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January 1928


Arch Intern Med (Chic). 1928;41(1):10-17. doi:10.1001/archinte.1928.00130130013002

It has long been an established clinical fact that diuresis may be produced by the administration of alkalis.1 M. Fischer emphasized the theoretical consideration that accumulation of water in tissues was due to an increased tissue acidity.2 For some time therapy in nephritis and in albuminurias has been directed toward alkalinization of the urine. Post and Thomas3 claimed decidedly beneficial results with this therapy in orthostatic albuminuria. A thorough review of this literature is unnecessary. It suffices to emphasize that in certain edematous states therapy with alkalis of various sorts has yielded a diuresis, but in certain cases has caused a dangerous exacerbation of the edema.

With the development of more accurate methods of study of the hydrogen ion concentration of the blood, and of the status of the alkali reserve in the presence of an acidosis, it has further been demonstrated that a diminished reserve of the fixed bases

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