About Bartter Syndrome
Bartter syndrome encompasses a group of autosomal recessive renal tubular disorders caused by mutations in genes encoding ion transporters in the thick ascending limb of the loop of Henle, resulting in salt wasting, hypokalaemic metabolic alkalosis, and secondary hyperaldosteronism. The neonatal forms (Types I and II) present with life-threatening polyuria, dehydration, and electrolyte disturbances in utero or at birth, while Type III (CLCNKB mutation) is more variable in severity. Long-term complications include nephrocalcinosis and progressive renal impairment.
Common Clinical Features
Clinical Trial Eligibility Tips
What to know before applying to Bartter Syndrome trials.
Genotype confirmation specifying Bartter subtype (I–V) is essential as disease severity, age of onset, and eligibility criteria differ substantially between subtypes.
Electrolyte profiles (potassium, chloride, bicarbonate, aldosterone, renin) at baseline and on current supplementation therapy must be documented; trials may require electrolytes to be within defined ranges at screening.
Some trials exclude patients on high-dose potassium supplementation or prostaglandin synthetase inhibitors; clarify medication requirements with the coordinating centre.
Patient Resources
Natural History Registry
European Rare Kidney Disease Reference Network (ERKNet) Registry
Join registry ↗Find recruiting Bartter Syndrome trials
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