腎性浮腫疾患における電解質代謝

抄録

Taking up acute nephritis and the nephrotic syndrome as the edema of renal origin, the abnormalities of the electrolyte, metabolism in these were researched. Because of having being unsettled the results about them as yet, the electrolyte metabolism in these were observed on the clinical data & then on the experimental data. As the cause for edema in acute nephritis, the capillary permeability by the antigen antibody reaction has much weight, the other hand, in the nephrotic syndrome, the hypoosmolality by hypoproteinemia. For these reasons, the electroly-te metabolism in anaphylaxy & plasmapheresis were observed. 1) The clinical data about acute nephritis was as follows. The decrease in total serumprotein & albumin fraction were comparatively slight. When the renal in-sufficiency was severe, the plasma k concentration was increased during the oliguric phase and then became low at the wend of the polyuric phase. But if the reneal isuff'iciency was relatively slight, it was in-creased after the onset of diuresis. The plasma Na & C1 concentration were high during the oliguric phase, became low at the end of the polyuric phase & then recover, d the normal value. The plama Ca concentration were low during the oliguric phase & then became normal after the onset of diuresis. The urinary excretion of Na & C1 had the peak of that during the polyuric phase and the peak of K excretion was always several days later. The peak of 17 ketosteroid excretion coincided mostly with that of K, which speaks the adreno-cortical hormone take part in these changes. 2) The early change of dogs in anaphylactic shock was mainly due to the liver congestion. When the severity of shock was slight, dogs relatively lived long & the capillary permiability was prominent. This time, the Hematocrit value was high, the total serum protein was decreased, the plasma Na & Cl concentration were elevated and the plasma K concentration was decreased. 3) Acute nephritis was induced in dogs by the antikidney serum. The change of electrolyte metabolism was similar to that in men. The early change of it was almost equal to the change in anaphylactic dogs which relatively lived long. 4) The clinical data about the nephrotic syndrome was as follows. The plasma Na concentration was decreased, which seems to be inversely interdepenent to the total serum cholesterol. Hypoproteinemia was attended mostly by the higher plasma C1 concenration. When the renal damage was severe, the plasma K concentration was elevated. During diuresis following the steroid therapy, the plasma K & C1 concntration became low, but Na concentration high. Comparing the ACTH the rapy with the Prednisolone therapy, the former had the inclination of keeping water & Na in the body before diuresis. 5) Hypoproteinemia was induced in dogs by plasmapheresis. The total serum protein & the albumin fraction were depressed much, neverthless, the total serum cholesterol wsa not so increased. They had no edema & no oliguric phase in spite of hypoproteinemia. The plasma Na concentration was slightly increased, but C1 & K concentration moderately decreased. 6) The experimental nephrotic syndrome was induced in rats by aminonucleoside. Hyperlipemia was observed, but the plasma electrolyte concentration had little change. The electrolyte contents of edematous tissues were as follows. The liver has little change. The Na & Cl content were increased in the muscle as well as in the kidney, but K content decreased in the former as it was increased in the latter. Considered as the carcass, total body Na & C1 appeared to be increased with water, but this tendency keep back by the NaCI defecit diet. The Ascitic fluid had the lower concentration than the plasma in Na, K & Cl concentration, bnt as to the Cl concentration, often became higher.