作者: Andrew Whelton
DOI: 10.1161/HYPERTENSIONAHA.112.198341
关键词:
摘要: See related article, pp 1148–1156 Rarely in clinical medicine is it possible to define a distinct laboratory abnormality associated, for unknown reasons, with specific disease entity and have one group of tenacious investigators resolve the conundrum contributing mechanisms. Nonetheless, this issue Hypertension such case as presented investigations Soletsky Feig.1 These now contributed decade or more animal human investigation by Feig Johnson their coworkers unraveling major mechanism that links hyperuricemia hypertension. This has been long-standing basic science quest.2 Gout, long-term manifestation hyperuricemia, metabolic process known from antiquity. Egyptian physicians described some 5000 years ago followed astute characterization disease, fifth century BC, Greek physician Hippocrates, “the unwalkable disease.”3 By mid-1800s AD Sir Alfred Baring Garod identified uric acid was cause gout not consequence disease. In addition, also coincided time framework which several speculated on linkage presence However, until contemporary studies colleagues we learned that, models, acute elevation serum urate induces prompt blood pressure chronic sustains abnormal irreversible vascular glomerular changes lead form salt-sensitive hypertension.4,5 Hence, lesson suggested humans, early treatment reduce associated increases might be successful, whereas attendant emergence …