Key result
Bartter's syndrome involves six interrelated abnormalities driven by complex feedback loops with no single primary cause.
Why the study?
The primary abnormality underlying the six interrelated features of Bartter's syndrome remains uncertain, as each abnormality could be either the proximate cause or a consequence of the others.
This review analyzes the complex feedback loops among the six core physiological abnormalities of Bartter's syndrome, highlighting the inability of current data to pinpoint a single proximate cause.
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Complicates mechanism-based therapy selection in Bartter syndrome; leaves open identification of a primary abnormality for further study.
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.
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Bourke et al. (2008) conducted a review in Bartter's syndrome. Bartter's syndrome involves six interrelated abnormalities that modulate each other via feedback loops, preventing definitive identification of a single primary abnormality.
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