Studies on the Rendl Changes induced by the Administration of Glucocorticold

1) Histological study of the renal tissues was performed on the autopsy cases, consisting of a Cushing's Syndrome, 13 of acute and chronic leukemia, and a malignant lymphoma in which considerable amounts of glucocorticoid was administered clinically. Besides the capsular drops in some of the glomeluli, fatty deposition was a prominent feature. Fat is stained as Sudan III positive granules and first appears in the viscinity of the basement membranes of the proximal tubuli, which, with increase in degree, spreads to the distal portions with concomitant increase in size and number. Study on the cause of this fat deposition suggested that the administration of glucocorticoid seemed to play a role rather than anoxia due to anemia. 2) In the experimental study of the fat deposition, 1.5 mg, 2.5 mg and 5.0 mg of prednisolone acetate was administerd daily, subcuteneousely, to the Wistar male rats, weighing 100 g, which were sacrificed on the 28 th 14 th, and 10 th day, respectively. In the animals, to which more than 2.5 mg of the glucocorticoid was given, exsudative lesions in some of the glomeluli, and prominent fatty deposition were observed in the tubuli ; a similar finding to that in human. Biochemical examination on the blood revealed a correlation between serum lipids (total cholesterol, FFA and trigricerides) and histological findings. 3) Measurement of lipid fraction in the renal tissues revealed a prominent increase of trigricerides, corresponding well with histological observation. 4) With a purpose of investigating this trigricerides accumulation, incorporation of 14c to renal lipids from glucose-U-14c, acetate-1-14^c palmitic-acid-1-14^c was studied in viva and in vitro. These experiments suggested that abundant supply FFA from the circulation, rather than the meta-bolic derangement of renal tubular cell, is the cause of the fatty accumulation. The investigation of HMP shunt, using gluose-1-14c and glucse-u-14c neither showed its predominace over the control groups. Dibenamine (2.5mg/100g I.P, mi.) was administred to the prednsolone treated rats in order to block FFA release from the adipose tissue. The result was a marked decrease of trigricerides in the renal tissue in proportion with that of serum FFA. This was confirmed by the absence of tubular fatty deposition in the histological study. It is therefore concluded that the renal tubular fatty deposition, induced by glucocorticid administration, is caused by the triglycerides accumulation which is mainly ascribed to the abundant supply of FFA from the circulation.