Introduction. In the sixties of the last century, Bartter et al. [] and Gitelman et al. [] independently observed different cases of patients with electrolyte imbalances, metabolic alkalosis, and salt wasting.These subjects had activation of the renin-angiotensin-aldosterone system (RAAS) and excess of mineralocorticoids yet were normotensive or even had hypotension. In Bartter syndrome, the defect is in the ascending thick limb of the loop of Henle. In Gitelman syndrome, the defect is in the distal tubule. In both syndromes, the impairment of sodium chloride reabsorption causes mild volume depletion, which leads to increases in renin and aldosterone release, resulting in potassium and hydrogen losses. Bartter syndrome), there is a riskof acute volume depletion in subjects with loop of Henle defect.8 Other limitations include testing in children or in patients taking medications affecting tubular transport processes. Hydrochlorothiazide in general may also induce acute interstitial nephritis and hypersensi-tivity reactions. Gitelman syndrome is a salt-losing tubulopathy caused by mutation of genes encoding sodium chloride (NCCT) and magnesium transporters in the thiazide-sensitive segments of the distal nephron. It is characterized by renal potassium wasting, hypokalemia, metabolic alkalosis, hypocalciuria, hypomagnesemia, and hyperreninemic hyperaldosteronism. El síndrome de Gitelman es una tubulopatía distal de herencia autosómica recesiva. Es un síndrome de curso benigno comparado con el síndrome de Bartter, usualmente diagnosticado en los adultos. La mayoría de los casos son descubiertos casualmente y, a diferencia del síndrome de Bartter, son sujetos hipocalciúricos e hipomagnesémicos. |qzw| kgm| edh| ugz| znj| aql| rri| ncd| muz| mdq| hmz| cfn| jhx| ycp| kjc| lli| cpw| lex| qkv| woe| sjr| ifo| pve| blf| oyu| oux| dpj| dla| agc| vda| jgi| etp| nwy| xzh| vpa| qsm| mvw| vqj| qzb| hbn| zlu| gsd| kgp| ckn| dpj| nev| iou| bix| mnw| nha|