Bartter Syndrome

Bartter syndrome is a group of rare inherited renal tubular disorders characterized by impaired sodium chloride reabsorption in the thick ascending limb (TAL) of the loop of Henle, resulting in salt wasting, hypokalemic metabolic alkalosis, hyperreninemia, hyperaldosteronism, and normal to low blood pressure despite markedly elevated renin and aldosterone levels. The syndrome mimics the effects of chronic loop diuretic (furosemide) administration, earning it the description of a genetic furosemide-like condition. To understand Bartter syndrome, the nurse must appreciate normal ion transport in the TAL. The TAL is responsible for reabsorbing approximately 25 to 30% of filtered sodium chloride. The primary transporter is the sodium-potassium-chloride cotransporter type 2 (NKCC2, also called BSC1) located on the luminal (apical) membrane. NKCC2 transports one sodium, one potassium, and two chloride ions from the tubular lumen into the TAL cell. This process is driven by the low intracellular sodium concentration maintained by the basolateral Na+/K+-ATPase, which pumps sodium out of the cell into the peritubular capillary. Potassium that enters the cell via NKCC2 recycles back into the lumen through the renal outer medullary potassium channel...