Bartter Syndrome

Question: What is the life expectancy for someone who is 40, with Bartter's Syndrome, and never got treatment for it? until soon? The person is starting to have kidney stones.

Answer: I have no idea, but I can promise the life expectancy will be a lot shorter if this person doesn't get that checked out. It's better to put out a small fire before it becomes a big fire.

Question: does anybody have a rare kidney problem called bartter syndrome i was just looking to chat with someone with

Answer: i dont know what that is but if u need to talk to some 1 my e mail fernandodefino@yahoo.com

Question: clinically,Gitemans,s syndrome is distinguished from bartter,s by? 1hypomagnesemia and hypocalciuria 2hypermagnesemia and hypocalciuria 3hypomagnesemia and hypercalciuria 4hypermagnesemia and hypercalciuria

Answer: GITELMANS syndrome, is diagnosed as an accident, in young people with mild hipokalemia, hypomagnesemia, hypocalcyuria, metabolic alkalosis, and normal or low blood pressure. (calcium urinary elimination or Sulkovitch test is generally normal) It is due to the mutation of the gene that controls the absorption of sodium chloride in the sodium chloride cotransported in the DISTAL convoluted tube... It mimicks tha abuse of high loop diuretics... Bartters syndrome is a more severe one...(due to deffects in the sodium transportation in the ascending loop of henle)detected from birth, following mental retardation and nephrocalcinosis..., and urinary calcium is normal or high...there is mild hypokalemia, and typically, there is no HYPERTENSION, and magnesium in blood and urine, is typically NORMAL, as it happens in Alports and Conns syndromes ( Hypertension with Hypokalemia with alkalosis)

Question: Differentiate Bartter syndrome form Gitelman syndrome...? especially antenatally...Thank you so much for your help...

Answer: Bartter: due to mutation of sodium transport proteins in kidney, causing low potassium, chloride and alkalosis, with low blood pressure despite high levels of hormones (renin, aldosterone) which would normally raise blood pressure. Gitelman: variant of Bartter with low magnesium and low urine calcium CLINICAL FEATURES The antenatal form of Bartter syndrome is a life-threatening disorder in which both renal tubular hypokalemic alkalosis and profound systemic symptoms are manifest (Seyberth et al., 1985; Deschenes et al., 1993; and Proesmans et al., 1985). The abnormalities begin in utero with marked fetal polyuria that leads to polyhydramnios between 24 and 30 weeks of gestation and, typically, premature delivery (Ohlsson et al., 1984). The amniotic fluid contains high chloride levels but normal concentrations of sodium, potassium, calcium, and prostaglandin E2. Affected neonates have severe salt wasting and hyposthenuria, moderate hypokalemic metabolic alkalosis, hyperprostaglandinuria, and failure to thrive. The International Collaborative Study Group for Bartter-like Syndromes (1997) noted that an essential manifestation of the antenatal variant is marked hypercalciuria, and as a secondary consequence, affected infants develop nephrocalcinosis and osteopenia. Fever, vomiting, and occasional diarrhea associated with the disorder have been attributed to the stimulation of renal and systemic prostaglandin E2 activity in affected infants; these symptoms are effectively treated with inhibitors of prostaglandin synthesis. Based on these clinical features, the antenatal form of Bartter syndrome has been referred to as the hyperprostaglandin E syndrome (Seyberth et al., 1987).