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Chloride – Cl–
Reference interval – examples
Distribution and physiological significance of chloride
Why measure chloride ?
Terms used in interpretation of chloride
Causes of hypochloremia and hyperchloremia
The value of chloride in the investigation of acid-base disturbance
Causes of ”high-AG” acidosis
Causes of ”normal-AG hyperchloremic”acidosis
Acid-base disturbances associated with abnormal chloride
Chloride (Cl–) is the major anion in the extracellular fluid and one of the most important anions in blood. The main function of Cl– is to maintain osmotic pressure, fluid balance, muscular activity, ionic neutrality in plasma, and help elucidate the cause of acid-base disturbances.
Reference interval – examples
Distribution and physiological significance of chloride
In common with sodium (Na+), most of the approximately 3200 mmol (113 g) of Cl– present in the human body is contained within the extracellular fluid. Extracellular (plasma) concentration is around 100 mmol/L, whereas intracellular-fluid concentration is closer to 2 – 5 mmol/L. As the second most abundant extracellular fluid ion after Na+, and the most abundant extracellular fluid anion, Cl– is essential for the maintenance of normal plasma osmolarity, contributing 100 of the 300 mOsmol of extracellular tonicity . In combination with Na+, Cl– determines water movement between extracellular and intracellular compartments and thereby regulation of blood volume and blood pressure. Cl– is essential for maintaining the electrochemical neutrality of plasma, contributing 70 % of all negative charges in plasma, bicarbonate (HCO3–) contributing most of the remaining.
Cl– ions are secreted from parietal cells of the stomach as hydrochloric acid, a constituent of gastric juice essential for many processes involved in the digestion and absorption of food, as well as the control of bacterial growth within the gastrointestinal tract.
Cl– is present at high concentrations (~70 mmol/L) in erythrocytes compared with all other cells (2 – 5 mmol/L). This high concentration enables the movement of Cl– between plasma and erythrocytes in exchange for bicarbonate (HCO3–) . This so-called ”chloride shift” is essential for the effective transport of carbon dioxide from tissues to lungs and the maintenance of normal blood pH (acid-base homeostasis).
Why measure chloride?
The clinical utility of measuring chloride concentration (cCl–) is to help elucidate the cause of acid-base disturbances, as abnormal Cl– levels alone usually signify a more serious underlying metabolic disorder, such as metabolic acidosis or alkalosis. It is also essential for the calculation of the anion gap (AG)  (see AG) that can be useful in the investigation of acid-base disturbance . In the absence of acid-base disturbance, cCl– almost invariably parallels sodium (cNa+), so that cCl– measurement is rarely of value in routine assessment of fluid and electrolyte balance; measurement of cNa+ is sufficient and cCl– provides no additional information .
Maintaining Cl– within normal limits principally depends on renal regulation of Cl– loss in urine. Daily dietary intake of Cl–, predominantly in the form of salt flavoring, ranges from 160 to 300 mmol (5.7 – 10.6 g) . This is far in excess of what is required to replace normal obligatory physiological losses of Cl– in urine, sweat and feces, so that most of this dietary intake must be excreted in urine to remain in balance. Renal regulation of Cl– excretion, like that of sodium excretion, depends on the hormone aldosterone and the renin-angiotensin pathway. Cl– excretion is linked to HCO3– reabsorption/regeneration, an important mechanism for renal regulation of blood pH that has implication for the role of Cl– in the pathogenesis of acid-base disturbance.
Cl– balance also depends on the ability of the gastrointestinal tract to absorb almost all of the Cl– present in gastrointestinal secretions, e.g. gastric juice, pancreatic juice, bile. Vomiting and/or diarrhea can lead to Cl– depletion.
Terms used in interpretation of chloride
Decreased cCl– (i.e. <98 mmol/L) is called hypochloremia .
Increased cCl– (i.e. cCl– >107 mmol/L) is called hyperchloremia .
Causes of hypochloremia and hyperchloremia
Since cCl– almost invariably closely parallels cNa+ in both health and disease, the causes of hypochloremia are identical with the causes of hyponatremia (see Na+) and the causes of hyperchloremia are identical with the causes of hypernatremia (see Na+)
The clinical value of measuring cCl– is confined to acid-base disturbance when cCl– may not parallel cNa+.
The value of chloride in the investigation of acid-base disturbance
Measurement of cCl– is useful in the investigation of patients with unexplained metabolic acidosis because it allows the distinction between ”high-AG” metabolic acidosis and ”normal-AG” metabolic acidosis (see AG) . The first, which is the more common of the two, is characterized by abnormal increase in unmeasured (non-chloride) anions derived from a causative non-volatile acid (e.g. lactic acid, keto acid). The second is characterized by an increase in measured anion (Cl–), so it is associated with hyperchloremia. In general terms, ”high-AG” metabolic acidosis is due to abnormal accumulation of an acid, such that the HCO3– buffer is consumed, and ”normal-AG, hyperchloremic” metabolic acidosis is due to primary loss of HCO3– buffer from the body, either via the gastrointestinal tract or the kidneys. The resulting decreased extracellular fluid HCO3– induces hyperchloremia to correct the anion deficit and maintain the electrochemical neutrality of extracellular fluid. This is a condition in which cCl– does not parallel cNa+; whatever the sodium concentration there is relative hyperchloremia.
Causes of ”high-AG” acidosis 
- Lactic acidosis (most common cause of metabolic acidosis)
- Diabetic ketoacidosis (DKA)
- Alcoholic ketoacidosis
- Starvation ketoacidosis
- Renal failure (acute and chronic)
- Toxins that metabolize to acids (e.g. ethylene glycol, methanol, salicylates)
Causes of ”normal-AG hyperchloremic” acidosis 
- Renal tubule acidosis
- Severe diarrhea
- Drainage of pancreatic or biliary secretion
- Bowel fistula
- Carbonic anhydrase inhibitor drugs (e.g. acetazolamide)
- Excessive administration of HCl or NH4Cl to correct metabolic alkalosis
- Fluid resuscitation (e.g. saline infusion)
Other acid-base disturbances associated with abnormal chloride
Hypochloremia can cause increased renal reabsorption of HCO3– and consequent metabolic alkalosis . This hypochloremia is usually the result of increased loss of Cl– via the gastrointestinal tract in vomit but can be the result of renal losses, usually secondary to diuretic therapy. Symptoms of hypochloremia are due to the metabolic alkalosis that it induces.
Renal compensation for respiratory acidosis involves increased reabsorption of HCO3– in exchange for Cl–, so that chronic respiratory acidosis is associated with increased loss of Cl– in urine and consequent hypochloremia.
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- Olsen TG, Barnes AA, King JA. Elevated HCG outside of pregnancy – diagnostic considerations and laboratory evaluation. Obstet Gynecol Surv 2007; 62: 669-74.
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Effective Date January 20th, 2023 (last updated January 20th, 2023)
ABOUT THIS POLICYRadiometer values your privacy and the protection of your personal data. This policy (“Policy”) explains how Radiometer its affiliates, subsidiaries or related companies, a full list of which can be located here (together, “Radiometer”, “our”, “us”, or “we”), collects, uses, shares, transfers and processes data collected from or about you.
“Personal Data” is any information that can be used to directly or indirectly identify an individual or that can be reasonably expected to link to an individual. This can include items such as name, address, telephone number, credit card details, email address, ID number, Internet Protocol (“IP”) address of an electronic device used by an individual, or other identifying code (even absent of other identifying information). Statistical and non-identifiable metric data are not considered Personal Data.
The Radiometer subsidiary, affiliate or related company with which you interact is, where applicable, the data controller (or equivalent under applicable law) responsible for the processing of your Personal Data. You can find a list of the relevant legal entities that act as data controllers in Appendix 1 to this Policy.
SCOPEThis Policy describes the types of Personal Data that we may collect, process or disclose about you and how you may govern this processing by exercising applicable legal rights. This Policy applies to both online and offline information collection, including your use of websites or subdomains operated by us, any mobile applications, when we provide products and/or services to you or notify you about prospective items of interest and in other situations where you interact with us in-person, by telephone or by mail where this Policy is posted or referenced.
There may be occasion where you have been provided with a circumstance-specific privacy notice that is separate from this policy, such as privacy notices for specific activities such as Recruitment. To the extent you were provided with a different notice, those notices apply and govern our interactions with you. If you provide Personal Data about parties other than yourself, you are responsible for ensuring their knowledge of how we will process their personal data, and, where applicable, obtaining any necessary consents required in advance.
We are committed to processing Personal Data in accordance with applicable laws. Please note that if you do not wish to provide your Personal Data to us, some products and/or services may become unavailable to you. Your use of any or all these platforms indicates you have been notified of our collection, use, transfer, and disclosure of your information as described in this Policy to the extent permitted by applicable law.Read more