Abstract
Investigation of the action of phloridzin in Bright's disease has a theoretical as well as a practical interest. The mechanism of kidney diabetes is as yet imperfectly understood. The original idea that it was due to a change in the permeability of the kidney epithelium has gradually lost support, and instead there is a growing belief in the hypothesis that, in kidney diabetes, the sugar owes its origin to an exaggerated katabolic condition of the kidney.
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