| Abstrakt: |
POTASSIUM Early workers in the study of blood potassium in nephritis, Blumenfeldt1 and, shortly afterward, Smillie,2 reported increases of this ion in the blood. The latter considered potassium retention accountable for the development of uremic symptoms. He based this assumption on the observation that in normal persons doses of potassium chloride are nontoxic, but in nephritic subjects these salts, while still readily absorbed, are poorly excreted and toxic symptoms develop. Later workers, Myers and Short,3 Loeb, Atchley and Palmer,4 Denis and Hobson,5 Wilkins and Kramer,6 all report the blood potassium in nephritis as being practically constant at the normal level. Such exceptions to normality as these reports contain are almost insignificant in degree, and might readily be attributed to extraneous factors such as secondary anemia, when the cells, which contain the greater part of the potassium, are reduced in volume. Denis7 was unable |
