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J. M. HAYMAN Jr., M.D.; J. A. BENDER, M.D.
Arch Intern Med (Chic). 1933;51(3):447-451. doi:10.1001/archinte.1933.00150220122009.
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Since the time of Bright, albuminuria has commonly been associated with disease of the kidneys. More recently the distinction has been made between non-nephritic and nephritic albuminuria. The former is most readily attributed to a transient and reversible increase in permeability of the glomerular membrane from partial asphyxia brought about by circulatory changes.1 From time to time, however, the suggestion has been made that nephritic albuminuria is the result of changes in the plasma proteins rather than any change in or damage to the kidney itself. Epstein2 saw in the albuminuria of nephrosis a disturbance of plasma protein formation; Kollert and Starlinger3 an increased tissue destruction leading to increase in fibrinogen; and Munk and his associates,4 an abnormality in the physicochemical state of the plasma colloids. The conception of extrarenal albuminuria is supported by the appearance of foreign proteins, such as egg albumin, in the urine


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