腎不全時の尿中ならびに血中 glucocorticoid の変動に関する臨床的研究 第1編: 急性腎不全時における血中 glucocorticoid の変動について,ことに侵襲の立場からみた血中 cortisol レベルならびに血球内Na,Kの変化について

Abstract

Adrenocortical function was studied on 25 cases of acute renal failure. 1) Plasma cortisol level before hemodialysis or peritoneal lavage was 38.35±4.48 pg/dl (normal value: 14.33±2.36µg/dl, p<0.001) and plasma corticosterone level was 5.00± 0.89µg/dl (normal value: 3.22±0.84µg/dl, p<0.01). Both levels were, therefore, significantly elevated. None of the patients showed normal pattern of diurnal change of plasma cortisol in which it is high in morning and low in evening. Percent relative change between 9.00 a.m. and 9.00 p.m. was +5.3% (normally -57.9% in average). 2) The high plasma cortisol level is probably, as in chronic renal failure, attributable to decrease of urinary excretion of 17-OHCS due to impaired renal function and simultaneous increase of the plasma conjugated 17- OHCS. Besides, in acute renal failure, stress such as surgery or trauma might have stimulated hypothalamo-pituitary-adrenocortical system promoting cortisol excretion from the adrenal. Disturbance of the diurnal rhythmic change in these patients may be explained by activity of ACTH-releasing system not controled by feedback regulation. 3) The patients in diuretic phase with almost normal blood chemistry, after passing oligoanuric phase through dialysis treatment, showed decrease of plasma cortisol level but not to the normal range. At this time, some diurnal difference began to appear (% relative change: -21.0%) but not so remarkable. Renal functional recovery in diuretic phase did not necessarily correlate with urinary 17-0HCS excretion. The further improved renal function of creatinine clearance over 10 ml/min somewhat coincided with lowering of the plasma cortisol level, but they did not correlate well. This is reasonable because renal clearance of plasma cortisol is extremely low. It is conjectured that the lowering of plasma cortisol is secondary to the return of ACTH excretion to the original resting state under normal feedback mechanism as well as to the accelerated conversion of the free form of 17-OHCS to the conjugated form. 4) In acute renal failure before treatment, blood cell sodium was 34.66±6.76mEq/L (normal value: 21.22±4.53 mEq/L), blood cell potassium was 68.61±9.66mEq/L (normal value: 84.88±7.20mEq/L). This increase or decrease was significant (p<0.01), but did not correlate with BUN or serum creatinine level. The plasma cortisol correlated, however, with blood cell sodium (r=0.75), potassium (r=-0.64), potassium/sodium ratio (r= -0.74) and extracellular/intracellular sodium ratio (r=-0.77). It did not correlate well with intracellular/extracellular potassium ratio (r= -0.21). The elevated plasma cortisol level might have acted toward inflow of sodium into the cell and outflow of potassium from the cells, but these changes of both cations seemed to proceed not synchronously. 5) There was no definite pattern of the plasma cortisol change during hemodialysis. The plasma cortisol kept high level and even elevated during dialysis with Kolff type artificial kidney probably because of stressful extracorporeal circulation. Two hours after dialysis wth Kiil type artificial kidney, the cortisol level lowered to some extent but not to the normal range (below 20µg/dl). Pre-and postdialysis value of the plasma cortisol was 33.2 and 37.5 pg/dl in Kolff type, while 37.84 and 32.4 pg/dl in Kiil type with slightly significant decrease (0.05<p<0.1). In vitro experiment, there was almost no cortisol movement beyond the dialysis membrane under concentration of the plasma level in acute renal failure. Intracellular sodium decreased through dialysis (from 34.6 to 27.7mEq/L in Kolff type and 49.8 to 41.1mEq/1 in Kiil type), and intracellular potassium increased significantly in Kolff type (from 70.4 to 78.5 mEq/l) but slightly in Kiil type (from 71.0 to 73.2mEq/I). These findings, however, could not be related to the plasma cortisol changes.