Experimental treatments that are being examined depend on the revelation that a few mutations causing Bartter<unk>  create carriers with normal function. In any case, the mutations bring about the sequestration of these carriers inside intracellular compartments with the goal that they neglect to effectively embed into the suitable cell membrane. When these proteins can be effectively embedded into the cell membrane, they can become functional and correct the defect. The delivery and insertion of these fully or partially functional proteins into the cell membrane and partially rescue sodium chloride reabsorption can be improved by the utilization of the molecular chaperones, such as 4-phenylbutyrate.
Bartter syndrome future or investigational therapies
Bartter syndrome medical therapy
Andersen-Tawil syndrome primary prevention
Bartter syndrome echocardiography or ultrasound
Fabry's disease echocardiography or ultrasound
Fabry's disease electrocardiogram
Neurofibromatosis type 1 secondary prevention
Brugada syndrome diagnostic criteria