Abstract
In a previous report 1 some of the factors influencing the albumin output through diseased kidneys in chronic nephrosis and in animal experiments were discussed. The present work is a continuation of this investigation, using three patients with chronic nephrosis.
With two of the patients the same sudden rise under high protein diet (130 gm. daily) occurred as in the previous experiments, with immediate fall to the original level upon return to a low protein diet (30 gm. daily). The globulin to albumin ratio in the urine remained approximately constant.
During a period of fever (body temperature about 38.5°) of one of the patients, the urinary proteins increased to a still higher level, and the globulin to albumin ratio also increased, indicating a greater permeability of the kidney. That the kidney was probably damaged was indicated by the slow return of the urinary proteins to their former level, as contrasted with the sudden fall after high protein feeding.
The third patient was a case of myxedenra combined with nephrosis and showed a metabolic rate of −30 at the beginning of the experiment. The induced increase of urinary protein was insignificant as compared with the result in other cases. After a short period on high protein intake, the patient was given thyroid extract daily, whereupon there occurred an immediate large rise in the protein output followed by a gradual decline during the ensuing period. This sudden increased output of protein is interpreted as a confirmation of the theory of Boothby 2 that the body contains part of its protein in the form of storage protein, which, in non-nephritic cases of myxedema is being mobilized by thyroid medication and eliminated as urinary non-protein nitrogen. In the case studied by us, the whole extra nitrogen output following the thyroid medication was in the form of urinary protein.
Get full access to this article
View all access options for this article.