The other subtypes of the syndrome involve mutations in other transporters that result in functional loss of the target transporter. Patients often admit to a personal preference for salty foods.The clinical findings characteristic of Bartter syndrome is hypokalemia, metabolic alkalosis, and normal to low blood pressure. These findings may also be caused by other conditions, which may cause confusion. When diagnosing a Bartters syndrome, the following conditions must be ruled out as possible causes of the symptomatology:
Chronic vomiting: These patients will have low urine chloride levels; they have relatively higher urine chloride levels. Abuse of diuretic medications  (water pills): The physician must screen urine for multiple diuretics before a diagnosis is made. Magnesium deficiency and calcium deficiency: These patients will also have low serum and urine magnesium and calcium.Patients with Bartter syndrome may also have elevated renin and aldosterone levels.Prenatal Bartter syndrome can be associated with polyhydramnios. Related conditions
Bartter and Gitelman syndromes are both characterized by low levels of potassium and magnesium in the blood, normal to low blood pressure, and hypochloremic metabolic alkalosis.However, Bartter syndrome is also characterized by high renin, high aldosterone, hypercalciuria, and an abnormal Na+-K+-2Cl− transporter in the thick ascending limb of the loop of Henle, whereas Gitelman syndrome causes hypocalciuria and is due to an abnormal thiazide-sensitive transporter in the distal segment. Pseudo-Bartters syndrome is a syndrome of similar presentation as Bartter syndrome but without any of its characteristic genetic defects. Pseudo-Bartters syndrome has been seen in cystic fibrosis, as well as in excessive use of laxatives.
Acquired hemolytic anemia is also encountered in burns and as a result of certain infections (e.g. malaria). Lead poisoning or poisoning by arsine or stibine causes non-immune hemolytic anemia. Runners can develop hemolytic anemia due to "footstrike hemolysis", the destruction of red blood cells in feet at foot impact. Low-grade hemolytic anemia occurs in 70% of prosthetic heart valve recipients, and severe hemolytic anemia occurs in 3%. Intravascular hemolysis
Intravascular hemolysis describes hemolysis that happens mainly inside the vasculature. As a result, the contents of the red blood cell are released into the general circulation, leading to hemoglobinemia and increasing the risk of ensuing hyperbilirubinemia.Intravascular hemolysis may occur when red blood cells are targeted by autoantibodies, leading to complement fixation, or by damage by parasites such as Babesia. Additionally, thrombotic microangiopathy (TMA) can result in hemolysis of red blood cells. TMA is frequently observed in aHUS patients where clots form in the small vessels of the kidney resulting in damaged red blood cells as they attempt to pass through the restricted vessels. Extravascular hemolysis
Extravascular hemolysis refers to hemolysis taking place in the liver, spleen, bone marrow, and lymph nodes. In this case little hemoglobin escapes into blood plasma. The macrophages of the reticuloendothelial system in these organs engulf and destroy structurally-defective red blood cells, or those with antibodies attached, and release unconjugated bilirubin into the blood plasma circulation.