The nephrons 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 blood capillaries waiting to reabsorb ions from the interstitial fluid to circulate in the body. The amount of chloride to be released in the urine is due to the receptors lining the nephrons and the glomerulus filtration. Normally, chloride reabsorption begins in the proximal tubule and nearly 60% of chloride is filtered here. In a person with<unk> , 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. In the proximal tubule chloride reabsorption occurs in two parts. In the 1st phase, organic solutes (such as phosphates, amino acids, 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. One suggested mechanism leading to<unk> , there is a decrease in chloride transporter proteins along the nephron. These proteins may include sodium-potassium-2 chloride co-transporter, chloride anion exchangers, and chloride channels. 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 diffusion of chloride in and out the tubule.
Hyperchloremia
Alkalosis
Hypernatremia
Hyperchloremic acidosis
Hyponatremia
Hyperaemia
Acidosis
Hyperammonemia