Serum Chloride Concentrations Research Articles

Retrospective evaluation of paired plasma creatinine and chloride concentrations following hetastarch administration in anesthetized dogs (2002-2015): 244 cases.

To evaluate changes in serum creatinine and chloride concentrations in anesthetized dogs that received 6% hydroxyethyl starch (HES) 670/0.7. Retrospective case series, 2002-2015. University veterinary teaching hospital. Two hundred forty-four client-owned dogs undergoing general anesthesia that received an HES solution. None. Medical records of dogs that received an HES solution (6%, 670/0.7) while under general anesthesia during the study period were reviewed. Information obtained from the medical record included patient signalment, reason for anesthesia or diagnosis, body weight, amount of HES solution administered, pre- and postanesthesia creatinine value, pre- and postanesthesia chloride value, and day interval between measurements. Corrected chloride values were used for all statistical analysis. Dogs received a median dose of 6.3 mL/kg hetastarch during anesthesia. Median preanesthesia creatinine and corrected chloride values were 79.5μmol/L (0.9mg/dL) (range 8.8-689.5μmol/L [0.1-7.8mg/dL]) and 111mmol/L (111mEq/L) (range 80-123mmol/L [80-123mg/dL]), respectively. Median postanesthesia creatinine was 57.4μmol/L (0.65mg/dL) (8.8-716μmol/L [0.1-8.1mg/dL]). Median postanesthesia corrected chloride was 115mmol/L (115mEq/L) (range 87.5-129.6mmol/L [87.5-129.6mEq/L]). Mann-Whitney test analysis revealed a significant decrease in creatinine (Δ Cr 17.7μmol/L [0.2mg/dL], P < 0.01) and a significant increase in corrected chloride (Δ Cl 4.1mmol/L [4.1mEq/L], P < 0.01) between pre- and postanesthesia values. In a mixed population of hospitalized dogs undergoing general anesthesia that received a median dose of 6 mL/kg of HES, creatinine was lower and chloride was higher in the postanesthetic than in the preanesthetic period. The clinical significance of these changes and the role that HES administration played in them relative to concurrent therapies is unknown.

Water intake after dehydration makes muscles more susceptible to cramp but electrolytes reverse that effect

ObjectiveNo previous study has compared water and oral rehydration solution (ORS) intake after dehydration induced by exercise in the heat for the effect on muscle cramps. The present study tested...

Effect of iodinated contrast media on serum electrolyte concentrations in patients undergoing routine contrast computed tomography scan procedure

Background and Objectives:Being hypertonic solutions, iodinated contrast media such as iohexol can cause a shift of fluids and electrolytes between different compartments of the body, but there is an ongoing discrepancy in data and current studies as to the effect of iodinated contrast media on serum electrolytes. Hence, this hospital-based prospective clinical observational study was carried out with objectives of evaluating the changes in serum electrolyte concentrations with intravenous iodinated contrast media administration in adult population and to correlate the changes in electrolyte concentrations, if any, with the demographic profile of the patients.Materials and Methods:We analyzed 103 numbers of adult patient samples over a period of 2 months by collecting blood both before administration of contrast and after 24 h of the contrast-enhanced computed tomography scan procedure. Serum concentrations of sodium, potassium, chloride, and ionized calcium were measured using Eschweiler Combiline analyzer based on ion-selective electrode principle.Results:The mean age of the study population in our study was 40.11 ± 20.51 years. We found that changes in serum sodium and chloride concentration after administration of contrast media are significant (sodium: 136.29 ± 3.53 vs. 132.49 ± 6.36 mmol/L and chloride: 100.03 ± 0.70 vs. 97.53 ± 0.70 mmol/L). Sodium concentration shows more decrease in females compared to males after administration of iodine contrast. The most probable reason for this decrease in serum electrolytes was secondary changes to hemodilution due to high osmolality of the contrast.Conclusions:Attending physicians must be alert for such possibilities of changes in electrolytes after contrast administration and be prepared to treat any adversity if one occurs.

CHOLESTEROL AND CHLORIDE IN ACUTE HEART FAILURE.

SUMMARYDetecting predictors of poor outcome is crucial for understanding the underlying pathophysiology of heart failure (HF) and thus creating new therapeutic concepts. It is well established that low serum lipid levels are associated with unfavorable outcomes in HF patients. Several studies examined the association between serum lipids and established predictors of mortality in HF patients. The aim of the present study was to examine the association of serum lipid and chloride concentrations, as well as their impact on survival in acute heart failure (AHF). The present study was performed as a prospective, single-centre, observational research. The study included 152 patients with AHF. Spearman’s correlation coefficient revealed a significant positive correlation of serum chloride levels with serum levels of total cholesterol (ρ 0.221, p=0.006), low-density lipoprotein cholesterol (LDL-c) (ρ 0.187, p=0.015) and high-density lipoprotein-cholesterol (HDL-c) (ρ 0.169, p=0.038). Binary logistic regression revealed a significant association of chloride, total cholesterol and LDL-c serum levels measured at admission with hospital survival (OR 1.077, CI 1.01-1.154, p=0.034), (OR 1.731, CI 1.090-2.748, p=0.020) and (OR 1.839, CI 1.033-3.274, p=0.038), respectively, as well as with 3-month survival (OR 1.065, CI 1.002-1.131, p=0.042), (OR 1.625, CI 1.147-2.303, p=0.006) and (OR 1.711, CI 1.117-2.622, p=0.014), respectively. In conclusion, positive statistical association between serum cholesterol (total cholesterol, LDL-c and HDL-c) and chloride levels may suggest their similar modulation by AHF pathophysiology. Serum levels of total cholesterol, LDL-c and chloride contribute to patient survival.

"I don't get no respect": the role of chloride in acute kidney injury.

Acute kidney injury (AKI) is a major public health problem that complicates 10-40% of hospital admissions. Importantly, AKI is independently associated with increased risk of progression to chronic kidney disease, end-stage renal disease, cardiovascular events, and increased risk of in-hospital and long-term mortality. The chloride content of intravenous fluid has garnered much attention over the last decade, as well as its association with excess use and adverse outcomes, including AKI. Numerous studies show that changes in serum chloride concentration, independent of serum sodium and bicarbonate, are associated with increased risk of AKI, morbidity, and mortality. This comprehensive review details the complex renal physiology regarding the role of chloride in regulating renal blood flow, glomerular filtration rate, tubuloglomerular feedback, and tubular injury, as well as the findings of clinical research related to the chloride content of intravenous fluids, changes in serum chloride concentration, and AKI. Chloride is underappreciated in both physiology and pathophysiology. Although the exact mechanism is debated, avoidance of excessive chloride administration is a reasonable treatment option for all patients and especially in those at risk for AKI. Therefore, high-risk patients and those with "incipient" AKI should receive balanced solutions rather than normal saline to minimize the risk of AKI.

Hyperchloremia Is Not an Independent Risk Factor for Postoperative Acute Kidney Injury in Pediatric Cardiac Patients

Hyperchloremia recently has been shown to have an association with the development of acute kidney injury (AKI) in critically ill patients. However, there is little information about the prevalence of an abnormal chloride concentration after pediatric cardiac surgery and its association with postoperative AKI. The aim of this study was to determine the prevalence of hyperchloremia and its association with AKI in pediatric patients after cardiac surgery. A retrospective single-center study. Referral high-volume pediatric cardiac center in a tertiary teaching hospital. Patients under 72 months of age with congenital heart disease who underwent cardiac surgery with the use of cardiopulmonary bypass. None. The primary outcome was development of AKI diagnosed by Kidney Disease Improving Global Outcomes consensus criteria. The associations of outcomes with the highest serum chloride concentration ([Cl-]max) and time-weighted average chloride concentration ([Cl-]ave) within the first 48 hours after surgery were investigated. Of 521 patients included in the study, 463 patients (88.9%) had hyperchloremia at least 1 time within the first 48 hours after surgery. Postoperative AKI occurred in 205 patients (39.3%). [Cl-]ave and [Cl-]max in the AKI group were significantly higher than those in the non-AKI group (112 [110-114] mEq/L v 111 [109-113] mEq/L, p = 0.001 and 116 [113, 119] mEq/L v 114 [112-118] mEq/L, p = 0.002, respectively). After adjustment for other predictors of AKI by multivariable analyses, neither [Cl-]ave nor [Cl-]max was associated independently with the development of AKI (odds ratio [OR] = 1.040, 95% confidence interval [CI]: 0.885-1.220, p = 0.63; OR = 0.992, 95% CI: 0.874-1.130. p = 0.90). Postoperative hyperchloremia was common and was associated with the development of AKI in pediatric patients after congenital cardiac surgery in univariate analysis. After adjustment for predictors of AKI by multivariate analyses, there was no significant relationship between postoperative chloride concentration and AKI.

Increase in serum chloride and chloride exposure are associated with acute kidney injury in moderately severe and severe acute pancreatitis patients

ObjectiveWe aimed to evaluate whether early (first 48 h) hyperchloremia and/or the change of serum chloride concentration are associated with acute kidney injury (AKI) in patients with moderately severe and severe acute pancreatitis (MSAP and SAP). MethodsWe retrospectively collected the data of patients with a primary diagnosis of MSAP or SAP from a tertiary center between January 2014 and June 2017. Consecutive chloride levels within the first 48 h after admission were retrieved for further calculation. Logistic regression analysis and receiving operating characteristic (ROC) curve were used to assess the relationship between hyperchloremia and AKI. Results145 patients were enrolled for analysis, of whom 33.5% (47/145) developed hyperchloremia during the observation period. The incidence of AKI was significantly higher in the hyperchloremia group (40.4% vs 7.1%; p < 0.001). On multivariate analysis, the increase in serum chloride (Δ[Cl-]) was independently associated with AKI [OR = 1.32 (1.00–1.74)], as was chloride exposure [OR = 1.01 (1.00–1.02)], and these associations were found to be stronger in patients identified as predicted SAP (PSAP). Moreover, even in patients without hyperchloremia, increase in serum chloride (Δ[Cl-]) was still associated with AKI [OR = 1.65 (1.18–2.32)]. Area under the curve of the ROC curve (AUCROC) analysis found that Δ[Cl-] is a good predictor of AKI with an optimal cutoff point at 3.5 mmol/L, showing an AUCROC of 0.81. ConclusionHyperchloremia is common in patients with AP and Δ[Cl−] and chloride exposure during the first 48 h were independent risk factors for AKI in MSAP and SAP patients.

Low-chloride versus high-chloride hypertonic solution for the treatment of subarachnoid hemorrhage-related complications (The ACETatE trial): study protocol for a pilot randomized controlled trial

BackgroundAneurysmal subarachnoid hemorrhage (aSAH) is a life-threatening condition that results from a ruptured cerebral vessel. Cerebral edema and vasospasm are common complications and frequently require treatment with hypertonic solutions, in particular hypertonic sodium chloride (NaCl). We have previously shown that hyperchloremia in patients with aSAH given hypertonic NaCl is associated with the development of acute kidney injury (AKI), which leads to higher morbidity and mortality. Our current trial aims to study the effect of two hypertonic solutions with different chloride content on serum chloride concentrations in patients with aSAH who are at risk for AKI.MethodsA low ChloridE hyperTonic solution for brain Edema (ACETatE) is a single center, double-blinded, double-dummy pilot trial comparing bolus doses of 23.4% NaCl and 16.4% NaCl/Na-Acetate for the treatment of cerebral edema in patients with aSAH. All patients will be enrolled within 36 h following admission. Randomization will occur once patients who receive hypertonic treatment for cerebral edema develop hyperchloremia (serum Cl− concentration ≥ 109 mmol/L). Subsequent treatment will consist of either NaCl 23.4% or NaCl/Na-Acetate 16.4%. The primary outcome of this study will be the change in serum Cl− concentrations during treatment. Secondary outcomes will include incidence of AKI, mortality, changes in intracranial pressure, and extent of hypernatremia.DiscussionIn patients with aSAH, hyperchloremia is a known risk factor for subsequent development of AKI. The primary goal of this pilot study is to determine the effect of two hypertonic solutions with different Cl− content on serum Cl− concentrations in patients with aSAH who have already developed hyperchloremia. Data will be collected prospectively to determine the extent to which the choice of hypertonic saline solution affects subsequent serum Cl− concentrations and the occurrence of AKI. This approach will allow us to obtain preliminary data to design a large randomized trial assessing the effects of chloride-sparing hypertonic solutions on development of AKI in patients with SAH. This pilot study is the first to prospectively evaluate the relationship between hypertonic solution chloride content and its effect on serum electrolytes and renal function in aSAH patients at risk of AKI due to hyperchloremia.Trial registrationClinicaltrials.gov, NCT03204955. Registered on 28 June 2017.

Dynamic changes in serum chloride concentrations during worsening of heart failure and its recovery following conventional diuretic therapy: A single-center study.

Background and aimsFew data are available regarding the dynamic changes in the serum chloride concentrations in heart failure (HF) pathophysiology. The aim of the present study was to investigate changes in the serum chloride concentration under worsening HF and its recovery following conventional diuretic therapy.MethodsBlood test data, including measurements of serum albumin/solutes and b‐type natriuretic peptide, at both worsening and recovery of HF status, were obtained from 47 patients with definite HF.ResultsAmbulatory patients with HF were enrolled and followed up at the outpatient clinic of Nishida Hospital between June 2003 and March 2009. From clinically stable to worsening HF, the serum sodium concentration increased from (mean ± SD) 139 ± 4.1 to 141 ± 5.07 mEq/L (P < 0.05, two‐way analysis of variance) and the serum chloride concentration increased from 101 ± 5.36 to 104 ± 5.44 mEq/L (P < 0.01) among all patients. After resolution of worsening HF by treatment with conventional diuretics, both the serum sodium concentration and serum chloride concentration decreased significantly to 138 ± 5.12 and 99.5 ± 5.33 mEq/L, respectively (P < 0.0001 for each). The absolute changes in the serum sodium concentration from clinically stable HF to worsening HF appeared to be lesser than those in the serum chloride concentration (1.70 ± 4.34 vs 2.72 ± 6.02 mEq/L, P = 0.079, t test), but this was not statistically significant. Absolute changes in the serum sodium concentration from worsening HF to its recovery following treatment with conventional diuretics were lesser than those in the serum chloride concentration (−2.87 ± 4.38 vs −4.45 ± 5.23 mEq/L, P = 0.0068, t test).ConclusionUnder conventional diuretic therapy, greater changes occur in the serum chloride concentration than in the serum sodium concentration under HF state transitions, suggesting that chloride dynamics might contribute more to HF pathophysiology under such therapeutic circumstance.

Perturbations in serum chloride homeostasis in heart failure with preserved ejection fraction: insights from TOPCAT.

Prior cohorts demonstrating the importance of serum chloride levels in heart failure either excluded or had partial representation of patients with heart failure with preserved ejection fraction (HFpEF). We aimed to examine the relationship between serum chloride concentration and outcomes in HFpEF. We included participants from the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist Trial (TOPCAT) who met the following criteria: met inclusion by the natriuretic peptide stratum, had recorded serum chloride levels, and were from the Americas (n = 942). Multivariable Cox proportional hazards models tested the association of serum chloride with clinical outcomes, and mixed effects modelling tested the association of spironolactone or loop diuretic on serial serum chloride levels. The median serum chloride level was 102 [25th-75th percentile 100-105 mmol/L (range 84-114 mmol/L)]. After multivariable adjustment, every standard deviation decrease in serum chloride (4.05 mmol/L) was associated with ∼50% increased risk for cardiovascular death [hazard ratio (HR) 1.51, 95% confidence interval (CI) 1.11-2.06, P = 0.008] and ∼30% increased risk for all-cause death (HR 1.29, 95% CI 1.02-1.62, P = 0.04), but not with the primary composite endpoint or heart failure hospitalization (P > 0.3 for both). There were no significant interactions between spironolactone use and the serum chloride-risk relationship (P > 0.1) for each endpoint. Spironolactone was not (P = 0.33) but loop diuretic use was associated with lower serial serum chloride levels (P < 0.001). Lower serum chloride was independently associated with increased risk of cardiovascular and all-cause death in HFpEF. Loop diuretic use, but not spironolactone, lead to a decrease in serum chloride levels over time.

Changes in red blood cell volume during transition of heart failure status: a reflection of cellular hydration status?

This study examined how changes in heart failure (HF) status induce changes in the index of erythrocyte hydration based on mean red blood cell volume (MCV). Data from 47 HF patients (32% men; 78.2 ± 9.7 years) that experienced worsening and recovery of HF were analysed. Blood tests included measurements of MCV, albumin, serum solutes and b-type natriuretic peptide (BNP). Among a total of 47 worsening HF events, changes in MCV were positively correlated with changes in body weight (r = 0.31, p = .034), serum sodium (r = 0.417, p = .0036), and chloride (r = 0.457, p = .0012), and negatively correlated with changes in blood urea nitrogen (r= −0.389, p = .0069) and creatinine (r= −0.494, p = .0004). At recovery from worsening of HF by conventional diuretic therapy, change in MCV was positively correlated with the change in body weight (r = 0.457, p = .0012), serum sodium (r = 0.466, p = .001) and chloride (r = 0.484, p = .0006). Multivariate regression analysis demonstrated an independent association between the increase in serum chloride and MCV from stability to worsening of HF (odds ratio [OR] 6.02, 95% confidence interval [CI] 1.09–33.2, p = .039) and the increase or absence of change in serum chloride concentration and preserved MCV after decongestion (OR 11.5, 95% CI 1.53–85.9, p = .017). In conclusion, this study demonstrates that the changes in MCV under transition in HF status do not reflect a change that occurs in parallel with changes in HF-related markers, such as body weight and serum BNP level, but is independently associated with a change in the serum chloride concentration. Whether changes in MCV actually reflect the bodily cellular hydration status warrants further research.

Serum chloride as a novel marker for adding prognostic information of mortality in chronic heart failure

BackgroundSerum chloride concentrations have clinical significance in the prognosis of heart failure (HF). Little is known regarding the prognostic value of serum chloride in patients with chronic heart failure (CHF). This study sought to investigate the prognostic ability of admission serum chloride for long-term mortality in CHF patients. MethodsWe identified 1021 consecutive patients diagnosed with CHF. Participants were followed up for all-cause mortality at 21 ± 9 months to establish the survival models and analyze the association between admission serum chloride concentrations and death risk. ResultsOf the 1021 patients, 905(88.6%) available cases were obtained. Admission serum chloride concentrations of patients were independently and inversely associated with long-term mortality (hazard ratio [HR]: 0.890; 95% CI: 0.863 to 0.918; p < 0.001). After multivariable risk adjustment for age, male sex, history of diabetes, LVEF, loop diuretic use, beta-blocker use, ACEI or ARB use, eGFR and NT-proBNP, chloride concentrations remained independently associated with mortality (HR:0.922; 95% CI:0.887 to 0.958; p < 0.001) but not independent of sodium concentrations (HR: 0.953; 95% CI: 0.900 to 1.009; p = 0.095). The optimal cut-off value of chloride concentrations predicting death was 102.8 mmol/l with an area under the curve (AUC) value of 0.686 (95% CI: 0.635 to 0.737; p < 0.001), with a sensitivity of 62% and specificity of 70%. The lower chloride concentrations could significantly increase the risk ratio of CHF patients in the setting of hyponatremia (p < 0.001). The cumulative survival estimates significantly differed across Na/Cl quartiles (log-rank χ2 19.14, p < 0.001), with higher mortality for higher Na/Cl ratio. Correlation analysis showed a positive correlation between serum chloride concentrations and sodium concentrations (r = 0.598; p < 0.001). An increased AUC was observed by combining chloride and sodium (AUC = 0.704, 95% CI:0.655–0.754, p < 0.001) compared to sodium only (AUC = 0.689, 95% CI:0.639–0.739, p < 0.001). ConclusionsIn a Chinese Han population, admission serum chloride concentrations are inversely associated with all-cause mortality of CHF patients and provide incremental prognostic information of serum sodium.

Use of Arginine Hydrochloride in the Treatment of Metabolic Alkalosis or Hypochloremia in Pediatric Patients.

Dosing of arginine for treatment of hypochloremia or metabolic alkalosis is laborious and has inherent variability in dose selection. The primary objective of this study was to determine the efficacy of arginine in the treatment of metabolic alkalosis and hypochloremia. Secondary objectives were to determine an optimal dose, route, and frequency for arginine administration in the treatment of these conditions. This single center, retrospective, descriptive study was conducted in children who received arginine for treatment of hypochloremia or metabolic alkalosis. Treatment success was assessed by measuring serum chloride and bicarbonate concentrations after arginine administration. Of the 464 orders analyzed, 177 met inclusion criteria in 82 unique patients. Fifty percent (n = 81) of arginine administrations used to manage hypochloremia saw normalization of abnormal chloride levels, and 83% (n = 62) of arginine administrations used to treat metabolic alkalosis saw normalization of abnormal bicarbonate levels. Patients who received arginine to resolve hypochloremia were statistically significantly more likely to have their hypochloremia resolve if they used alternative dosing methods compared to established dosing methods (76 vs. 5, p = 0.001). However, this relationship was not seen for patients with metabolic alkalosis (11 vs. 51, p = 1.000). The median percentage of calculated daily dose of arginine needed for resolution of hypochloremia was 59% and was 35% for metabolic alkalosis. Arginine is effective to improve metabolic alkalosis and hypochloremia. Established dosing methods are not more effective than other methods in resolving metabolic alkalosis or hypochloremia. Further prospective studies are warranted to validate these results.

Case 3: Fever, Vomiting, and Altered Mental Status in a 17-year-old Boy

1. Jonathan Pelletier, MD* 2. Kathleen Bartlett, MD* 1. *Duke Children's Hospital and Health Center, Durham NC A 17-year-old boy with a history of restrictive eating disorder and orthostatic hypotension presents via emergency medical services from an eating disorder facility with 1 week of dizziness and confusion and 1 day of fever. He also reports months of daily first-morning, nonbloody, and nonbilious vomiting. On presentation to the emergency department he is febrile (temperature, 102.9°F [39.4°C]), tachycardic (heart rate, 112 beats/min), and hypotensive (blood pressure, 91/46 mm Hg) and requires oxygen via nasal cannula. His weight is 114.2 lb (51.8 kg) (3rd percentile), height is 64.6 in (164 cm) (5th percentile), and BMI is 19.3 (15th percentile). General physical examination findings are normal. Shortly after arrival, the patient develops a brief episode of upper extremity tonic extension, unresponsiveness, and desaturation. He recovers spontaneously without an apparent postictal period. Repeated neurologic examination reveals slowed but appropriate responses to questioning. Cranial nerves, strength, sensation, and reflexes are normal. Upper extremity coordination is normal, but he has right greater than left ataxia with heel-to-shin testing. The patient is unable to stand for gait and Romberg testing due to dizziness. Laboratory tests before fluid therapy are remarkable for a serum sodium concentration of 149 mEq/L (149 mmol/L) (reference range, 135–145 mEq/L [135–145 mmol/L]), a serum chloride concentration of 118 mEq/L (118 mmol/L) (reference range, 96–108 mEq/L [96–108 mmol/L]), leukocytosis, and normocytic anemia. Urinalysis results are normal, …

The effect of a commercial feed additive on the immune-metabolic axis, liver function and predicted carcass quality in purebred Angus steers

To determine the effect of the commercial feed additive OmniGen-AF® on immune, physiological, and carcass ultrasound variables in steers during backgrounding, transition, and finishing phases, nine purebred Angus half-sibling steers were randomly assigned to one of two treatment groups: Control (n = 4) and OmniGen-AF (OG; n = 5). Cattle were offered 0 (Control) or 56 g daily of OG throughout a 28-d backgrounding period (limit-fed a predominantly forage diet), a 14-d transition period, and a 56-d finishing period on a high concentrate diet (104 days total). During the three feeding periods, whole blood and serum was collected to evaluate markers of immune function and physiology, respectively. Across basal diet phases, OG supplementation increased serum chloride (P = 0.02) and haptoglobin (P = 0.03) concentrations and decreased serum NEFA (P = 0.001) concentrations. At the end of the high-concentrate finishing period, OG supplementation vs. Control attenuated the decrease in serum paraoxonase and the increase in AST concentrations, a marker of liver cell necrosis. Carcass prediction measurements, collected in 30-day intervals during the finishing phase, indicated lower predicted numerical yield grades (P = 0.03) due to higher REA (P = 0.009) and a tendency for less 12th rib fat (P = 0.06) in Control vs. OG steers. Weight gain, feed intake, feed efficiency, and predicted quality grades did not differ between treatments. In conclusion, OG may act on the immune-metabolic axis across the three studied basal diet phases to support healthier livers and improved predicted yield grades in Angus steers by decreasing fat deposition and increasing REA.

Changes of macrominerals and calcitropic hormones in serum of periparturient dairy cows subject to subclinical hypocalcaemia.

The aims of the study reported in the Research Communication were to evaluate changes of macrominerals and major calcitropic hormone concentrations in 51 healthy dairy cows over the peripartum period, and to compare those cows with 51 cows subject to subclinical hypocalcaemia (SCH) on calving day. The results showed that serum calcium (Ca) and potassium (K) concentrations were lowest in the healthy periparturient dairy cows at parturition, while sodium (Na) and parathyroid hormone (PTH) concentrations were highest. Serum magnesium (Mg), chloride (Cl) and phosphorus (P) concentrations were highest 1 wk prepartum, however, the concentration of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] was highest 1 wk postpartum. The dairy cows with subclinical hypocalcaemia (SCH) had significantly lower serum levels of Ca, K, Na, Mg, Cl, 1,25(OH)2D3 and glucose and had significantly higher levels of serum P, non-esterified fatty acids (NEFA) and β-hydroxybutyrate (BHBA) than their healthy counterparts on calving day. However, the serum calcitonin and PTH concentrations were not significantly different between the two groups. These data demonstrated that the concentrations of macrominerals and major calcium regulating hormones of cows change dramatically over the peripartum period. Furthermore, SCH was associated with a risk of the development of ketosis and fatty liver.

Balanced Crystalloid Solution Versus Normal Saline on Biochemical Outcomes in Acute Medical and Surgical Patients

Background: Concerns have been raised regarding the use of various intravenous fluids resulting in hyperchloremic acidosis and associated acute kidney injury; however, this has primarily been in the context of resuscitation and critical care, and not ward-based medical or surgical patients who receive lower volumes of infusion fluid. We aimed to determine whether normal saline use is more likely to produce hyperchloremic metabolic acidosis than compound sodium lactate, in acute general medical and surgical patients. Methods: This was a retrospective study, conducted in 2015 in a metropolitan hospital in Melbourne, Australia, and of 1,158 sequentially admitted general medical and surgical patients receiving either intravenous normal saline or compound sodium lactate. Demographics, admission diagnosis, comorbidities, and medications were compared. Serum biochemistry results 24 - 48 h post-infusion were analyzed. Primary outcome was incidence of serum hyperchloremia post-infusion. In addition, mean shift in serum chloride concentration as well as mean normalized chloride concentration (mmol/L per day per L of infusion) were calculated. Acute kidney injuries and deaths during admission were also reported. Results: A total of 221 patients (169 medical and 52 surgical patients) were included for analysis (mean age 71.6 years, 72% female), with 174 normal saline and 61 compound sodium lactate infusions. No difference in hyperchloremia rate was found (normal saline vs. compound sodium lactate; n = 8 (4.6%) vs. n = 2 (3.3%), P = 1.0). Post-infusion serum chloride concentration was also not significantly different (99.0 ± 5.1 mmol/L vs. 100.0 ± 3.4 mmol/L, P = 0.1700) between infusion groups. Normal saline infusions resulted in an increase of mean normalized chloride concentration compared to compound sodium lactate (1.2 ± 4.0 mmol/L per day/L vs. -0.3 ± 1.5, P = 0.0121). Conclusions: We conclude that 2 - 3 L normal saline infusions in this population do not appear to be associated with hyperchloremic acidosis more frequently than compound sodium lactate infusions, allaying concerns of normal saline use in wards. World J Nephrol Urol. 2018;7(2):39-44 doi: https://doi.org/10.14740/wjnu339w

Effects of intraoperative and early postoperative normal saline or Plasma-Lyte 148® on hyperkalaemia in deceased donor renal transplantation: a double-blind randomized trial

BackgroundAdministration of saline in renal transplantation is associated with hyperchloraemic metabolic acidosis, but the effect of normal saline (NS) on the risk of hyperkalaemia or postoperative graft function is uncertain. MethodsWe compared NS with Plasma-Lyte 148® (PL) given during surgery and for 48 h after surgery in patients undergoing deceased donor renal transplantation. The primary outcome was hyperkalaemia within 48 h after surgery. Secondary outcomes were need for hyperkalaemia treatment, change in acid–base status, and graft function. ResultsTwenty-five subjects were randomized to NS and 24 to PL. The incidence of hyperkalaemia in the first 48 h after surgery was higher in the NS group; 20 patients (80%) vs 12 patients (50%) in the PL group (risk difference: 0.3; 95% confidence interval: 0.05, 0.55; P=0.037). The mean (sd) peak serum potassium was NS 6.1 (0.8) compared with PL 5.4 (0.9) mmol litre−1 (P=0.009). Sixteen participants (64%) in the NS group required treatment for hyperkalaemia compared with five (21%) in the PL group (P=0.004). Participants receiving NS were more acidaemic [pH 7.32 (0.06) vs 7.39 (0.05), P=0.001] and had higher serum chloride concentrations (107 vs 101 mmol litre−1, P<0.001) at the end of surgery. No differences in the rate of delayed graft function were observed. Subjects receiving PL who did not require dialysis had a greater reduction in creatinine on day 2 (P=0.04). ConclusionsCompared with PL, participants receiving NS had a greater incidence of hyperkalaemia and hyperchloraemia and were more acidaemic. These biochemical differences were not associated with adverse clinical outcomes. Clinical trial registrationAustralian New Zealand Clinical Trials Registry: ACTRN12612000023853.

Hyperchloremia Is Associated With Acute Kidney Injury in Patients With Subarachnoid Hemorrhage.

To assess the prevalence of acute kidney injury in patients with subarachnoid hemorrhage patients. Retrospective analysis of all subarachnoid hemorrhage admissions. Neurocritical care unit. All patients with a diagnosis of subarachnoid hemorrhage between 2009 and 2014. None. Of 1,267 patients included in this cohort, 16.7% developed acute kidney injury, as defined by Kidney Disease Improving Global Outcome criteria (changes in creatinine only). Compared to patients without acute kidney injury, patients with acute kidney injury had a higher prevalence of diabetes mellitus (21.2% vs 9.8%; p < 0.001) and hypertension (70.3% vs 50.5%; p < 0.001) and presented with higher admission creatinine concentrations (1.21 ± 0.09 vs 0.81 ± 0.01 mg/dL [mean ± SD], respectively; p < 0.001). Patients with acute kidney injury also had higher mean serum chloride and sodium concentrations during their ICU stay (113.4 ± 0.6 vs 107.1 ± 0.2 mmol/L and 143.3 ± 0.4 vs 138.8 ± 0.1 mmol/L, respectively; p < 0.001 for both), but similar chloride exposure. The mortality rate was also significantly higher in patients with acute kidney injury (28.3% vs 6.1% in the non-acute kidney injury group [p < 0.001]). Logistic regression analysis revealed that only male gender (odds ratio, 1.82; 95% CI, 1.28-2.59), hypertension (odds ratio, 1.64; 95% CI, 1.11-2.43), diabetes mellitus (odds ratio, 1.88; 95% CI, 1.19-2.99), abnormal baseline creatinine (odds ratio, 2.48; 95% CI, 1.59-3.88), and increase in mean serum chloride concentration (per 10 mmol/L; odds ratio, 7.39; 95% CI, 3.44-18.23), but not sodium, were associated with development of acute kidney injury. Kidney recovery was noted in 78.8% of the cases. Recovery reduced mortality compared to non-recovering subgroup (18.6% and 64.4%, respectively; p < 0.001). Critically ill patients with subarachnoid hemorrhage show a strong association between hyperchloremia and acute kidney injury as well as acute kidney injury and mortality.

Proposal for heart failure progression based on the 'chloride theory': worsening heart failure with increased vs. non-increased serum chloride concentration.

AimsChloride (Cl) is an established key electrolyte for the activation of the renin–angiotensin–aldosterone system. Recent studies have shown the serum Cl as a key electrolyte for the regulation of body fluid distribution in heart failure (HF) patients. The clinical differences of worsening HF status according to the changes in serum Cl concentration are unclear.Methods and resultsData from 47 chronic HF patients were analysed. Upon worsening HF, each patient exhibited at least two HF‐related signs. Blood tests included haemoglobin (Hb), haematocrit (Ht), mean red blood cell volume (MCV), albumin, serum solutes, and b‐type natriuretic peptide. The relative change in the plasma volume (%PV) from stable to worsening HF was estimated as follows: 100 × {Hb (stable) × [1 − Ht (worse)]}/{Hb (worse) × [1 − Ht (stable)]} − 100. When patients were divided into two groups based on changes in serum Cl concentration from stable to worsening HF, the pathophysiologic features of the patients with increased Cl (range 1–23 mEq/L; n = 31) included a greater increase in serum sodium (2.94 ± 4.15 vs. −0.69 ± 3.75 mEq/L, P = 0.005), higher vascular expansion (12 ± 11.1 vs. 4.81 ± 7.94%, P = 0.026), a tendency towards a greater MCV (1.23 ± 2.36 vs. −0.06 ± 1.88 fL, P = 0.065), and preserved renal function defined by the absence of an increase of serum creatinine (−0.24 ± 0.39 vs. −0.05 ± 0.12 mg/dL, P = 0.057) compared to patients with non‐increased Cl (range −9 to 0 mEq/L; n = 16). Clinically, the increased Cl group had fewer HF signs (2.65 ± 0.71 vs. 3.31 ± 0.79, P = 0.005) although the change in symptoms did not differ between groups (48% vs. 63%, P = 0.54).ConclusionsThe present study suggests a new clinical entity of worsening HF status, that is, HF with increased vs. non‐increased serum Cl concentration from clinical stability to worsening HF.