It was not until 1931 that the disease was recognized as a disease in its own right when researchers Allen Graham et al from Cleveland reported its symptoms and presentation in the same detailed manner as Hakaru.In 1956, Drs. Rose and Witebsky were able to demonstrate how immunization of certain rodents with extracts of other rodents thyroid resembled the disease Hakaru and other researchers were trying to describe. These doctors were also able to describe anti-thyroglobulin antibodies in blood serum samples from these same animals.Later on in the same year, researches from the Middlesex Hospital in London were able to perform human experiments on patients who presented with similar symptoms. They purified anti-thyroglobulin antibody from their serum and were able to conclude that these sick patients have an immunological reaction to human thyroglobulin. From this data, it was proposed that Hashimotos struma could be an autoimmune disease of the thyroid gland. In 1957, it was recognized as an autoimmune disorder and was the first organ-specific autoimmune disorder identified.Following this recognition, the same researchers from Middlesex Hospital published an article in 1962 in Lancet which ended up including a portrait of Hakaru Hashimoto. The disease was able to become so much more well known from that moment and Hashimotos disease became to appear more frequently in textbooks.Since those discoveries, a number of autoimmune diseases have been able to be discovered with several of them having to do with thyroid-specific antibodies.
This charge gradient is obligatory for the paracellular reabsorption of both calcium and magnesium ions.Proper function of all of these transporters is necessary for normal ion reabsorption along the thick ascending limb, and loss of any component can result in functional inactivation of the system as a whole and lead to the presentation of Bartter syndrome. Loss of function of this reabsorption system results in decreased sodium, potassium, and chloride reabsorption in the thick ascending limb, as well as abolishment of the lumen-positive voltage, resulting in decreased calcium and magnesium reabsorption. Loss of reabsorption of sodium here also has the undesired effect of abolishing the hypertonicity of the renal medulla, severely impairing the ability to reabsorb water later in the distal nephron and collecting duct system, leading to significant diuresis and the potential for volume depletion. Finally, increased sodium load to the distal nephron elicits compensatory reabsorption mechanisms, albeit at the expense of potassium by excretion by principal cells and resulting hypokalemia. This increased potassium excretion is partially compensated by α-intercalated cells at the expense of hydrogen ions, leading to metabolic alkalosis.Bartter and Gitelman syndromes can be divided into different subtypes based on the genes involved:

Diagnosis
People with Bartter syndrome present symptoms that are identical to those of patients who are on loop diuretics like furosemide, given that the loop diuretics target the exact transport protein that is defective in the syndrome (at least for type 1 Bartter syndrome).