabolic engineering of this organism to increase the amount of DHA produced per biomass could result in additional increases in titer.