It is now a well-known and generally recognized fact that acidosis may occur in the course of nephritis, particularly in the terminal stages. Among the evidences of acidosis are a diminished carbon dioxid tension of the alveolar air, an increased hydrogen ion concentration of the blood or serum, a diminution of the alkali reserve and of the oxygen combining power of the hemoglobin.
It is not yet clear on what this acidosis depends. It is surely not due to an accumulation of the acetone bodies, for they do not appear in the urine nor are they increased in the blood. It has been suggested that lactic acid may be responsible for the acidosis. The studies of Lewis, Ryffell and others1 have shown that lactic acid is not increased in the blood in sufficient amount to account for the acidosis. There is no direct evidence nor, so far as