Although the incidence of corrosive esophagitis due to various corrosive chemicals is on the decrease since 1950 accidental ingestion of such chemicals among young infants is still quite common. There had been numbers of investigations and reports on the corrosive esophagitis caused by lye but these reports were mainly dealed with the clinical aspects on the esophagus itself. Furthermore, carefully followed experimental studies on the corrosive esophagitis had been really few and the aspect of general effects had been neglected. It is the purpose of this paper to investigate the aspect of general effects produced by ingestion of acetic acid which is the most commonly responsible chemicals for the corrosive esophagitis. Corrosive esophagitis was produced with the acetic acid on the rabbits and the histopathologic changes in the kidney were carefully followed. The finding in the kidney begins from the first day after the ingestion of acetic acid. These changes are characterized by congestion and dilatation of blood vessels, including capillaries of glomeruli. It is accompanied by necrosis of tubular epithelium in the medulla. The changes become progressively severe and reach its maximum at the end of the 7th day. The congestion and edema of small and medium-sized vessels as well as glomerular capillaries begin to improve at the end the 4th week. The regenerative acitivity in the medulla is evident all throughout this period and the changes in general are somewhat less than that of the cortex. Scattered mixtures of regenerated tubules and the edematous degenerated tubules can be observed around this tissues. At the end of the 5th week these various changes more or less subside completely from the cortex and there is a proliferation of fibrous connective tissue including newly formed capillaries in the medulla. Although there is a good deal of morphologic evidence of improvement, the improvement by no means is complete even at the end of the 5th week. From above observations, it is shown that absorbed acetic acid begin to cause slight damage to the kidney even from the first day and reach its maximum at the 7th day. From approximately 10th day to the end of the 4th week, the nephrotic changes of the kidney continues probably due to excretion of degenerated products of proteins from other organs (and of kidney itself). It is also found that the changes do not improve completely even at the end of the 5th week.