Serum Chloride Concentrations Research Articles

Balanced Solution versus Normal Saline in Predicted Severe Acute Pancreatitis: A Stepped Wedge Cluster Randomized Trial.

To compare the effect of balanced multielectrolyte solutions(BMES) versus normal saline(NS) for intravenous fluid on chloride levels and clinical outcomes.in patients with predicted severe acute pancreatitis (pSAP). Isotonic crystalloids are recommended for initial fluid therapy in acute pancreatitis, but whether the use of BMES in preference to NS confers clinical benefits is unknown. In this multicenter, stepped-wedge, cluster-randomized trial, we enrolled patients with pSAP (APACHE II score ≥8 and C-reactive protein >150mg/L) admitted within 72 hours of the advent of symptoms. The study sites were randomly assigned to staggered start dates for one-way crossover from the NS phase (NS for intravenous fluid) to the BMES phase(Sterofudin for intravenous fluid). The primary endpoint was the serum chloride concentration on trial day3. Secondary endpoints included a composite of clinical and laboratory measures. Overall, 259 patients were enrolled from eleven sites to receive NS(n=147) or BMES(n=112). On trial day3, the mean chloride level was significantly lower in patients who received BMES(101.8mmol/L(SD4.8) versus 105.8mmol/L(SD5.9), difference -4.3mmol/L [95%CI -5.6 to -3.0mmol/L];P<0.001). For secondary endpoints, patients who received BMES had less systemic inflammatory response syndrome(19/112,17.0% versus 43/147,29.3%, P=0.024) and increased organ failure-free days (3.9d(SD2.7) versus 3.5days(SD2.7), P<0.001) by trial day7. They also spent more time alive and out of ICU(26.4d(SD5.2) versus 25.0days(SD6.4), P=0.009) and hospital(19.8d(SD6.1) versus16.3days(SD7.2), P<0.001) by trial day30. Among patients with pSAP, using BMES in preference to NS resulted in a significantly more physiological serum chloride level, which was associated with multiple clinical benefits(Trial registration number: ChiCTR2100044432).

Goal-Directed Fluid Therapy Using Normal Saline versus Ringer's Lactate in Pediatric Neurosurgical Patients: A Randomized Controlled Trial

Abstract Background Ringer's lactate (RL) and 0.9% sodium chloride (NS) are used intraoperatively in pediatric surgical patients. The fluid of choice in pediatric neurosurgical patients is still under research. Hence, we compared NS and RL intraoperatively with a primary objective of measuring the absolute difference in serum chloride concentrations (ΔCl-) after surgery from baseline. Secondary objectives included changes in other electrolytes, osmolarity, pH, creatinine, brain relaxation score (BRS), and neurological outcome at discharge using a modified Rankin scale (mRS). Methods This prospective randomized trial was conducted in American Society of Anesthesiologists status I to II children, aged 6 months to 14 years, after Institutional Ethical Committee approval and written informed consent. Forty patients were randomized in group-S (received 0.9% Saline) and group-R (received RL). The fluid administration was guided by Pleth Variability Index (target &lt;13%). Arterial blood samples were taken at the start of surgery, during tumor resection, and at the end of surgery. Results Twenty-one patients in NS and 19 patients in RL were enrolled. ΔCl- was 12 (9–16) mmol/L in NS group and 4 (2–15) mmol/L in RL group, p = 0.03. NS group developed more metabolic acidosis (6 [28.6%] vs. 0 [0.0%], p = 0.021). There was no difference in the other electrolytes, serum osmolarity, BRS, perioperative creatinine, and mRS between groups, p = 0.36, p = 0.096, p = 0.658, and p = 0.168, respectively. Conclusion Intraoperative use of NS causes derangement in chloride balance, leading to metabolic acidosis compared to RL in children undergoing neurosurgical procedures. However, there was no difference in the other parameters, including serum osmolarity, BRS, and mRS.

Exploration of Risk Factors of the Onset of Antibiotics-induced Acute Kidney Injury and Its Transfer to Chronic Kidney Disease Using the Medical Information Database

Drug-induced acute kidney injury (AKI) is a serious adverse drug reaction, which results in a significant decline in renal function and is known to progress to chronic kidney disease (CKD). Therefore, appropriate drug therapy is important to avoid the risk of drug-induced AKI and CKD, which are serious concerns in clinical practice. In this study, using the medical information database of Hamamatsu University Hospital, we investigated the risk factors that accelerate the onset of drug-induced AKI or its progression to CKD in patients who received aminoglycoside antibiotics (AGs) or glycopeptide antibiotics (GPs), which are strongly associated with drug-induced AKI and CKD. We performed logistic regression analysis using patients' background, laboratory test results, and concomitant drug use, among other such factors as explanatory variables and drug-induced AKI or CKD onset as objective variables to explore the risk factors for drug-induced AKI and CKD. Our results showed that co-administration of amphotericin B, piperacillin-tazobactam and other AGs and GPs, increased serum creatinine (Scr) and chloride concentrations, serum lactate dehydrogenase activity, and decreased serum albumin concentration were risk factors for drug-induced AKI onset. Moreover, a reduced blood urea nitrogen:Scr ratio at drug-induced AKI onset served as a risk factor for CKD. These results suggest that careful monitoring of the aforementioned factors is important to ensure appropriate usage of these drugs in patients treated with AGs and GPs.

Neurohormonal Activation and Renal Chloride Avidity in Acute Heart Failure: Clinical Evidence Supporting the “Chloride Theory”

Introduction: Heart failure (HF) progression according to changes in the serum chloride concentration ([sCl−]) was recently proposed as the “chloride (Cl) theory” for HF pathophysiology. The present study examined the association of neurohormones and renal Cl avidity to determine their contribution to acute HF and their involvement to the “Cl theory.” Methods: Data from 29 patients with acute HF (48% men; 80.3 ± 12 years) were analyzed. Blood and urine samples were obtained before decongestive therapy. Clinical tests included peripheral blood, serum and spot urinary electrolytes, b-type natriuretic peptide (BNP), and plasma neurohormones. Results: In the 29 patients, urinary Cl concentrations ([uCl−]) inversely correlated with log (plasma renin activity [PRA]) (r = −0.64, p = 0.0002) and log (plasma aldosterone concentration) (r = −0.50, p = 0.006). The [sCl−]‒[uCl−] difference positively correlated with log PRA (r = 0.63, p = 0.0002) and log (plasma aldosterone concentration) (r = 0.49, p = 0.008). Patients were divided into 2 groups according to the [sCl−]‒[uCl−] difference, an excretion (low renal Cl avidity) group and an absorption (high renal Cl avidity) group. Compared with the excretion group (−77 to ‒5 mEq/L; n = 14), the absorption group (1–84 mEq/L; n = 15) exhibited greater renal impairment (serum creatinine; 1.45 ± 0.63 vs. 1.00 ± 0.38 mg/d, p = 0.029) and cardiac burden (log BNP; 2.99 ± 0.3 vs. 2.66 ± 0.32 pg/mL, p = 0.008), higher log PRA (0.20 ± 0.58 vs. −0.25 ± 0.35 ng/mL/h, p = 0.018), and lower fractional urinary Cl excretion (1.34 ± 1.3 vs. 5.33 ± 4.1%, p Conclusion: Renal Cl avidity differs in acute HF, i.e., excretion (low renal Cl avidity) versus absorption (high renal Cl avidity) types, involving renin-aldosterone-angiotensin activity as the underlying mechanism, which provides the neurohormonal background for the “Cl theory.” A version of this study was presented in part at the annual international scientific assembly (ACC.23) of the American College of Cardiology, March 4–6, 2023.

A machine learning approach for predicting treatment response of hyponatremia.

Hyponatremia leads to severe central nervous system disorders and requires immediate treatment in some cases. However, a rapid increase in serum sodium (s-Na) concentration could cause osmotic demyelination syndrome. To achieve a safety hyponatremia treatment, we develop a prediction model of s-Na concentration using a machine learning. Among the 341 and 47 patients admitted to two tertiary hospitals for hyponatremia treatment (s-Na <130 mEq/L), those who were admitted to the general unit with urine sodium <20 mEq/L or treated with desmopressin were excluded. Ultimately, 74 and 15 patients (342 and 146 6-hourly datasets) were included in the learning and validation data, respectively. We trained the prediction model using three regression algorithms for shallow machine learning to predict s-Na every 6 h during treatment with the data of patients with hyponatremia (median s-Na: 112.5 mEq/L; range: 110.0-116.8 mEq/L) from one hospital. The model was validated externally using the data of patients with hyponatremia (median s-Na: 117.0 mEq/L; range: 112.9-120.0 mEq/L) from another hospital. Using 5-7 predictors (water intake, sodium intake, potassium intake, urine volume, s-Na concentration, serum potassium concentration, serum chloride concentration), the support vector regression model showed the best performance overall (root mean square error = 0.05396; R2 = 0.92), followed by the linear regression and regression tree models. The predicted s-Na levels, using explainable machine learning algorithms and clinically accessible parameters, correlated well with the actual levels. Thus, our model could be applied to the treatment of hyponatremia in clinical practice.

Urine sodium concentration after intravenous furosemide in dogs with acute congestive heart failure and correlation with treatment efficacy.

Poor natriuresis is a potential marker of diuretic resistance in dogs with acute congestive heart failure (CHF) but little is known about the relationship between urine sodium concentration (uNa) and frequency of successful decongestion. Supplemental O2 is a common treatment in dogs with severe CHF. The time from start to discontinuation of supplemental O2 therapy (DCSO2 ) typically reflects the time course and ease of decongestion. Urine Na concentration after IV administration of furosemide will be correlated with duration of treatment with supplemental O2 (timeO2 ) and the cumulative frequency of successful DCSO2 during hospitalization. Fifty-one dogs with acute CHF. Retrospective observational single center study. Dogs with low uNa had significantly longer mean timeO2 than dogs with high uNa (uNa <87 mmol/L, 24.2 ± 2.6 hours vs uNa ≥87 mmol/L, 16.6 ± 1.7 hours; P = .02). Low uNa was correlated with lower cumulative frequency of DCSO2 (12 hour, 28%; 24 hour, 42%; 36 hour, 73%) compared to high uNa (12 hour, 28%; 24 hour, 88%; 36 hour, 96%; P = .005). History of PO loop diuretics, low serum chloride concentration (sCl), and high PCV were associated with low uNa. Urine Na concentration outperformed other metrics of diuretic responsiveness including weight loss. Urine Na concentration after IV furosemide predicted timeO2 and cumulative frequency of DCSO2 in dogs with acute CHF, which likely reflects important aspects of diuretic responsiveness. Urine Na can assess diuretic responsiveness and treatment efficacy in dogs with CHF.

L-Shaped Association of Serum Chloride Level With All-Cause and Cause-Specific Mortality in American Adults: Population-Based Prospective Cohort Study.

Chloride is the most abundant anion in the human extracellular fluid and plays a crucial role in maintaining homeostasis. Previous studies have demonstrated that hypochloremia can act as an independent risk factor for adverse outcomes in various clinical settings. However, the association of variances of serum chloride with long-term mortality risk in general populations has been rarely investigated. This study aims to assess the association of serum chloride with all-cause and cause-specific mortality in the general American adult population. Data were collected from 10 survey cycles (1999-2018) of the National Health and Nutrition Examination Survey. All-cause mortality, cardiovascular disease (CVD) mortality, cancer mortality, and respiratory disease mortality data were obtained by linkage to the National Death Index through December 31, 2019. After adjusting for demographic factors and relevant lifestyle, laboratory items, and comorbid factors, weighted Cox proportional risk models were constructed to estimate hazard ratios and 95% CIs for all-cause and cause-specific mortality. A total of 51,060 adult participants were included, and during a median follow-up of 111 months, 7582 deaths were documented, 2388 of CVD, 1639 of cancer, and 567 of respiratory disease. The weighted Kaplan-Meier survival analyses showed consistent highest mortality risk in individuals with the lowest quartiles of serum chloride. The multivariate-adjusted hazard ratios from lowest to highest quartiles of serum chloride (≤101.2, 101.3-103.2, 103.2-105.0, and ≥105.1 mmol/L) were 1.00 (95% CI reference), 0.77 (95% CI 0.67-0.89), 0.72 (95% CI 0.63-0.82), and 0.77 (95% CI 0.65-0.90), respectively, for all-cause mortality (P for linear trend<.001); 1.00 (95% CI reference), 0.63 (95% CI 0.51-0.79), 0.56 (95% CI 0.43-0.73), and 0.67 (95% CI 0.50-0.89) for CVD mortality (P for linear trend=.004); 1.00 (95% CI reference), 0.67 (95% CI 0.54-0.84), 0.65 (95% CI 0.50-0.85), and 0.65 (95% CI 0.48-0.87) for cancer mortality (P for linear trend=.004); and 1.00 (95% CI reference), 0.68 (95% CI 0.41-1.13), 0.59 (95% CI 0.40-0.88), and 0.51 (95% CI 0.31-0.84) for respiratory disease mortality (P for linear trend=.004). The restricted cubic spline analyses revealed the nonlinear and L-shaped associations of serum chloride with all-cause and cause-specific mortality (all P for nonlinearity<.05), in which lower serum chloride was prominently associated with higher mortality risk. The associations of serum chloride with mortality risk were robust, and no significant additional interaction effect was detected for all-cause mortality and CVD mortality (P for interaction>.05). In American adults, decreased serum chloride concentrations were independently associated with increased all-cause mortality, CVD mortality, cancer mortality, and respiratory disease mortality. Our findings suggested that serum chloride may serve as a promising cost-effective health indicator in the general adult population. Further studies are warranted to explore the potential pathophysiological mechanisms underlying the association between serum chloride and mortality.

Use of serum osmolality to identify heart disease stage in dogs and relationship to mathematical chloride correction.

Heart failure-associated hypochloremia can be depletional from diuretics or dilutional from water retention. Serum osmolality reflects water balance but has not been evaluated in dogs with heart disease. To determine if serum osmolality is related to heart disease stage and amount of mathematical correction of serum chloride (Cl- ) concentrations in healthy dogs and dogs with myxomatous mitral valve degeneration (MMVD). Seventy-seven dogs (20 healthy, 25 Stage B MMVD, 32 Stage C/D MMVD). Serum Cl- concentrations were mathematically corrected. Osmolality was calculated (calOsm) and directly measured by freezing point depression (dmOsm) and compared by Bland-Altman analysis. Biochemical variables and osmolality were compared among healthy, Stage B, and Stage C/D dogs. Correlations were explored between osmolality and biochemical variables. Median and range are presented. P < .05 was considered significant. The calOsm was different among groups (P = .003), with Stage B (310 mOsm/kg; 306, 316) and C/D dogs (312 mOsm/kg; 308, 319) having higher calOsm than healthy dogs (305 mOsm/kg; 302, 308). Osmolality methods were moderately correlated (P < .0001, rs = .46) but with proportional bias and poor agreement. The amount of Cl- correction was negatively correlated with calOsm (P < .0001, rs = -.78) and dmOsm (P = .004, rs = -.33). Serum bicarbonate concentration was negatively correlated with Cl- (P < .0001, rs = -.67). Dogs with Stage B and Stage C/D heart disease had higher calOsm than healthy dogs. Osmolality was inversely related to the amount of Cl- correction, which supports its use in assessing relative body water content. Poor agreement between calOsm and dmOsm prevents methodological interchange.

Prevalence of neoplasia and concurrent diseases in dogs and cats with hypercobalaminemia: A retrospective case-control study.

Hypercobalaminemia is infrequently reported in companion animals and is considered of low clinical significance. Recent studies have described its association with inflammatory, immune-mediated, endocrine, and neoplastic conditions in dogs and cats. We aimed to investigate the association between hypercobalaminemia and neoplasia in companion animals and to identify other concurrent diseases or clinicopathologic changes. This is a retrospective, case-control study. Medical records of patients with measured serum cobalamin concentration (2015-2020) and no history of prior supplementation were reviewed. Hypocobalaminemic animals were excluded. Variables were compared between groups (hypercobalaminemic vs. normocobalaminemic) using non-parametric statistics. Data are presented as median (range). Thirty-five dogs and eight cats were hypercobalaminemic. At baseline, neoplasia was confirmed in 4/35 hypercobalaminemic dogs versus 11/70 control dogs (P = 0.77) and 0/8 hypercobalaminemic cats versus 3/16 control cats (P = 0.53). Cases without neoplasia at baseline were followed for 409 (13-1854) days (dogs, n = 78) and 395 (28-1670) days (cats, n = 21). During follow-up, neoplasia was diagnosed in 4/27 hypercobalaminemic dogs versus 3/51 control dogs (P = 0.23) and 1/8 hypercobalaminemic cats versus 0/13 control cats (P = 0.38). Pancreatitis was more frequent in hypercobalaminemic dogs (P = 0.006). Hypercobalaminemic dogs had higher serum total protein (P = 0.014), globulin (P = 0.001), and CRP (P = 0.032) concentrations and lower serum sodium (P = 0.012) and chloride (P = 0.033) concentrations than controls. Hypercobalaminemic cats had higher serum total protein concentrations than controls (P = 0.008). Our results suggest that hypercobalaminemia is not associated with the presence or development of neoplasia in dogs and cats but may be associated with systemic inflammatory conditions, including pancreatitis, in dogs.

Nephrolithiasis and/or nephrocalcinosis is significantly related to renal dysfunction in patients with primary Sjögren's syndrome.

The present study compared the clinical features of patients with primary Sjögren's syndrome (pSS) with and without nephrolithiasis and/or nephrocalcinosis to determine factors related to renal dysfunction. The clinical features of 68 patients with anti-Sjogren's syndrome antigen A (SSA)/Ro-antibody-positive pSS with and without nephrolithiasis and/or nephrocalcinosis who underwent abdominal computed tomography and/or ultrasonography were retrospectively analysed. Of the 68 patients with anti-SSA-antibody-positive pSS, 23 (33%) had renal nephrolithiasis and/or nephrocalcinosis, whereas 45 (67%) did not. Fourteen (20%) patients had renal dysfunction at diagnostic imaging. Among five patients who underwent renal biopsy, four patients with renal nephrolithiasis and/or nephrocalcinosis were diagnosed with tubulointerstitial nephritis, and one without nephrolithiasis and/or nephrocalcinosis was diagnosed with minimal change nephrotic syndrome. Estimated glomerular filtration rate at diagnostic imaging was significantly lower in patients with than without nephrolithiasis and/or nephrocalcinosis group (P = 0.010). In addition to nephrolithiasis and/or nephrocalcinosis (odds ratio [OR], 3.467; P = 0.045), the gap between serum sodium and chloride concentrations (OR, 10.400; P = 0.012) and increased urinary β2-microglobulin (OR, 5.444; P = 0.033) were associated with renal dysfunction at the time of diagnostic imaging. Nephrolithiasis and/or nephrocalcinosis, normal anion gap metabolic acidosis, and tubulointerstitial damage are associated with renal dysfunction in patients with pSS.

Effect of renal function on the prognostic importance of chloride in patients with heart failure.

Hypochloremia has recently gained interest as a potential marker of outcomes in patients with heart failure (HF). The exact pathophysiologic mechanism linking hypochloremia to HF is unclear but is thought to be mediated by chloride-sensitive proteins and channels located in kidneys. This analysis aimed to understand whether renal dysfunction (RD) affects the association of hypochloremia with mortality in patients with HF. Using data from a nationwide registry, 438 cases with complete data on serum chloride concentration and 1-year survival were included in the analysis. Patients with an estimated glomerular filtration rate of <60 mL/min/m2 at baseline were accepted as having RD. Hypochloremia was defined as a chloride concentration <96 mEq/L at baseline. For HF patients without RD at baseline, patients with hypochloremia had a significantly higher 1-year all-cause mortality than those without hypochloremia (41.6% vs 13.0%, log-rank p < 0.001) and the association remained significant after multivariate adjustment (odds ratio (OR): 2.55, 95% confidence interval (CI): 1.25-5.21). The evidence supporting the association was very strong in this subgroup (Bayesian Factor (BF)10: 48.25, log OR: 1.56, 95% CI: 0.69-2.43). For patients with RD at baseline, there was no statistically significant difference for 1-year mortality for patients with or without hypochloremia (36.3% vs 29.7, log-rank p = 0.35) and there was no evidence to support an association between hypochloremia and mortality (BF10: 1.18, log OR :0.66, 95% CI: -0.02 to 1.35). In patients with HF, the association between low chloride concentration and mortality is limited to those without RD at baseline.

Early Hyperchloremia and Outcomes After Severe Traumatic Brain Injury: Analysis of Resuscitation Outcomes Consortium Hypertonic Saline Trial.

Post hoc analysis of Resuscitation Outcomes Consortium Hypertonic Saline (ROC HS)-TBI trial. A total of 114 North American emergency medical services agencies in the ROC. A total of 991 patients with severe TBI and Glasgow Coma Scale score of less than or equal to 8. Prehospital resuscitation with single IV dose (250 cc) of 7.5% saline in 6% dextran-70, 7.5% saline (no dextran), or crystalloid. Patients with increased serum chloride concentrations (110 mmol/L or greater) 24 hours after randomization were identified. Hyperchloremia was graded into one or greater than or equal to 2 occurrences in the first 24 hours. Logistic regression analyses were performed to determine the effects of hyperchloremia on: 1) death or severe disability at 180 days and 2) death within 180 days after adjusting for confounders. Compared with patients without hyperchloremia, patients with greater than or equal to 2 occurrences of hyperchloremia had significantly higher odds of death or severe disability at 180 days (odds ratio [OR], 1.81; 95% CI, 1.19-2.75) and death within 180 days (OR, 1.89; 95% CI, 1.14-3.08) after adjustment for confounders. However, the total volume of fluids administered during the first 24 hours was an independent predictor of death within 180 days; therefore, after adding an interaction term between the total volume of fluids administered during the first 24 hours and greater than or equal to 2 occurrences of hyperchloremia, patients with greater than or equal to 2 occurrences of hyperchloremia had significantly higher odds of death within 180 days (OR, 2.35; 95% CI, 1.21-4.61 d) but not of composite outcome of death or severe disability at 180 days. After modifying for the effect of the total volume of fluids administered during the first 24 hours, multiple occurrences of hyperchloremia in the first 24 hours were associated with higher odds of death within 180 days in patients with severe TBI.

Lower serum chloride concentrations are associated with an increased risk of death in ICU patients with acute kidney injury: an analysis of the MIMIC-IV database.

The association between baseline serum chloride levels and mortality in patients with severe acute kidney injury (AKI) is unknown. Our aim was to investigate the relationship between baseline blood chloride levels and 28-day mortality in patients with AKI admitted to the ICU and to detect possible effect modifiers in this population. AKI patients with severe critical illness were extracted from the MIMIC-IV. During ICU admission, chloride levels were measured for the first time. Our primary outcome was 28-day mortality in patients with AKI after 24 hours in the ICU. Multivariable logistic regression was used to examine the association between three groups of chloride levels and 28-day mortality, and logistic regression with restricted cubic spline was applied to detect the non-linear trendy. A total of 24,166 patients with critically ill AKI were included in this retrospective cohort study. The total 28-day mortality rate in the ICU was 15.9%. Overall, there was a U-shaped relationship between baseline serum chloride levels and 28-day mortality (non-linear P<0.001). Accordingly, patients with low serum chloride (<96 mEq/L) had a significantly increased risk of death compared to patients with normal serum chloride (96-108 meq/L) (adjusted OR=1.94, 95% CI: 1.68-2.24, P<0.001). None of the variables, including age, gender, 24-hour fluid intake, continuous renal replacement therapy, ventilation, Atrial fibrillation, Sequential Organ Failure Assessment score, whether to measure lactate and AKI stage, significantly modified the association between lower chloride levels and 28-day mortality. Low serum chloride levels at baseline were associated with death at 28 days in intensive illnesses with AKI.

Changes in Serum Electrolytes, Urea and Creatinine in Nicotiana tabacum-treated Rats

Tobacco, which is a product of Nicotiana tabacum, has nicotine as its principal phytochemical. Nicotine has been reported to be an addictive drug and the leading cause of tobacco addiction worldwide with consequent renal implications. Therefore, this study was conducted to investigate the effect of the aqueous extract of Nicotiana. tabacum on serum electrolytes, urea and creatinine levels as indices of renal function in male rats. A total of 18 male wistar rats weighing 140-230g were used for this study. The animals were randomly divided into three groups (A, B and C), containing 6 rats each. Group A served as control while Group B and C were orally administered sublethal doses of 20 and 30 mg/kg body weight of the Nicotiana. tabacum extract respectively once per day for three weeks. At the end of the experimental period, all the animals were sacrificed. Blood samples were collected for biochemical assay.The results showed a significant increase (p&lt;0.05) in the serum concentration of sodium, potassium and urea levels of rats treated with the extract when compared with the control. However, serum concentrations of chloride, bicarbonate and creatinine showed no significant appreciable differences between the treated groups and the control group (p&lt;0.05).In conclusion, the study showed that aqueous extract of Nicotiana tabacum is associated with renal dysfunction with consequent hypernatremia and hyperkalemia, and may also suggest impaired urea clearance by the kidneys in male wistar rats.

Effect of initial serum chloride level on the association between intravenous chloride load and mortality in critically ill patients: A retrospective cohort study.

To assess the effect of intravenous chloride load on prognosis in intensive care unit (ICU) patients with different initial serum chloride levels. Participants from the Medical Information Mart for Intensive Care IV database were divided into low, normal (>100 and ≤110 mEq/L), and high chloride groups according to initial chloride levels. Records of intravenous fluids were extracted to calculated the volume adjusted chloride load (VACL) and VACL per body weight (VACL-W). The associations of VACL, VACL-W, and changes in serum chloride concentration (ΔCl) with mortalities were investigated in different initial chloride groups. Respectively, 4593 (20.9%), 13,364 (60.9%), and 3978 (18.1%) patients had a low, normal, and high initial chloride level. Interactions were found between initial chloride levels and VACL, VACL-W, and ΔCl on mortality risks. In normal and high chloride groups, increased VACL, VACL-W, and ΔCl were associated with higher ICU and hospital mortalities. However, in the low chloride group, multivariable models found no associations between VACL, VACL-W, or ΔCl with mortalities. High chloride load and increased serum chloride level were associated with poor outcomes in patients with normal or high initial chloride levels, but not in those with a low initial chloride level.

Assessment of Hematological and Electrolytes Levels and Oxidative Stress Predictive Factors by Logistic Regression Analysis of Acute Ischemic Stroke Disease

Background: Ischemic stroke is a common disease that affects the blood vessels in the brain. This disease is considered one of the most dangerous ailments that affect the nervous system all over the world. Objectives: The aim of this study was to evaluate some hematological and biochemical parameters in men with ischemic disease in Touggourt (Algeria) region. Methods: The study was done on 40 voluntary individuals divided into healthy men reserved as control with Mean±SD age of 56.13±3.32 years and ischemic stroke man (patients) with Mean±SD age of 57.75±4.01 years; their origin covered the whole Touggourt (Algeria) region. Some hematological and biochemical parameters were analyzed, Sensitivity and specificity of oxidative stress biomarkers in serum, erythrocytes, and leucocytes were estimated using a receiver operating characteristics curve (ROC) design. Results: The results suggest that when compared to the controls, blood glucose levels significantly increased (P&gt;0.05) while serum sodium, potassium, and chloride concentrations and serum alkaline phosphatase activity significantly decreased (P&lt;0.05) in stroke patients. Red blood cell, hemoglobin, glutathione (GSH), and total thiol levels significantly decreased (P&lt;0.05) while white blood cell, neutrophile, platelets, malondialdehyde (MDA), superoxide dismutase (SOD), total antioxidant capacity (TAC) and vitamine C levels significantly increased (P&lt;0.05) in ischemic stroke patients compared to the controls with high sensitivity and specificity values of oxidative stress markers. Conclusion: The results indicate that change in electrolytes, hematological, alkaline phosphatase, and oxidative stress markers contributes to the development or complications of ischemic stroke. Investigations on oxidative stress markers can early identify predictors of stroke disease.

Mechanistic insights into chloride-related heart failure progression according to the plasma volume status.

AimsTwo types of heart failure (HF) progression were recently proposed on the basis of an increased vs. non‐increased serum chloride concentration. The applicability of this concept to real‐world HF pathophysiology requires further investigation. The present study evaluated the mechanisms of HF progression to a different type according to changes in the estimated plasma volume status (ePVS).Methods and resultsData from 47 patients (32% men; 78.2 ± 9.7 years of age) with stable to worsening HF (37.5 ± 16 days) were analysed. Physical examination, standard blood tests, and b‐type natriuretic peptide (BNP) measurements were conducted. The ePVS was calculated as follows: ePVS (dL/g) = [100 − haematocrit (%)]/[haemoglobin (g/dL)]. For the study subjects as a whole (n = 47), changes in the ePVS correlated positively with changes in the serum chloride concentration from stable to worsening HF (r = 0.398, P = 0.0056). When divided into two groups of worsening HF with an increased (n = 31) vs. non‐increased serum chloride concentration (n = 16), no significant baseline differences in body weight, serum logBNP, or ePVS were detected between groups. Under worsening HF, the increase in body weight (2.34 ± 1.12 vs. 2.59 ± 1.56 kg, P = 0.57) and logBNP (0.39 ± 0.30 vs. 0.54 ± 0.31 pg/mL, P = 0.13) did not differ between groups, but the increase in the ePVS was smaller in the group with a non‐increased serum chloride concentration compared with that with an increased serum chloride concentration (0.292 ± 0.49 vs. 0.653 ± 0.60 dL/g, P = 0.044). An increase in the %change in ePVS ≥ 10% was less common in patients with a non‐increased chloride concentration (37% vs. 71%, P = 0.03). Patients with a non‐increased serum chloride concentration had more HF signs (3.31 ± 0.79 vs. 2.65 ± 0.71, P = 0.005) and a higher incidence of pulmonary rales (63% vs. 16%, P = 0.0024) than those with an increased serum chloride concentration.ConclusionsAccording to the changes in the ePVS, HF progression may result from a difference between two HF types (i.e. increased vs. non‐increased serum chloride concentration) in the cardiac reserve in response to a given cardiac burden by modulating plasma volume status via the possible tonicity potential of chloride.

Estimation of Plasma Renin Activity on the Basis of Serum and Urinary Chloride Concentrations versus Sodium Concentrations

Introduction: The present study examined the possible estimation of plasma renin activity (PRA) by serum and urinary concentrations of chloride versus sodium in acute and chronic heart failure (HF). Methods: Data from 29 patients with acute HF (48% men; 80.3 ± 12 years) and 26 patients with recovery of HF after decongestive therapy (50% men; 81.2 ± 12 years) were analyzed. Blood and urine samples were obtained immediately before decongestive therapy in acute HF patients. Clinical tests included peripheral blood tests, serum and spot urinary electrolytes, and plasma neurohormones. Sodium- or chloride-related indices included serum ([sNa⁺] or [sCl⁻]) and urinary ([uNa⁺] or [uCl⁻]) concentrations, their differences, and their ratio. Linear regression analysis was used for correlation coefficients. Results: PRA levels higher than the normal range were detected in only 5 (17%) of 29 patients with acute HF, but in as many as 11 (42%) of 26 patients with chronic HF. In the 29 patients with acute HF, all the chloride- and sodium-related indices except for [sNa⁺] were correlated with PRA: the [sCl⁻]/[uCl⁻] ratio was best correlated with PRA (R² = 0.84, p < 0.0001) followed by the [sNa⁺]/[uNa⁺] ratio (R² = 0.64, p < 0.0001). In the 26 patients with chronic HF, however, both the [sCl⁻] (R² = 0.36, p = 0.001) and [sNa⁺] (R² = 0.22, p = 0.016) were only weakly correlated with PRA. Conclusion: In acute HF, chloride-related indices derived from serum and urinary concentrations were firmly associated with PRA or better than sodium-related indices. In chronic HF, either chloride- or sodium-related indices were not firmly associated with PRA, presumably due to influence of cardiovascular medication.

Utilization of serum chloride level from post mortem blood in determination of time since death- A critical analysis

The potential to unravel many unfolded medico legal mysteries lies within the post mortem clocking. Despite the large amount of research undertaken, the post mortem interval remains one of the most challenging variables to be quantified and established. The aim of our project was to study the pattern of serum chloride (cl-) concentration change after death and to correlate it with post mortem interval. Post mortem blood samples collected from external jugular vein of total 150 subjects with documented time of death, were analyzed in a period of one & half years during January 2020 to June 2021to assess the changing pattern of cl- concentration with respect to their time since death. Serum cl- concentration was found to be decreased almost linearly with progression of time within 6-33 hours after death. Coefficient co-relation of mean post mortem cl- concentration and time since death was (-0.94). Average decrease rate of serum cl- concentration was found to be 0.85meq/L per hour. The present study also showed that 95% confidence limit of over ± 17.18 hours limits the usefulness of this method in estimating time since death.

Hypochloraemia following admission to hospital with heart failure is common and associated with an increased risk of readmission or death: a report from OPERA-HF.

Hypochloraemia is common in patients hospitalized with heart failure (HF) and associated with a high risk of adverse outcomes during admission and following discharge. We assessed the significance of changes in serum chloride concentrations in relation to serum sodium and bicarbonate concentrations during admission in a cohort of 1002 consecutive patients admitted with HF and enrolled into an observational study based at a single tertiary centre in the UK. Hypochloraemia (<96 mmol/L), hyponatraemia (<135 mmol/L), and metabolic alkalosis (bicarbonate >32 mmol/L) were defined by local laboratory reference ranges. Outcomes assessed were all-cause mortality, all-cause mortality or all-cause readmission, and all-cause mortality or HF readmission. Cox regression and Kaplan-Meier curves were used to investigate associations with outcome. During a median follow-up of 856 days (interquartile range 272-1416), discharge hypochloraemia, regardless of serum sodium, or bicarbonate levels was associated with greater all-cause mortality [hazard ratio (HR) 1.44, 95% confidence interval (CI) 1.15-1.79; P = 0.001], all-cause mortality or all-cause readmission (HR 1.26, 95% CI 1.04-1.53; P = 0.02), and all-cause mortality or HF readmission (HR 1.41, 95% CI 1.14-1.74; P = 0.002) after multivariable adjustment. Patients with concurrent hypochloraemia and natraemia had lower haemoglobin and haematocrit, suggesting congestion; those with hypochloraemia and normal sodium levels had more metabolic alkalosis, suggesting decongestion. Hypochloraemia is common at discharge after a hospitalization for HF and is associated with worse outcome subsequently. It is an easily measured clinical variables that is associated with morbidity or mortality of any cause.