Editing Hyperchloremia (section)

==Mechanism ==
The [[nephron]]s in the [[kidney]] are responsible for regulating the level of chloride in the blood. The general mechanism is that as filtrate fluid passes through the nephrons varying concentrations of ions will be secreted into the [[interstitial fluid]] or absorbed into the lumen. All along the nephrons are [[Capillary|blood capillaries]] waiting to reabsorb ions from the interstitial fluid to circulate in the body.<ref name=":0">{{Cite book|title=Textbook of Medical Physiology|last=Hall, J|first=Guyton, A|publisher=Elsevier|year=2016|isbn=978-1455770052}}</ref> The amount of chloride to be released in the urine is due to the receptors lining the nephrons and the glomerulus filtration.{{cn|date=November 2024}}

Normally, chloride reabsorption begins in the [[proximal tubule]] and nearly 60% of chloride is filtered here.<ref name=":4">{{Cite journal|date=2016-07-01|title=Hyperchloremia – Why and how|journal=Nefrología (English Edition)|volume=36|issue=4|pages=347–353|doi=10.1016/j.nefroe.2016.06.006|pmid=27267918|issn=2013-2514|last1=Nagami|first1=Glenn T.|doi-access=free}}</ref> In a person with hyperchloremia, the absorption of chloride into the interstitial fluid and subsequently into the blood capillaries is increased. This means the concentration of chloride in the filtrate is decreased, therefore, a decreased amount of chloride is being excreted as waste in the urine.<ref name=":0" /> In the proximal tubule chloride reabsorption occurs in two parts. In the 1st phase, organic solutes (such as [[phosphate]]s, [[amino acid]]s, [[glucose]] and [[anions]]), sodium ions, and [[hydronium]] ions are reabsorbed from the filtrate fluid into the interstitial fluid.  This is an important step because this creates the concentration gradient in which chloride concentration in the lumen will increase in comparison to the chloride concentration in the interstitial fluid. In phase 2, chloride will diffuse along the concentration gradient, which means chloride ions will travel from areas of high concentration to areas of low concentration.<ref name=":1">{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK309/|title=Clinical Methods: The History, Physical, and Laboratory Examinations|last=Morrison|first=Gail|date=1990|publisher=Butterworths|isbn=978-0409900774|editor-last=Walker|editor-first=H. Kenneth|edition=3rd|location=Boston|pmid=21250151|editor-last2=Hall|editor-first2=W. Dallas|editor-last3=Hurst|editor-first3=J. Willis}}</ref>

One suggested mechanism leading to hyperchloremia, there is a decrease in chloride [[Transport protein|transporter proteins]] along the nephron. These proteins may include sodium-potassium-2 chloride co-transporter, chloride anion exchangers, and [[chloride channel]]s.  Another suggested mechanism is a depletion in concentration gradient as a result of the reduced activity in these transporters.  Such concentration gradient depletion would allow for the [[Passive transport|passive diffusion]] of chloride in and out the tubule.<ref name=":4" />