At this point the use of epsilon-aminocaproic acid may be recommended to break down clots but its use can increase risk of obstructive nephropathy.In children, the administration of multiple blood transfusions has been shown to decrease overall kidney damage, but it is unclear how long this effect lasts. Maintaining good hydration is important in those with SCN because of the risk of dehydration from increased urination and there is a major concern of sickle cell crisis that can be prevented with adequate fluid intake.To manage proteinuria a low protein diet should be avoided because of the decrease in energy and growth in those with SCN but limiting protein to the maximum daily requirement without exceeding it is beneficial in retaining kidney function. A low protein diet may be considered in end stage renal disease (ESRD) alongside phosphate binders, and vitamin D, with the potential of using dialysis or kidney transplants. Medications
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are beneficial in reducing proteinuria by 50% over a  period of at least six months alongside a slight reduction in GFR but there is an unclear effect in overall CKD progression. If the medication is stopped then the symptoms return to similar levels to what it was before starting the medications. The lowering of nocturia has also been shown most likely from the decrease in GFR. This addition can be done regardless of baseline blood pressure.
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).