Bartter's syndrome - a dilemma of cause and effect.
Six interrelated abnormalities of Bartter's syndrome are analyzed-juxtaglomerular hyperplasia, angiotensin resistance, altered kallikrein-kinin system, hyperprostaglandinuria, hypokalemia, and chloride-losing nephropathy. Arguments are advanced that any one of these could be the proximate cause and result in all the others. By the same token, each abnormality could be a consequence of any of the others and, furthermore, modulate the others by negative or positive feedback. Despite many recent insights, available data do not permit a definitive conclusion as to the locus of the primary abnormality. Rather, the syndrome presents as a remarkable biological counterpart to an electronic integrated circuit. The altered physiology of Bartter's syndrome is reviewed and the pathogenesis of the syndrome analyzed in the light of recent literature.
D000804:Angiotensin II / Q000037:antagonists & inhibitors / Q000502:physiology; D001477:Bartter Syndrome / Q000150:complications / Q000209:etiology* / Q000378:metabolism; D006801:Humans; D006929:Hyperaldosteronism / Q000209:etiology*; D006965:Hyperplasia / Q000473:pathology; D007008:Hypokalemia / Q000209:etiology; D007606:Juxtaglomerular Apparatus / Q000473:pathology; D007610:Kallikreins / Q000502:physiology; D007705:Kinins / Q000502:physiology; D009399:Nephrons / Q000378:metabolism; D011453:Prostaglandins / Q000502:physiology; D012965:Sodium Chloride / Q000378:metabolism
D007705:Kinins; D011453:Prostaglandins; D000804:Angiotensin II; D012965:Sodium Chloride; D007610:Kallikreins