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Although hypochloremia is strongly associated with adverse prognosis in acute heart failure (AHF), it is unknown whether incorporating hypochloremia into the preexisting risk model improves the model performance. We calculated the Get With The Guidelines-Heart Failure (GWTG-HF) risk score in 1,428 patients with AHF (derivation cohort) and developed 2 risk scores incorporating brain natriuretic peptide (BNP) into the GWTG-HF risk score (GWTG-BNP risk score) and incorporating both BNP and hypochloremia (GWTG-BNP-Cl risk score). Hypochloremia was defined as

The increasing burden of heart failure (HF) and emerging knowledge regarding chloride as a prognostic marker in HF have increased the interest in the pathophysiology and interactions of chloride abnormalities with HF-related factors and treatments. Chloride is among the major electrolytes that play a unique role in fluid homeostasis and is associated with cardiorenal and neurohormonal systems. This review elucidates the role of chloride in the pathophysiology of HF, evaluates the effects of treatment on chloride (eg, diuretic agents cause higher urinary chloride excretion and consequently serum hypochloremia), and discusses recent evidence for the association between chloride levels and mortality.

A 6-year-old castrated male American Pit Bull Terrier dog was presented for evaluation of acute onset of tonic-clonic seizures, anorexia, and vomiting. On physical examination, neurologic signs, such as generalized proprioceptive ataxia, salivation, circling to the right, and absent patellar reflexes bilaterally, were noted. A complete blood cell count revealed mild hemoconcentration and an inflammatory leukogram, while a chemistry panel showed severe azotemia, marked hypochloremia, and a severe titrational metabolic acidosis, suggesting possible ethylene glycol intoxication. However, an irregularly round, small mass was identified in the large intestine on abdominal ultrasound. Additionally, bilateral hyperechoic renal cortices with medullary rim sign were suggestive of acute nephritis or tubular necrosis. The cytologic evaluation of a fine-needle aspiration biopsy of the abdominal mass revealed a large population of mesenchymal cells, suggesting the presence of neoplasia. Due to the worsening of symptoms, the dog was humanely euthanized. Necropsy confirmed ethylene glycol intoxication, and the incidental finding of a neoplastic intestinal mass was diagnosed as spindle cell sarcoma. Immunohistochemical staining showed strong, diffuse positivity for CD117, smooth muscle actin, and S-100, indicating the final diagnosis of a spindle cell type gastrointestinal stromal tumor (GIST). This report briefly discusses the classifications of nonlymphoid, nonangiogenic intestinal mesenchymal tumors, characteristics of GISTs, and the importance of the immunohistochemical classification of mesenchymal tumors of the gastrointestinal tract. Accepted version

Objective Chloride is an important electrolyte in the body. In this study, we aimed to evaluate the associations between chloride levels on emergency department (ED) admission and neurologic outcomes by stratifying patients undergoing targeted temperature management (TTM) after out-of-hospital cardiac arrest (OHCA) into three groups (hyper/normo/hypochloremia); we also assessed the effect of changes in chloride levels from baseline over time on outcomes. Methods This retrospective, observational cohort study of 346 patients was conducted between 2011 and 2019. The chloride levels were categorized as hypochloremia, normochloremia, and hyperchloremia by predetermined definitions. The primary endpoint was poor neurologic outcomes after hospital discharge. We evaluated the associations between chloride levels on ED admission and neurologic outcomes and assess the effect of changes in chloride levels over time on clinical outcomes. Results On ED admission, compared with normochloremia, hypochloremia was significantly associated with unfavorable neurologic outcomes (OR, 2.668; 95% CI, 1.217–5.850, P = 0.014). Over time, unfavorable neurologic outcomes were significantly associated with increases in chloride levels in the hyperchloremia and normochloremia groups after ED admission. The rates of poor neurologic outcomes in the hyperchloremia and normochloremia groups were increased by 14.2% at Time-12, 20.1% at Time-24, and 9.3% at Time-48 with a 1-mEq/L increase in chloride levels. Conclusion In clinical practice, chloride levels can be routinely and serially measured cost-effectively. Thus, baseline chloride levels may be a promising tool for rapid risk stratification of patients after OHCA. For fluid resuscitation after cardiac arrest, a chloride-restricted solution may be an early therapeutic strategy.

Introduction. Recurrent vomiting is a commonly overlooked debilitating symptom which causes significant impact on the quality of life. There are several causes for vomiting, ranging from commonly known causes to rare causes. Nonfunctioning pituitary macroadenomas generally present with visual disturbances, headache, and symptoms due to anterior pituitary hormone deficiencies. This case report is about an atypical presentation of a nonfunctioning pituitary macroadenoma in which the patient presented with cyclical vomiting with severe hyponatremia. Case Report. A 23-year-old girl presented with four to five episodes of vomiting per day for two days duration. She had a history of similar episodes of vomiting since 2016, with each episode generally lasting for 4-5 days and occurring in every four to six months. All episodes exhibited similar symptomatology and she was free of symptoms in-between. Generalized body weakness, postural dizziness, reduced appetite, and secondary amenorrhea were other symptoms she has had since 2016. Examination findings showed a low body mass index (BMI) (16 kg/m2) with normal system examination. Investigations showed severe hyponatremia (110 mmol/L) with hypokalemia (3.2 mmol/L) and hypochloremia (74 mmol/L). Her urinary excretion of potassium, sodium, and serum osmolality was low. Urine osmolality was mildly elevated compared to serum osmolality. Blood urea was normal. Severe hyponatremia with minimal hyponatremic symptoms was suggestive of chronic hyponatremia, which was accentuated by ongoing vomiting and possible reduced intake of salt. Further investigations showed evidence of secondary hypoadrenalism, central hypothyroidism, hypogonadotropic hypogonadism, and mild hyperprolactinemia. Magnetic resonance imaging (MRI) revealed a pituitary macroadenoma with mass effect on the optic chiasma. Hydrocortisone and levothyroxine were started, and she underwent transsphenoidal resection of the pituitary tumor. She recovered from cyclical vomiting. Conclusion. There can be multiple overlapping aetiologies for every observed symptom, sign, and abnormal investigation finding. Therefore, aetiological diagnosis is challenging, especially in the presence of an atypical clinical presentation. Cyclical vomiting and severe hyponatremia are atypical presentations of nonfunctioning pituitary macroadenomas.

Electrolyte serum disorders are associated with poor outcome in chronic heart failure. The aim of this study sought to identify the main driver of incident hypochloremia in chronic HF (CHF) outpatients and to determine the prognostic value of baseline and incident hypochloremia.Consecutive CHF outpatients were enrolled and clinical, laboratoristic and echocardiographic evaluations were performed at baseline and repeated yearly in a subgroup of patients. Baseline and incident hypochloremia were evaluated. During an up to 5-year follow-up, all-cause mortality was the primary end-point for outcome.Among 506 patients enrolled, 120 patients died during follow-up. At baseline, hypochloremia was present in 10% of patients and it was associated with mortality at univariate (HR: 3.25; 95%CI: 2.04-5.18; p0.001) and at multivariate analysis (HR 2.14; 95%CI: 1.23-3.63; p: 0.005) after correction for well-established CHF prognostic markers. Among patients with repeated evaluations and without baseline hypochloremia, in 13% of these, incident hypochloremia occurred during follow-up and furosemide equivalent daily dose was its first determinant (HR for 1 mg/die: 1.008; 95%CI: 1.004-1.013; p0.001) at forward stepwise logistic regression analysis. Finally, incident hypochloremia was associated with mortality at univariate (HR: 4.69; 95%CI: 2.69-8.19; p0.001) as well as at multivariate analysis (HR: 2.97; 95%CI: 1.48-5.94; p: 0.002).In CHF outpatients baseline and incident hypochloremia are independently associated with all-cause mortality, thus highlighting the prognostic role of serum chloride levels which are generally unconsidered. Future studies should evaluate if the strict monitoring and correction of hypochloremia could exert a beneficial effect on prognosis.

In patients visiting the emergency department (ED), a potential association between electrolytes disturbance and coronavirus disease 2019 (COVID-19) has not been well studied. We aim to describe electrolyte disturbance and explore risk factors for COVID-19 infection in patients visiting the ED. We carried out a case–control study in three hospitals in France, including adult ED inpatients (≥ 18 years old). A total of 594 ED case patients in whom infection with COVID-19 was confirmed, were matched to 594 non-COVID-19 ED patients (controls) from the same period, according to sex and age. Hyponatremia was defined by a sodium of less than 135 mmol/L (reference range 135–145 mmol/L), hypokalemia by a potassium of less than 3.5 mmol/L (reference range 3.5–5.0 mmol/L), and hypochloremia by a chloride of less than 95 mmol/L (reference range 98–108 mmol/L). Among both case patients and controls, the median (IQR) age was 65 years (IQR 51–76), and 44% were women. Hyponatremia was more common among case patients than among controls, as was hypokalemia and hypochloremia. Based on the results of the multivariate logistic regression, hyponatremia, and hypokalemia were associated with COVID-19 among case patients overall, with an adjusted odds ratio of 1.89 [95% CI 1.24–2.89] for hyponatremia and 1.76 [95% CI 1.20–2.60] for hypokalemia. Hyponatremia and hypokalemia are independently associated with COVID-19 infection in adults visiting the ED, and could act as surrogate biomarkers for the emergency physician in suspected COVID-19 patients.

Water has a pH of around (7.0), making it neither alkaline nor acidic. Alkaline is defined as a pH value greater than (7.0). The power of water to neutralize acids is measured by its alkalinity. The pH scale ranges from (pH = 0 to 14), with anything above (pH = 7.0) being alkaline, and anything below (7.0) being acidic. Much of the research up to now has been investigating the effect of adding alkaline substances to the water to increase the pH levels. Recent evidence suggests that using baking soda (sodium bicarbonate), which is an alkaline substance with a pH of about (9). While studies have shown that adding soda to water increases its alkalinity, it has a number of negative health consequences. For instance, Hypokalemia, Hypochloremia, High levels of sodium in the blood, Worsening kidney disease, Worsening heart failure, Muscle weakness and spasm, and Increased stomach acid production. The main aim of this study is to investigate a natural substance consisting of environmental elements i.e., it is derived from silica by the thermal fusion method (prepared by the authors) that raises the pH of water with a physical field of 80 cm without adding any components to the water. The results showed the effectiveness of this natural substance in its solid and liquid forms in raising the pH of water to reach 8.5 from a distance range = 80 cm, without any side effects on human health.

Introduction: Malaria is life threatening protozoal infection caused by plasmodium species and it is major health problem in India. Electrolyte alternation is commonly occurring in infections like malaria due to effects of parasitaemia on host cells. The objectives of study were to assess serum level of sodium, potassium and chloride in malaria cases and to find association of electrolyte alteration with severity of malaria infection in different type of malaria. Materials and Methods: Total 70 cases of P. falciparum, 70 cases of P. vivax and 70 age matched healthy controls were included in the study. Diagnosis of malaria was confirmed by QBC (Quantified buffy coat) malaria test. Estimation of electrolyte was done by direct ISE method. Result: There were significantly decreased in mean sodium, potassium and chloride level in P. falciparum malaria cases compare to controls (P Conclusion: Hyponatraemia, hypokalaemia and hypochloremia are found in malaria particularly in P. falciparum type. Hyponatremia and hypokalemia are associated with severity of malaria infection. Keywords: Hyponatraemia, Hypokalaemia, Hypochloremia, Malaria, Serum electrolytes.

Chronic Kidney Disease (CKD) is a syndrome composed of numerous comorbidities such as the failure of excretion of toxins and nitrogenous compounds from metabolism, as well as the failure to maintain endocrine, water, electrolyte and acid-base homeostasis in all mammals. As it is a non-regenerative and progressive disease, any endogenous or exogenous insults in the organ in question will lead to the intensification of all these mentioned disorders associated with decreased urinary output. Several studies in humans and animals recommend the use of renal replacement therapy, especially in those who already have CKD, and who are in uremic syndrome. This report aims to demonstrate that the use of intermittent hemodialysis (HI) in sheep is a therapeutic alternative in those in renal failure. A six-year-old Bergamasca sheep was presented with lateral decubitus, dyspnea, dark liquid diarrhea, apathy, anorexia and pulmonary crepitation on auscultation. Laboratory tests showed azotemia and electrolyte changes such as hypocalcemia, hypokalemia, hypochloremia, isosthenuria (1,012), pyuria, glycosuria, and a protein: creatinine ratio of 0.88. In ultrasonography, the real resistivity index was above 0.54, being suggestive of loss of renal perfusion. The treatment chosen consisted of electrolytic and fluid replacement, associated with HI. After HI, the sheep showed great clinical and laboratory improvement as expected, however, despite not having survived, the histopathological findings of the necropsy pointed out segments of glomerulosclerosis, thus reinforcing the hypothesis that the animal already had a CKD which was aggravated due to the association of hypovolemia, hypotension by anesthetic drugs and the indiscriminate use of NSAIDs. Despite the death of the sheep, HI again proved to be a therapy of rapid clinical and laboratory improvement of the patient compared to conventional clinical treatment, thus being an important treatment alternative for sheep with a high impact on reproduction, production, and research.

Background Hypochloremia associated with congestive heart failure (CHF) in dogs is likely multifactorial. Loop diuretics cause 1:2 sodium [Na+]:chloride [Cl−] loss, whereas water retention causes a 1:1 [Na+]:[Cl−] dilution. Mathematical [Cl−] correction separates these effects on [Cl−]. Hypothesis We hypothesized that corrected [Cl−] (c[Cl−]) would not differ from measured [Cl−] (m[Cl−]) in dogs with controlled CHF because of loop diuretics, and dogs with refractory CHF would have higher c[Cl−] than m[Cl−], indicating relative water excess. Animals Seventy‐one client‐owned dogs with acquired heart disease, without CHF (NO‐CHF), 76 with Stage C CHF and 24 with Stage D CHF. Methods Clinicopathological data from a previous study were retrospectively analyzed. Corrected [Cl−], m[Cl−], and differences were compared among NO‐CHF, Stage C CHF, and Stage D CHF, using the formula: c[Cl−] = (mid‐reference range [Na+]/measured [Na+]) × m[Cl−]. Results Corrected [Cl−] and m[Cl−] were lower in Stage D vs Stage C and NO‐CHF (all P 2 mmol/L. Conclusions and Clinical Importance Serum [Cl−] increased after mathematical correction in Stage D CHF dogs but not in Stage C and NO‐CHF dogs. Although c[Cl−] was higher than m[Cl−] in Stage D dogs supportive of relative water excess, hypochloremia persisted, consistent with concurrent loop diuretic effects on electrolytes. Future study correlating c[Cl−] to antidiuretic hormone concentrations is warranted.

Background This systematic review discusses a clinical physiology aspect of chloride in fluid therapy. Crystalloid solutions are one of the most widely used remedies. While generally used in medicine for almost 190 years, studies focused largely on their safety have only been published since the new millennium. The most widely used solution, normal saline, is most often referred to in this context. Its excessive administration results in hyperchloremic metabolic acidosis with other consequences, including higher mortality rates. Methods Original papers and review articles eligible for developing the present paper were identified by searching online in the electronic MEDLINE database. The keywords searched for included hyperchloremia, hypochloremia, and compound words containing the word “chloride,” infusion therapy, metabolic acidosis, renal failure, and review. Results A total of 21,758 papers published before 31 May 2020 were identified; of this number, 630 duplicates were removed from the list. Upon excluding articles based on their title or abstract, 1850 papers were screened, of which 63 full-text articles were assessed. Conclusions According to the latest medical concepts, dyschloremia (both hyperchloremia and hypochloremia) represents a factor indisputably having a negative effect on selected variables of clinical outcome. As infusion therapy can significantly impact chloride homeostasis of the body, the choice of infusion solutions should always take into account the potentially adverse impact of chloride content on chloremia and organ function.

Our objective was to determine in children in the intensive care unit (ICU) the incidence of hyperchloremia (>110 mmol/L) and hypochloremia (

Diarrhea is the most common cause of death in calves, and remains a major health challenge Although there are many studies on the related pathogens, the understanding of the clinicopathological changes is limited This study aimed to identify the pathogens and observe the clinicopathological changes in electrolytes and acute phase proteins (APPs) associated with diarrhea Blood samples and fecal samples were collected from 141 calves for the determination of APPs, electrolyte and acid-base status and identification of enteropathogens, respectively Single or co-infections with enteropathogens, including virus (bovine viral diarrhea virus, coronavirus, and rotavirus), Eimeria, Cryptosporidium, and Escherichia coli K99 were detected in both non-diarrheic and diarrheic calves Levels of APPs such as serum amyloid A, haptoglobin and fibrinogen were comparable between diarrheic and non-diarrheic calves Hypoglycemia, high blood urea, electrolytes and acid-base imbalance (hyponatremia, hypochloremia, and decreased bicarbonate), and strong ion difference (SID) acidosis showed a significant association in diarrheic calves (p < 0 01) Particularly, significant hyponatremia, bicarbonate loss, SID acidosis, hypoglycemia, and elevated blood urea nitrogen were found in rotavirus-infected calves Monitoring the clinicopathological parameters of APPs and electrolyte levels could be vital in the clinical management of diarrheic calves © 2020 Korean Society of Veterinary Science All rights reserved

BACKGROUND The European Society for Clinical Nutrition and Metabolism Guidelines for Parenteral Nutrition in Geriatric Patients state metabolic complications are more frequent in elderly patients. However, literature provides limited information about metabolic complications in older patients receiving parenteral nutrition (PN). Consequently, the purpose of this study was to compare the development of metabolic complications in older vs younger patients receiving PN. METHODS Patients receiving PN from May 1, 2014, to February 7, 2017, at Cooper University Hospital were included. Metabolic complications assessed included acid-base disturbances, hepatic complications, hypercapnia, hyperchloremia, hyperglycemia, hypernatremia, hypertriglyceridemia, hypochloremia, hypoglycemia, hypokalemia, hypophosphatemia, and refeeding syndrome. RESULTS 595 patients were included (older group [≥65 years]: n = 245, median age: 76 years; younger group [

Cystic fibrosis (CF), an autosomal recessive disorder, occurs due to mutations in CFTR gene resulting in impaired cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel function in various epithelia. In addition to the well-known pulmonary and pancreatic morbidities, CF is characterized by electrolyte and acid-base abnormalities- hypochloremia, hyponatremia, hypokalemia and metabolic alkalosis. These are collectively known as Pseudo-Bartter syndrome, as similar abnormalities are seen in Bartter syndrome- an inherited tubulopathy affecting thick ascending limb of loop of Henle. There may be a significant clinical overlap between the Classic Bartter syndrome, Gitelman syndrome and CF presenting as Pseudo-Bartter syndrome, especially in early childhood. This review focuses on Pseudo-Bartter syndrome in CF, its pathogenesis and differentiation from Bartter/Gitelman syndrome. Other causes of metabolic abnormalities resembling Bartter syndrome are also highlighted.

Background: The strong ion model (SIM) is an alternative paradigm in the characterization of acid‐base disturbances particularly in complex disorders. Hypothesis/Objectives: To compare the acid‐base changes in dogs with parvoviral enteritis (PE) using the Henderson‐Hasselbalch (HH) approach, with 2 strong ion approaches. Animals: Forty‐four dogs with PE, and 16 age‐matched control dogs. Methods: Prospective controlled observational study. Acid‐base status was evaluated using the HH model, Fencl‐Stewart (FS) approach and a validated strong ion model (VDM). The acid‐base changes according to each model were classified and compared. Statistical correlations between pH, CO2, and various SIM variables were performed, as well as between the sum of effects (SOE) of the SIM and the individual variables comprising the SOE. Results: The HH model identified acid‐base disorders in 31/44 cases of which 16/31 were mixed with metabolic acidosis and concurrent respiratory alkalosis the most common (10/31). Using the FS approach, metabolic changes were present 36/42 cases, with changes in free water (FW), chloride, and unmeasured anions (UA) being the most prevalent. Both FW and UA correlated well with pH; however, UA were most consistently abnormal in severe acidemia. Similarly to the HH, the VDM detected acid‐base disturbances in 28/44 cases. Major contributors to the acid‐base changes were hyponatremia, hypochloremia, and Atot acidosis because of elevated globulins and increased UA. Conclusions and Clinical Importance: Acid‐base changes are common and complex in dogs with PE, and were easier to understand using a SIM paradigm. Increases in UA have not been documented in PE in dogs.

Four 2‐month‐old foals were presented to an equine hospital with acute kidney injury caused by Leptospira interrogans infection. Clinical signs were nonspecific and included lethargy, fever, and unwillingness to nurse. The most important hematologic and clinicopathologic findings were azotemia, anemia, thrombocytopenia, hyponatremia, and hypochloremia. The diagnosis was based on urinary real‐time PCR, serology using a microscopic agglutination test, or both. The most important serovars involved were L. interrogans serogroup australis serovar Bratislava and Australis. Treatment consisted of IV fluid therapy and antimicrobial treatment. Renal replacement therapy with hemodiafiltration was performed in 1 of the foals. All foals survived to discharge. This report highlights the importance of early diagnosis and treatment in foals with acute kidney injury caused by L. interrogans infection.

Background: Underestimation of leptospirosis cases is happening in many countries. The most common factor of underreporting is misdiagnosis. Considering the limitations of direct detection of pathogen and serological diagnosis for leptospirosis, clinical features and blood tests though non-specific are usually referred in making presumptive diagnosis to decide disease management. Methods: In this single-centre retrospective study, comparative analysis on clinical presentations and laboratory findings was performed between confirmed leptospirosis versus non-leptospirosis cases. Results: In multivariate logistic regression evidenced by a Hosmer-Lemeshow significance value of 0.979 and Nagelkerke R square of 0.426, the predictors of a leptospirosis case are hypocalcemia (calcium

Purpose The objective of this study was to assess selected serum electrolytes imbalance and associated factors in diabetic patients attending their follow up appointments in Jimma University Medical Center (JUMC) from February 1 to April 1, 2019. Patients and methods A cross sectional study design was used to assess the selected serum electrolytes in diabetic patients attending their follow up appointments at Jimma University Medical Center (JUMC) chronic illness clinic. A convenience sampling technique was used to include 279 diabetic patients in the study and an interviewer based questionnaire was used to include all necessary data from each diabetic patient. Five milliliters of blood were collected from each subject and processed and analyzed for blood glucose and serum electrolyte determination by ABX Pentra400 and Humalyte plus5 ion-selective electrode (ISE) system clinical chemistry analyzers. Pearson's correlation coefficient model and multivariate logistic regression were used respectively to assess the correlation and significant association between abnormal serum electrolytes and independent variables. Results A high prevalence of one or more serum electrolyte abnormalities was determined in diabetic patients. The overall prevalence was 42.0% (n=116/276) in which hyponatremia was the highest followed by hypochloremia and hypercalcemia, 40.6%, 14.9% and 10.9% respectively. Age, type of medication, and high body mass index (BMI) had strong positive correlations with abnormal serum concentration levels of sodium (r=0.611, P=0.731), potassium (r=0.752, P=0.812) and chloride (r=0.645, P=0.459). Being employed (AOR: 3.933, 95% C.I: 1.057-14.637, P value: 0.041), treated with mixed medications (AOR: 2.9, 95% C.I: 1.292-6.441, P value: 0.010) and being unable to control blood glucose level or being hyperglycemic (AOR: 3.2, 95% C.I: 2.179-5.721, P value: 0.000) were statistically identified as risk factors for serum electrolyte abnormalities in diabetic patients. Conclusion The serum electrolyte concentration level was highly abnormal in diabetic patients. The prevalence of abnormal concentration was more common in diabetic patients with advanced age, and some variables had strong positive correlation with abnormal serum electrolyte level in diabetic patients.

Objective: The aim of this work was to study the effects of antihypertensive therapies on certain metabolic parameters in hypertensive patients. Methods: A cross-sectional and analytical study conducted within the Bafoussam Regional Hospital on 343 patients including 99 normotensives and 244 hyperten-sives distributed in 71 patients naive to treatment and 173 patients under treatment (84 under monotherapy, 67 under bitherapy and 21 under trithera-py). The antihypertensive medications were recorded from the medical records. A questionnaire survey was administered to study participants and potential risk factors for hypertension sought. Blood and urine samples were collected for lipid, renal and hepatic disorder analysis. Two blood pressure measure-ments enabled us to diagnose hypertensive patients. Measurements of biochemical parameters such as total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, creatinine, glucose, aspartate aminotransferase (ASAT), alanine aminotransferase (ALT), potassium, chloride and calcium were done in serum by methods resulting from commercial kits. Results: Calcium Channel Blockers were significantly associated with increases in blood potassium (odd-ratios (OR) = 8.63, p = 0.036) and sodium (OR = 0.20, p = 0.037). Angiotensin-converting enzyme/Angiotensin II receptor blockers were significantly associated with an increase in plasma activity of ASAT (OR = 0.12, p = 0.03) whereas Diuretics were significantly associated with an increase in ALAT plasma activity (OR = 0.003, p = 0.012). Dual therapies were associated with highest frequencies of hypercreatininemia (41.8%) and hyperglyce-mia (44.8%) whereas hypocholesterolemia HDL (38.1%) was most observed in hypertensive patients on triple therapy. The different therapies resulted in very low frequencies of abnormal liver profiles (in general almost all below 10%). Tritherapy had the most beneficial effects on the different profiles, with no cases of hyperkalemia, glycosuria, hypochloremia, hematuria, hyponatremia, total hypercholesterolemia, ALAT and ASAT hyperactivity. Conclusion: Triple therapy should be recommended as it has the most beneficial effects on metabolic parameters in the study population.

The current study evaluated the clinical, ruminal, haemato-biochemical, and ultrasonographic findings of abomasal disorders’ affected buffaloes grouped as abomasal impaction (n = 18) and abomasal ulcers (n = 15). The abomasal disorders’ screening was based on clinical examination and confirmed by ultrasonography. The most common clinical findings of the buffaloes affected with abomasal disorders include depressed demeanour (96.97%), absence of rumination (87.88%), abdominal guarding (87.88%), sunken eye balls (81.82%), tachycardia (78.79%), tachypnea (72.73%), and kyphosis (63.64%). The average rumen motility, respiratory rate, and pulse rate for abomasal impaction and abomasal ulcers were 0.28, 33.37, and 83.44, and 0.33, 35.87, and 92.60, respectively. The faecal occult blood test (benzidine test) revealed the presence of melena in all the buffaloes diagnosed with abomasal ulcers (100%). The ultrasonographic examination of the abomasal impaction group revealed increased abomasal size with no movement of the abomasal contents. The ultrasonographic imaging of abomasal ulcer-affected buffaloes showed irregularity in the abomasal wall-outline with moderately echogenic abomasal contents and a layer of fibrin at the affected area. Nine buffaloes had ultrasonographic evidence of peritonitis. The abomasal contents of buffaloes with positive benzidine test (n = 15) were screened for Clostridium perfringens by a polymerase chain reaction and were found positive for cpa toxin yielding 900-bp length. The rumen protozoal count was higher in healthy buffaloes, while the sedimentation test, (time) methylene blue reduction test, (time) and chloride levels were higher (P

Hypochloremia is an electrolyte disturbance characterized by low serum concentration of chloride ions, often occurring in acute illnesses and characterized by nonspecific signs and symptoms. It rarely results from decreased intake and is predominantly due to either renal or extra-renal losses. We report a case of severely worsening symptomatic hypochloremia resulting from an extra-renal loss of chloride ion in a 58-year-old female patient presenting for prolonged protracted vomiting. Chloremia reached a surprising level of 48 mEq/L, the lowest level reported in the literature. The patient was eventually diagnosed with a rare signet ring cell carcinoma that occurred in the ampulla of Vater, leading to a malignant gastric outlet obstruction and causing extra-renal loss of chloride.

Gitelman and Bartter syndromes are rare inherited diseases that belong to the category of renal tubulopathies. The genes associated with these pathologies encode electrolyte transport proteins located in the nephron, particularly in the Distal Convoluted Tubule and Ascending Loop of Henle. Therefore, both syndromes are characterized by alterations in the secretion and reabsorption processes that occur in these regions. Patients suffer from deficiencies in the concentration of electrolytes in the blood and urine, which leads to different systemic consequences related to these salt-wasting processes. The main clinical features of both syndromes are hypokalemia, hypochloremia, metabolic alkalosis, hyperreninemia and hyperaldosteronism. Despite having a different molecular etiology, Gitelman and Bartter syndromes share a relevant number of clinical symptoms, and they have similar therapeutic approaches. The main basis of their treatment consists of electrolytes supplements accompanied by dietary changes. Specifically for Bartter syndrome, the use of non-steroidal anti-inflammatory drugs is also strongly supported. This review aims to address the latest diagnostic challenges and therapeutic approaches, as well as relevant recent research on the biology of the proteins involved in disease. Finally, we highlight several objectives to continue advancing in the characterization of both etiologies.

Bartter's syndrome (BS) is an inherited renal tubular disorder characterized by hypochloremia, hypokalemia, metabolic alkalosis. Prognosis of Bartter's syndrome depends on the severity of the receptor dysfunction. In many cases the prognosis is good and patients are able to have fairly normal lives. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease of unknown cause that can affect virtually any organ of the body. The prognosis of SLE is quite variable, depending on the severity of the disease, the clinical course and organs involved. The last decades, there is a marked improvement in patient survival due to earlier diagnosis and treatment. Despite these improvements, patients with SLE still have higher mortality rates ranging from two to five times higher than that of the general population. Leishmaniasis is a disease caused by an intracellular protozoan parasite transmitted by the bite of a female phlebotomine sandfly. We report herein the case of a 22-year-old man with Bartter's syndrome (BS) and Systemic lupus erythematosus (SLE), who was hospitalized in the clinic of internal medicine because of Leishmaniasis. In the third day of his hospitalization the patient underwent Hartmann's operation for perforation located on descending colon. Management of patients with many severe diseases is very difficult for medical professionals.

Haozhang Huang,1,2,* Ziling Mai,1,3,* Liling Chen,4,* Qiang Li,1 Shiqun Chen,1 Kunming Bao,4 Ronghui Tang,5 Wen Wei,4 Yaren Yu,6 Zhidong Huang,1 Wenguang Lai,1,3 Bo Wang,1 Ning Tan,1– 3 Jiyan Chen,1– 3 Jin Liu,1 Yong Liu1– 3 1Department of Cardiology, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Cardiovascular Institute, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, People’s Republic of China; 2The Second School of Clinical Medicine, Southern Medical University, Guangzhou, 510515, People’s Republic of China; 3Guangdong General Hospital, Affiliated with South China University of Technology, Guangzhou, 510515, People’s Republic of China; 4Department of Cardiology, Longyan First Hospital Affiliated with Fujian Medical University, Longyan, 364000, People’s Republic of China; 5Yunnan Fuwai Cardiovascular Hospital, Department of Ultrasound Imaging, Yunnan, 650000, People’s Republic of China; 6The First People’s Hospital of Foshan, Foshan, Guangdong Province, 528000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yong Liu; Jin LiuDepartment of Cardiology, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Cardiovascular Institute, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, People’s Republic of ChinaTel +86 2083827812-10528Fax +86 2083851483Email liuyong@gdph.org.cn; ljaw397017568@163.comPurpose: Hypochloremia is a predictor for short-term mortality in patients with cardiovascular disease, but its association with coronary artery disease (CAD) is still unclear. We aimed to assess the impact of hypochloremia on all-cause mortality (short-and long-term) among patients with CAD.Patients and Methods: Based on the registry at Guangdong Provincial People’s Hospital in China, we analyzed data of 49,025 hospitalized patients who underwent coronary angiography (CAG) and were diagnosed with CAD from January 2007 to December 2018. To assess the association between hypochloremia and the study endpoints, a logistic-regression model (for 30-day all-cause mortality) and a Cox regression model (for long-term all-cause mortality) were fitted.Results: Overall, 4.4% of the study population showed hypochloremia (< 98 mmol/L). During a median follow-up of 5.2 (3.1– 7.8) years, a total of 6486 (13.2%) patients died. Patients with hypochloremia were generally older and at risk for diabetes, cardiorenal dysfunction, and morbidity than those without hypochloremia. After adjustment for confounders, hypochloremia remained a significant predictor of mortality risk (30-day all-cause death: adjusted odds ratio [aOR], 1.99; 95% confidence interval, 1.08– 3.18; P=0.017 and long-term all-cause death: adjusted hazard ratio [aHR], 1.32; 95% confidence interval, 1.19– 1.47; P< 0.001).Conclusion: Hypochloremia is mildly common in patients with CAD and is associated with increased short-and long-term mortality. Meanwhile, it is necessary to further investigate effective and preventive measures and the potential mechanisms of hypochloremia in patients with CAD.Keywords: hypochloremia, coronary artery disease, prevalence, short- and long-term mortality

Visual Abstract, Highlights • Small molecule inhibition of WNK1 (WNK463) signaling mitigates upregulation of the membrane glucose channels GLUT1 and GLUT4, restores levels of several glucose metabolites, and decreases protein O-GlcNAcylation and glycation in the RV. • Quantitative proteomics of RV mitochondrial enrichments shows WNK463 treatment prevents down-regulation of several mitochondrial enzymes in the tricarboxylic acid cycle, fatty acid oxidation pathway, and the electron transport chain complexes. • Integration of proteomics and metabolomics analysis suggests WNK463 reduces glutaminolysis induction and lipotoxicity caused by impaired mitochondrial fatty acid oxidation. • WNK463 augments RV systolic and diastolic function independent of PAH severity. • Hypochloremia, a condition of predicted WNK1 activation in patients with PAH, is associated with more severe RV dysfunction., Summary Small molecule inhibition of with no lysine kinase 1 (WNK1) (WNK463) signaling activates adenosine monophosphate-activated protein kinase signaling and mitigates membrane enrichment of glucose transporters 1 and 4, which decreases protein O-GlcNAcylation and glycation. Quantitative proteomics of right ventricular (RV) mitochondrial enrichments shows WNK463 prevents down-regulation of several mitochondrial metabolic enzymes. and metabolomics analysis suggests multiple metabolic processes are corrected. Physiologically, WNK463 augments RV systolic and diastolic function independent of pulmonary arterial hypertension severity. Hypochloremia, a condition of predicted WNK1 activation in patients with pulmonary arterial hypertension, is associated with more severe RV dysfunction. These results suggest WNK1 may be a druggable target to combat metabolic dysregulation and may improve RV function and survival in pulmonary arterial hypertension.

Background The main symptoms of congenital chloride diarrhea (CCD) main symptoms are watery diarrhea, hypochloremia, and hypokalemic metabolic alkalosis. Silver–Russell syndrome (SRS) is a heterogeneous imprinting disorder characterized by severe intrauterine retardation, poor postnatal growth, and facial dysmorphism. Methods Parent‐offspring trio whole‐exome sequencing was used to identify the causal variants. Sequencing reads were mapped to the reference of human genome version hg19. Sanger sequencing was performed as a confirmatory experiment. Results The proband was a patient with SRS caused by maternal uniparental disomy 7. The CCD of the proband was caused by homozygous variant c.1515–1 (IVS13) G>A; both mutated alleles were inherited from her mother. Conclusion We report the first clinical case of CCD and SRS occurring together. Patients with milder phenotypes may be difficult to diagnose in early stage, but close monitoring of potential complications is important for identification., We report the first case of a female child presenting with CCD accompanied by maternal segmental UPD of chromosome 7 confirmed by molecular diagnosis. The proband was the only patient in the family and harbored a SLC26A3 variant (NM_000111.3:c.1515‐1G>A). The mother of the patient was heterozygous, whereas the father was wild‐type. After treatment of CCD, the patient still failed to thrive and had a typical dysmorphic feature. In the second genetic analysis, we found that at least 86.51 Mb of genome 7q11q36 (chr7: 65446986–151960086) was maternal uniparental disomy. We revised the diagnosis to CCD combined with SRS.

Several studies have recently challenged the sodium-centric view that has been dominating the field of heart failure (HF) and cardiorenal syndrome. The previously observed benefits of severe dietary restriction of salt do not seem to be consistently reproduced by contemporary studies. Moreover, there is evidence that too low intake may paradoxically lead to adverse outcomes in more advanced stages of HF. Facing the escalating controversy, investigators have shifted their focus from sodium to its often overlooked counter ion in salt, the chloride. Emerging data suggest that serum chloride levels could portend robust independent prognostic value in a wide range of HF syndromes possibly stronger than that of sodium. The untoward impact of hypochloremia on the outcomes could be mechanistically linked to renal tubular regulatory pathways, neurohormonal activation, and diuretic resistance. As such, it can be a potential target of therapy in this setting. In this article, the authors provide a brief overview of the role of serum chloride as a cardiorenal connector and explore the context in which the contemporary data should be interpreted. Implementation of predictive and therapeutic strategies incorporating the emerging evidence would be refined through discussion of nuances of such findings as well as their biological and clinical relevance.

Background Refractory congestive heart failure (CHF) and associated diuretic resistance are not well defined. Objectives To characterize renal function, electrolyte concentrations, indices of diuretic efficacy, and renin-angiotensin-aldosterone system (RAAS) activation in dogs with naturally occurring heart disease (HD) in American College of Veterinary Internal Medicine stages B1, B2, C, and D and to determine their usefulness in defining HD stages. Animals Group 1:149 dogs with HD stages B1, B2, C, and D. Group 2:22 dogs with HD stages C and D. Methods Group 1: Renal parameters, serum and urine electrolyte and diuretic concentrations, and urine aldosterone concentrations were measured. Medication dosages and measured variables were compared among stages. Correlation of furosemide dosages to serum concentrations was explored. Group 2: Angiotensin-converting enzyme activity and RAAS components were measured and compared among CHF stages. Results Serum chloride concentration was the best differentiator of HD stage. Furosemide PO dosages (≤6 mg/kg/day) were weakly correlated with serum furosemide concentrations, whereas higher dosages were not significantly correlated. Angiotensin-converting enzyme inhibitor dosage and RAAS inhibition were greater in stage D, compared to stage C dogs. Conclusions and clinical importance Hypochloremia is a useful marker for stage D HD in dogs. Poor furosemide dosage correlation to serum concentration may indicate variable and poor absorption, especially at higher dosages, advanced disease, or both. A small number of stage D dogs met proposed criteria for diuretic resistance. Greater RAAS inhibition in stage D versus stage C indicates effectiveness of RAAS-suppressive treatments in this group of dogs with refractory CHF.

Congenital chloride diarrhea (CCD) is an autosomal recessive hereditary disease manifested by persistent, watery, profuse diarrhea with high chloride concentration (>90 mmol/L). Postnatally, neonates suffer from hypochloremia, hyponatremia, hypokalemia, metabolic alkalosis, dehydration, developmental retardation, or even death. Prenatal diagnosis is of great importance for the prognosis of CCD. We report a prenatal recurrent case of CCD. Prenatal ultrasound revealed fetal diffuse intestinal dilation with the typical honeycomb sign and polyhydramnios with high amniotic fluid index. The whole exome capture and massively‐parallel DNA sequencing showed an abnormal mutation of Solute Carrier Family 26, Member 3 (SLC26A3), c.1039G>A (p.Ala347Thr), and the mutation sites were verified by sanger sequencing. When prenatal ultrasound shows polyhydramnios and diffuse intestinal dilation, CCD should be suspected. Molecular genetic testing can be helpful for the diagnosis.

Aim: This study aimed to describe the clinicopathological and necropsy findings in neonatal dairy calves affected with right torsion of the abomasum. Materials and Methods: The history and findings of clinical examination, hematology and serum biochemical analyses and necropsy were described in six neonatal Holstein calves with a confirmed diagnosis of right torsion of the abomasum. Furthermore, a review of the literature was carried out using internet search engines such as PubMed and Google Scholar concerning abomasal displacement in calves. Only published papers in scientific and refereed journals were reviewed. Results: Six neonatal Holstein calves (four females and two males) aged between 7 and 21 days were diagnosed with right torsion of the abomasum during necropsy. The calves were presented with peracute signs of anorexia, dehydration, abdominal pain, and abdominal distension. Hematology and serum biochemical analyses revealed hemoconcentration and azotemia, hyponatremia, hypochloremia, and hypokalemia. Conclusion: Abomasal torsion in neonatal calves must be placed on the deferential diagnostic list of calves suffering from peracute signs of abdominal pain and distension. Although the underlying etiopathological factors are not fully known, correction of nutritional mismanagement is required to prevent the condition.

The authors provide a review of current clinical guidelines regarding medical care provided to children with Bartter’s syndrome — impaired renal tubular function (loop of Henle) with the development of hypokalemia, hypochloremia, metabolic alkalosis and hyperreninemic hyperaldosteronism. The specifics of disease epidemiology, etiology and pathogenesis are described. The issues of differential diagnosis and treatment based on the principles of evidence are covered.

Diabetic Nephropathy(DN) is a complex disease manifested by persistence microalbuminuria occurring due to the interaction between hemodynamic and metabolic pathway that activates the local renin-angiotensin-aldosterone system resulting in a decline in renal functions. This study aimed to quantify the associations between serum aldosterone concentration and fetuin- A as a marker of calcification in type 2 diabetic patients with and without microalbuminuria from one side, and study the possible relationship between aldosterone and fetuin-A with glycemic indices, serum electrolyte, renal function and microalbuminuria and body mass index from the other side. A case-control study involved eighty-six adult subjects classified into three groups after testing urine microalbumin including thirty-two diabetics type 2 patients with positive microalbuminuria and twenty-eight diabetics type 2 patients with negative microalbuminuria and 26 healthy subjects during their visit to AL kindy specialized Center for Endocrinology and Diabetes / Baghdad. Those patients were compared to control group of 26 apparently healthy subjects, fasting blood samples was obtained from each of them in one occasion only to measure: fasting serum glucose, electrolyte, aldosterone, fetuin-A, urea, and creatinine. In addition to glycoheamoglobin, glomerular filtration rate and body mass index. Despite the presence of microalbuminuria in thirty-two of the studied diabetics, there was no positive correlation between aldosterone and fetuin- A, besides that no significant variations in serum aldosterone ,glomerular filtration rate(GFR) values, while both groups showed a significant increase in fasting serum glucose and glycaoheamoglobin ,significant decrease in serum sodium and chloride in comparison with the control group , significant increase was detected in serum fetuin-A mean values in microalbuminuric diabetics. Whereas, negative microalbuminuric diabetics measures expressed a positive correlation between both serum sodium and chloride levels and fetuin -A. The conclusion of this study diabetic patient are prone to vascular calcification (VC) might be due to increase in aldosterone level or due to diabetic itself from this study we can conclude microalbuminuria can occur without a decline in renal function or a change in estimated GFR ,no definite correlation occur between aldosterone and fetuin- A, fetuin- A mean values are higher in diabetic patient with microalbuminuria compared to diabetic patients without microalbuminuria and control group and this referred to uncontrolled diabetes ,aldosterone show a correlation with weight and body mass index while fetuin- A does not show such correlation. In general, electrolyte disturbances (hypernatremia) is more obvious in this study , and its occurrence is due to diabetic (osmotic diuresis) or drugs, while sodium retention which is a sign of aldosterone increment does not occur. Hypochloremia that occur in this study is due to chloride and it is in parallel with sodium level.

Background X-linked Adrenal Hypoplasia Congenita (AHC) is a rare cause of primary adrenal insufficiency due to mutations in the NR0B1 gene, causing a loss of function of the nuclear receptor protein DAX-1. Adrenal insufficiency usually appears in the first 2 months of life, but can sometimes emerge during childhood. Hypogonadotropic Hypogonadism is often associated later in life and patients may develop azoospermia. We describe an unusual onset of AHC started with isolated hypoaldosteronism as first and only sign of the disease. Case presentation A 18-days-old newborn presented with failure to thrive and feeding difficulties. Blood tests showed severe hyponatremia, hyperkalemia and hypochloremia. Renin was found over the measurable range and aldosterone was low whereas cortisol level was normal with a slightly increased ACTH. In the suspicion of Primary Hypoaldosteronism, correction of plasmatic electrolytes and replacement therapy with Fludrocortisone were promptly started. The subsequent evidence of low plasmatic and urinary cortisol and increased ACTH required the start of Hydrocortisone replacement therapy and it defined a clinical picture of adrenal insufficiency. Genetic analysis demonstrated a novel mutation in the DAX-1 gene leading to the diagnosis of AHC. Conclusions AHC onset may involve the aldosterone production itself, miming an isolated defect of aldosterone synthesis. NR0B1/DAX-1 mutations should be considered in male infants presenting with isolated hypoaldosteronism as first sign of adrenal insufficiency.

Background This study investigated the associations of fluctuations in serum chloride (Cl−) levels with 30-day mortality after intensive care unit (ICU) admission among critically ill patients. Methods We retrospectively analyzed the medical records of adult patients (≥18 years old) admitted to the ICU between January 2012 and December 2017. Positive and negative fluctuations in Cl− were defined as the differences between the Cl− upon ICU admission (baseline Cl−) and the maximum and minimum Cl− levels, respectively, measured within 72 h after ICU admission. Results The final analysis included 18,825 adult patients. In multivariable Cox regression analyses, the risk of 30-day mortality increased by 8% per 1-mmol L− 1 positive fluctuation in Cl− within 72 h (hazard ratio = 1.08, 95% confidence interval: 1.04–1.11, P 10%), normochloremia (97–110 mmol L− 1) or hyperchloremia (> 110 mmol L− 1) upon ICU admission. Furthermore, a negative fluctuation in the Cl− level during the first 72 h of an ICU stay was associated with a negative cumulative FB (

To determine association between electrolyte disturbances and mortality in patients with severe traumatic brain injury.Medical records of patients with severe traumatic brain injury and Glasgow Coma Scale score8 and electrolyte alterations were reviewed in a retrospective cohort study. Electrolyte levels were analyzed to establish an association between patients who died and patients who survived. Bivariate analysis was performed using χThere was a significant relationship between hypochloremia and increased risk of mortality in 23.1% of deceased patients (P = 0.03). Furthermore, there was a significant correlation with age (P0.01) and with the Acute Physiology and Chronic Health Evaluation APACHE II (P0.01).Hypochloremia could be an important prognostic factor to determine mortality risk and to improve treatment in patients with severe traumatic brain injury.

Background: Mechanical ventilation (MV) is one of the most important components of modern intensive care practice. Longer MV time is associated with increased morbidity and mortality. Therefore, it is important to identify the risk factors associated with longer duration of MV. The objective of this study was to determine the clinical and the laboratory risk factors for prolonged invasive MV in the pediatric intensive care unit (PICU). Methods: We performed a retrospective analysis of the records of all patients admitted to our PICU between October 2016 and March 2018. Patients with invasive MV were included in the study. Results: A total of 121 children with a mean age of 3.58 ± 4.84 years were enrolled in this study. The most frequent diagnosis at the time of admission to the PICU was primary respiratory disease (31.4%), followed by neurological diseases (22.3%), and sepsis (17.4%). Pressure control was the most commonly used MV method in 97 (80.2%) patients. Pressure regulated volume control was used in the other (19.8%) patients. The mean duration of mechanical ventilation was 9.17 ± 8.12 days. Risk factors for prolonged MV in the PICU included red blood cell (RBC) transfusion, hypochloremia, high gamma-glutamyl transferase (GGT), and low body mass index (BMI). The logistic regression analysis showed that hypochloremia prolonged MV by 3.234 fold, neuromuscular blocker drug uses prolonged MV by 3.689 fold, and RBC transfusion prolonged MV by 8.031 fold. Conclusion: Hypochloremia, need for RBC transfusion, and neuromuscular blocker drug use may be early predictors of prolonged MV in critically ill children.

Background: Diuretic resistance is among the most challenging problems that the cardio-nephrologist must address in daily clinical practice, with a considerable burden on hospital admissions and health care costs. Indeed, loop diuretics are the first-line therapy to overcome fluid overload in heart failure patients. The pathophysiological mechanisms of fluid and sodium retention are complex and depend on several neuro-hormonal signals mainly acting on sodium reabsorption along the renal tubule. Consequently, doses and administration modalities of diuretics must be carefully tailored to patients in order to overcome under- or overtreatment. The frequent and tricky development of diuretic resistance depends in part on post-diuretic sodium retention, reduced tubular secretion of the drug, and reduced sodium/chloride sensing. Sodium and chloride depletions have been recently shown to be major factors mediating these processes. Aquaretics and high-saline infusions have been recently suggested in cases of hyponatremic conditions. This review discusses the limitations and strengths of these approaches. Summary: Long-term diuretic use may lead to diuretic resistance in cardio-renal syndromes. To overcome this complication intravenous administration of loop diuretics and a combination of different diuretic classes have been proposed. In the presence of hyponatremia, high-saline solutions in addition to loop diuretics might be beneficial, whereas aquaretics require caution to avoid overcorrection. Key Messages: Diuretic resistance is a central theme for cardio-renal syndromes. Hyponatremia and hypochloremia may be part of the mechanisms for diuretic resistance. Aquaretics and high-saline solutions have been proposed as possible new therapeutic solutions.

Introduction: VIPoma is a neuroendocrine tumor that secrets vasoactive intestinal peptide and produces a well-defined clinical syndrome characterized by watery diarrhea, hypokalemia, hypochlorhydria and metabolic acidosis. The aim of this study to investigate clinical studies about diagnostic and therapeutic modalities of vipoma patients. In this retrospective study, all patients of vipoma were investigated. Clinical features, laboratory data at initial presentation, management and outcomes were collected. Subjects and Methods: The paper has written based on searching PubMed and Google Scholar to identify potentially relevant articles or abstracts. Categorical variables as percentage and continuous variables were reported as mean ± standard deviation (SD). Results: All the patients presented with watery diarrhea (30/30, 100%) and dehydration was reported in 33.3% of them. Prevalence of laboratory findings in these patients were assessed for hypokalaemia (25/30, 83.3%), metabolic acidosis (9/30, 33.6%), hypochloremia and achlorhydria (2/30, 6.6%). Elevated VIP levels have been seen in 73.3% patients with mean values of 882.85 ± 1134.87 pg/ml. Prevalence of diagnostic methods included CT scan in 19 patients (19/30, 63.3%), ultrasonography (15/50, 50%), and somatostatin receptor scintigraphy (8/30, 26.6%). Medical treatments included somatostatin and analogues in 18 patients (18/30, 60%). Surgery included less percentage of treatment in these patients. Conclusion: CT scan can be used as a reliable modality for diagnosis of vipoma and somatostatin analogues can be used as the most effective treatment in vipoma patients. Surveillance of these patients needs to close monitoring of patients via history, physical examination, laboratory and imaging.

Background Congenital chloride diarrhea (CCD, OMIM 214700) is a rare autosomal recessively inherited condition characterized by watery diarrhea, hypochloremia and metabolic alkalosis. Mutations of the solute carrier family 26, member 3 (SLC26A3, OMIM 126650) gene are responsible for the disease. The gene encodes a transmembrane protein, which is essential for intestinal chloride absorption. Case presentation Here we report a Hungarian boy, presenting the clinical phenotype of CCD. The patient born at 32 weeks of gestation and underwent surgery for abdominal distension and intestinal obstruction related to malrotation. After recovery, electrolyte replacement therapy was necessary due to several periods of diarrhea. After exclusion of other possible causes, increased chloride concentration in the feces supported the diagnosis of CCD. The diagnosis was confirmed by molecular genetic testing. Direct sequencing revealed compound-heterozygosity for a frameshift mutation c.1295delT (p.Leu432Argfs*11) and the known Polish founder mutation c.2024_2026dupTCA (p.Ile675_Arg676insLeu). Conclusions Here we present the clinical symptoms of the first patient in Hungary diagnosed with CCD. Based on the clinical symptoms, stool analysis and genetic testing, the diagnosis of CCD was established. Our study provides expansion for the mutation spectrum of the SLC26A3 gene and the genetic background of CCD.

Background Cirrhosis can be complicated by electrolyte abnormalities, but the major focus has been concentrated on the clinical significance of serum sodium levels. Emerging studies have identified hypochloremia as an independent prognostic marker in patients with chronic heart failure and chronic kidney disease. The aim of this study was to investigate whether serum chloride levels were associated with mortality of critically ill cirrhotic patients. Methods Critically ill cirrhotic patients were identified from the Multi-parameter Intelligent Monitoring in Intensive Care III Database. The primary outcome was ICU mortality. Logistic regression was used to explore the association between serum chloride levels and ICU mortality. The area under the receiver operating characteristic curves (AUC) was used to assess the performance of serum chloride levels for predicting ICU mortality. Results A total of 1216 critically ill cirrhotic patients were enrolled in this study. The overall ICU mortality rate was 18.8%. Patients with hypochloremia had a higher ICU mortality than those with non-hypochloremia (34.2% vs. 15.8%; p p = 0.002) in contrast to serum sodium levels, which were no longer significant (OR 1.03; 95% CI 0.99–1.08; p = 0.119). The AUC of serum chloride levels (AUC, 0.600; 95% CI 0.556–0.643) for ICU mortality was statistically higher than that of serum sodium levels (AUC, 0.544; 95% CI 0.499–0.590) (p Conclusions In critically ill cirrhotic patients, serum chloride levels are independently and inversely associated with ICU mortality, thus highlighting the prognostic role of serum chloride levels which are largely overlooked.

Background and Aims Recently, serum chloride has gained greater importance in the assessment of patients with heart failure and sepsis. Hypochloremia has been associated with higher mortality. On the other hand, COVID-19 pandemic continues to be, to date, a threat to public health. Patients with cardiovascular comorbidity or chronic kidney disease are particularly vulnerable. There are some studies that show a trend towards a lower serum chloride concentration in patients with a positive PCR test for SARS-CoV-2. Therefore, the objective of our study was to determine if there is a relationship between serum chloride levels at the time of diagnosis and a greater tendency to develop COVID-19 pneumonia in chronic hemodialysis patients. Method Retrospective cohort study. We analyzed the serum chloride, C-reactive protein (CRP), procalcitonin, neutrophil-lymphocyte (NLR) and platelet-lymphocyte (PLR) ratios of 11 chronic hemodialysis patients with a positive SARS-CoV-2 TMA PCR test during the second wave of the pandemic in our hospital (August-December 2020). We collected the length of hospital stay, the diagnosis of pneumonia (yes/no) and the final state of the infection (cure or death). The patients were divided into two groups taking the median serum chloride as the cut-off point (1: 97mEq / L) Results The mean age was 57 ± 13 years and 36.36% (N = 4) were women. All patients required hospital admission and mean hospitalization time was 19 ± 13 days. 3 patients (27.3%) died. The medians of the parameters were the following: serum chloride 97 mEq / L (IQR 94-99); CRP 29.04 mg / L (IQR 8.53-76.13); NLR 4.13 (IQR 2.67-8.48) and PLR 244.06 (IQR 208.08-320). 81.8% (N = 9) had COVID-19 pneumonia. Group 1 patients (Chloride Conclusion Chronic hemodialysis patients with SARS-CoV-2 infection and lower serum chloride levels at hospital admission were more likely to develop pneumonia.

Purpose We sought to describe the association between serum chloride levels and mortality among unselected cardiac intensive care unit (CICU) patients. Materials and methods We retrospectively reviewed adult patients admitted to our CICU from 2007 to 2015. The association of dyschloremia and hospital mortality was assessed in a multiple variable model including additional confounders, and the association of dyschloremia and post-discharge mortality were assessed using Cox proportional-hazards analysis. Results 9,426 patients with a mean age of 67±15 years (37% females) were included. Admission hypochloremia was present in 1,384 (15%) patients, and hyperchloremia was present in 1,606 (17%) patients. There was a U-shaped relationship between admission chloride and unadjusted hospital mortality, with increased hospital mortality among patients with hypochloremia (unadjusted OR 3.0, 95% CI 2.5–3.6, p Conclusion Abnormal serum chloride on admission to the CICU is associated with increased short- and long-term mortality, with hypochloremia being a strong independent predictor.

BackgroundHyperchloremia and chloride load have been associated with worse clinical outcomes in critically ill patients. We sought to evaluate the electrolyte profile and clinical outcomes associated with a unit-wide transition from saline to balanced fluids for resuscitation and maintenance fluids in a pediatric intensive care unit (PICU).MethodsA before and after analysis of all patients admitted to the PICU in a large, urban, academic hospital between August 2018 and March 2020. The transition from the use of saline to the use of balanced fluids for both resuscitation and maintenance fluid as standard care occurred in June 2019. The primary outcome was day 3 acute kidney injury (AKI). The secondary outcomes included mortality, ventilator-free days (VFDs), need for renal replacement therapy (RRT), hospital length of stay (LOS), and electrolyte abnormalities.ResultsOverall, 2863 patients (47% female) with a day 3 AKI rate of 12.9% (n = 130) and a mortality rate of 2.8% (n = 79) were included. After adjusting for confounders (age, PRISM III, mechanical ventilation, and immunocompromised state, septic shock), there were no significant differences in the odds of day 3 AKI (pre 13%, post 12.5%; adjusted odds ratio [aOR] 0.96, 95%CI 0.65–1.42). There were no differences in the secondary outcomes. The post-intervention period had fewer patients with hyperchloremia (pre 15.5% vs. post 10.4%,p = p = 0.02) and more patients with hypochloremia (pre 9.5% vs. post 14.4%,p = p = ConclusionsFollowing a unit-wide implementation of balanced fluids as standard care, there were no differences in rates of day 3 AKI or other clinical outcomes. However, there were lower rates of hyperkalemia and hyperchloremia and higher rates of hypokalemia and hypochloremia. Further evaluation of the effect of balanced fluids and the clinical significance of electrolyte abnormalities in critically ill children is needed.