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Arch Intern Med (Chic). 1926;38(2):259-275. doi:10.1001/archinte.1926.00120260117010.
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Nearly a century has elapsed since Richard Bright made his celebrated "statements and conjectures regarding the dependence of a peculiar class of Dropsies on disease and irritation of the Kidneys."1 Since then numerous additions have been made to our knowledge of the symptomatology of Bright's disease, the most significant, perhaps, being arterial hypertension, albuminuric retinitis, and the so-called uremic phenomena largely involving the central nervous system. The systemic manifestations of kidney disease are so variegated, and their association with one another so inconstant, that it was early realized they could not all be due to the same pathogenetic factor. In attempts to explain the connection between the kidney lesions and the associated systemic phenomena, two main paths have been pursued:

1. The study of extrarenal factors. This dates back to the classic investigations of Gull and Sutton2 on cardiac hypertrophy and Cohnheim and Lichtheim3 on edema. In the case of


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