On the basis of ten cases of poisoned kidnies due to organic phosphorous pathologic study has been attempted. For confirming the organic poisoning activity of cholinesterase in the blood serum was examined with modified method of Michel. All cases revealed to be positive. These are deviled into three groups according to the life span calculated from the time of poison swallowing to the death. While the early group (a few hours of life span) showed marked vasodilation in the kidney, the middle and late group (several to over ten hours of life span) revealed more or less circulation disturbance which is characterised by pronouncing juxtamedullary circulation in sacrifying the subcapsular one. Also was noticed epithelial degeneration mainly of the proximal tubule running parallel to the deviation of the intrarenal circulation. The conclusion can, therefore, be drawn that the pathologic changes of the kidney encountered consist of parenchymatous attack as well as of the circulation disturbance within the kidney.

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It has been said that prognosis of acute glomerulonephritis is different between adult and child, and that the former cases are apt to progress into the chronic stage more frequently than the latter. Adult cases, however, seem to include those of acute aggravation progressed from chronic glomerulonephritis. On the basis of renal biopsies and clinical findings the authors made the compara tive study on the prognosis of seemingly initial attack of acute glomerulonephritis in adults (over 15 years of age) and in children (under 15 years of age)The conclusions are as follows :1) No difference was noticed between 48 adult cases and 58 child cases in this series of healing, remission and chronic process.2) In adults the frequency and duration of hypertension were observed more often than in children, while those of hematuria were revealed more seldom.3) In child patients, increase of non-protein nitrogen and decrease of A/G ratio in serum protein were frequently found as compared with adult patients.

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In order to study the progress of chronic glomerulonephritis, the end-results of the treatment of 95 patients with chronic glomerulonephritis among the 239 patients with renal disease hospitalized at our clinic during the past 12 years were investigated and then the patients were examined. The group in which the preceding infection was unknown had poor results of the attack of the disease than the group in which there was a definite preceding infection. Patients who had had hyper-tension and hematuria clinically had poorer results. Of all the laboratory findings, renal clearance values and biopsy findings proved useful in prognostication. Then attempt were made to determine the factors involved in the exacerbation of nephritis. Those who had not followed physician's instruction or those who had had an increased tendency to upper respiratory infection had poor results. There were those in whom exacerbation could not be accounted for. It was thought that the production of autoantibodies in patients' bodies might be a factor in the exacerbation. So direct and indirect Coombs' tests were carried out to detect autoantibodies in the samples of sera of patients with chronic nephritis. They were all negative, Then a method for antigloburin consumption test was developed to detect a minute amount of incomplete antibodies. By this method, it was proved that there was a considerably high incidence of the production of incomlete antibodies in the above sample of sera. Moreover, these antibodies were absorbed by the renal tissue. This shows that these antibodies are the autoantibodies produced with the renal tissue as antigens. It was shown that during the phase of acute exacerbation the antigen-antibody reaction in the kidney became so vigorous that autoantibodies were consumed, with the result that the autoantibodies in the blood were reduced in number or disappeared. Patients who were positive for antiglobulin consumption test had poor results. In order to see how much the kidney are damaged by the antigen-antibody reaction there, a method of DPI reaction test was developed and performed on patients. This method is based on the discoloration of pigments by the reducing process brought about by cell respiration in the organs. Using this method, it was proved that autoantibodies damaged only the kidney through their reaction with antigens. It was shown in the present experiments that the autoantibodies detected by the author are a factor in the exacerbation of chronic nephritis.

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1) For the purpose of exploration of the renal Lymphatics 49 rabbits were available either in the normal or in the hydronephrotic and pyelonephrotic states. The method employed consists of injection of SKY BLUE dye into either directly cortical subcapsular tissue or in the pelvic soft tissue with coincidental application of ligation of main lymphatic channels. Observation was continued from 12 hours to 40 days. Direct implantation of Proteus bacilli in appropriate amount was performed for producing pyelonephritis. Following conclusions can be drawn: a. Cortical lymphatics is observed subcapsular and periglomerular spaces with communication to the peritubular regions along the interlubular arteries in irregular arrangement. No positive finding is gained within the glomerulus. Emphasis is placed at the corticomedullary junction where dilated lymphatics filled with SKY BLUE are prominent. Small lymphatics running through the medulla is eminent along the tubules particulary along the vasa recta. Marked dilatation of lymphatics can be seen at the fornix closely attached the pelvic mucosa. b. The lymphatics show marked dilatation at the corticomedullary junction and the renal medulla lnspite of collaps of lymphatics in the cortex. The inflammatory infiltrate initiates at the fornix of the calyces extending through the medulla as well as almost simultaneus initiation at the subcapsular area. c. The renal lymphatics is thought to play an important role in the water reabsorption and reabsorption of some electrolytes, particulary in form of interstitial edema. d. The dilatation of the lymphatics at the hydronephrosis is considered mainly due to exaggarated pyelonephritic or tubulolymphatic blackflow which may in the normal state serve as a shunt for lymphdrainage. e. The inflammatory infiltrate of ascending pyelonphritis extends rather rapidly to the subcapsular legion of the renal cortex with gradual subsequent speading throughout.

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Since it has been clarified that acridone was metabolized to 2-OH-acridone in the kidneys, it can be presumed that renal impairment is accompanied by a decrease in the activity of acridonehydroxylase involved in the metabolism and by marked changes in the urinary excretion of 2-OH-acridone. On the basis of experiments designed to establish the relationship between acridone metabolism and renal function, the present author arrived at the following conclusions: 1) Acridone was administered to nephrectomized rabbits, and their organs and intestinal contents were examined for its metabolic products, but 2-OH-acridone was never perceived. Therefore it was confirmed that the formation of acridone to 2-OH-acridone by metabolism occurred in the kidneys alone. 2) The urinary excretion of acridone and 2-OH-acridone in rabbits given acridone by the intravenous route came to end in a short time. 3) Intravenous injection of acridone had no effects on the P. S. P.-excreting capacity of rabbits. 4) Acridone was administered to rabbits with experimental renal impairment due to various kidney-impairing agents, and the excretion of acridone and 2-OH-acridone in their 24-hour urine collections was determined. When compared with healthy rabbits, it is evident that there was a highly significant decrease in the amount of 2-OH-acridone. Speaking of experimental renal impairment, its extent cannot be expressed in numerical terms and therefore no detailed information is available regarding the extent. However, the foregoing results were observed to a particularly remarkable extent in rabbits with severe disturbance of the vascular system and proximal renal tubules. 5) Healthy male subjects were given acridone by mouth and their 24-hour urine collections were examined for its metabolic products. Quite similarly to rabbits, glucuronides and sulfides of 2-OH-acridone and acridone were detected in untreated urine and 2-OH-acridone and acridone in hydrolyzed urine. Accordingly, acridone metabolism was the same in man and rabbits. These metabolic products were completely excreted in the urine within 24 hours. From the above-mentioned results it can be postulated that the calculation of the concentration ratio between acridone and 2-OH-acridone in 24-hour acridone urine permits clinical testing for renal impairment.

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