Ans. is 'b' i.e., Hypokalemia o In Bartter's syndrome the B.P. is low to normal despite increased level of aldosterone.Pathogenesis of Bartter Syndrome|Defect in sodium chloride and potasium transportin the ascending loop of henle|Loss of sodium and chloride|Volume contraction|Stimulation of Renin angiotensin|Increased secretion of Aldosterone|Promotes sodium uptake and potassiumexcretion|Hypokalemia -(Polyuria & Nocturia)Increased prostaglandin E|Further activates the reninangiotensin axiso Classic Bartter *s syndrome presents during childhoodo Weakness and cramps occur secondary to hypokalemiaQo Polyuria and nocturia are common due to hypokalemiaQo Nephrocalcinosis (due to hvpercalciuria)Diagnosis of Bartter's Svndrome :o Hypo kalemiaQo Metabolic alkalosisQo Blood pressure is usually normalQo Urinary-potassium, calcium and sodium elevatedQ.o Serum renin, aldosterone and postaglandin E elevatedQ.o Renal function is typically normalQ.There are two types ofBartter syndromeAntenatalClassicBartter syndromeBartter syndromeo More severe o Presents in infancy o Polyhydramnios (associated) o Salt wasting o Severe dehydration Also know,Gitteman's Syndromeo Autosomal recessive traito Caused due to mutation in thiazide sensitive Na-Cl transporterQ.o Loss of activity of the thazide sensitive transporter increases tubular calcium reabsorption leading toclassic finding of hypoclaciuria in Gitleman's syndrome.o There is also decrease in Na+ reabsorptionQ leading to volume depletion and hypokalemia.Gitleman's syndrome is a close differential diagnosis of Barter's syndrome -SimilaritiesDifferenceso Hypokalemiao Hypomagnesemiao Metabolic acidosiso Hypocalciuriao Salt wasting o Elevated renin and aldosterone o Normal blood pressure It is usually diagnosed during adolescence or adulthood with fatigue, weakness, muscle cramps, nocturia.