The role of the kidney fixing antibodies (KFAb) in duck nephrotoxic sera (NTS) and of the rabbit antiduck globulin antibodies (anti-DG) was studied in nephrotoxic nephritis of rabbits. 1) The values of KFAb were measured. Six picograms of antibodies fixed per mm² of the glomerular filtration surface were enough to induce renal injury with moderate degree of proteinuria after several days of latent period. The fixed heterologous antibodies act as "sensitizing antigens" of the basement membrane, in which they reacts with the autologous antibodies to the duck globulin. 2) Passive immunization to duck globulin in rabbits, 24 hours after the injection of NTS, could ac-celerate the onset of proteinuria. 3) Isologous anti-DG, passively given 5 weeks after the injection of NTS into nephritic rabbits, sus tamed proteinuria without subsiding tendency. 4) The adjuvant immunization to duck globulin in nephritic rabbits increased the host response to the antigen and induced aggravation of nephritis. 5) It appears from these data that the anti-duck globulin plays an important role in the onset and development of rabbit nephritis induced with duck nephrotoxic sera.

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Thirty-four rabbits were given 20 mg of prednisolone intramuscularly daily and sacrificed at 2, 5, , 11, 24, 42 and 91 days by air-infusion. Kidneys were investigated by histochemistry, immunofluores cent studies and electronmicroscopy. Results were as follows: 1) In glomeruli, fresh exudations, so-called exudative lesions, intracapillary microthrombi and focal capillary dilatations were noticed. Lesions observed at 2 and 5 days were composed of fresh, eosinophilic exudations but lesions from 11 days to 91 days chiefly of eosinophilic, finely granular or fibrillar, exudative ones. Healing processes of those were observed at 42 and 91 days. Incidences of these lesions gradually increased with times of injec-tion. Histochemical studies showed that exudative lesions contained various quantities of fibrin or fib-rinoid, plasma protein, mucopolysaccharide, lipid and hyaline material. 2) Immunofluorescent studies for IgG, beta 1c-globulin, fibrinogen and platelet depositions revealed localizations of those in exudative and other minimal glomerular lesions. The fluorescence of these two were more striking than others generally. 3) When viewed in the electronmicroscope, exudative lesions were found to be composedd principally of an intra-luminal mass of amorphous debris, almost of it posessing a fine-fibrillar quality. The capillary walls surrounding these lesions displayed various changes ; absence of endothelial cells and foot processes, destruction of the basement membrane, and mesangial swelling, etc. In mesangial matrix and epithelial cytoplasm, the electron-dense, fibrillar substances appeared andd communicated with the intraluminal same ones. Conclusions are as follows: 1) Thrombocapillaropathy induced by intracapillary microthrombi of glomeruli is an essential process in the pathogenesis of steroidnephropathy. 2) Gradually increasedd incidences of exudative lesions during observation, and the coexistence of healing processes, so-calledd exudative lesions and fresh exudations in 42 and 91 days-groups suggest that these lesions are formed repeatedly during prednisolone administration.

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The role of the renin-angiotensin system in the pathogenesis of experimental renal hypertension remains still obscure. Until the recent years the renin-angiotensin system had been believed to play a primary role in the initial rise of blood pressure in experimental renal hypertension. Overdosage with sodium retaining corticoids and salt is known to decrease renal renin content and plasma renin activity in dogs. It is therefore interest to investigate whether renal hypertension can develop in DOCA and salt treated animals with hyporeninaemia. The objects of the following experiments was primarily to determine whether right renal constriction and subsequent left nephrectomy produces the same degree of hypertension in renin depleted as in nomal dogs, or not, and secondarily to study the effect of the constriction and nephrectomy on plasma renin activity and sodium balance in DOCA and salt treated dogs. The following results were obtained. 1) Plasma renin activity was within 10 ng/ml/12 hrs. on 3 or 5 days after DOCA and salt overloading (Fig. 3). Significant hypertension was not obtained in DOCA and salt treated dogs throughout the ex-periment. Sodium balance was positive after DOCA and salt overloading. There was 3 or 5 times "escape" phenomenon throughout the experiment. Serum potassium showed gradually lower level (2.7-3.0 mEq/L). 2) After right renal constriction, plasma renin activity and blood pressure were increased temporarily, returned to control level on 7 th day. After left nephrectomy plasma renin activity was increased 2.5-4 times than control level on the next day, gradually returned to control level on 7 th day, and blood pressure was increased by 160 mmHg on 3 or 5 day, and it remained approximately 160 mmHg throughout the experiment (Fig. 4-A, B). 3) Experimental renal hypertension could develop in DOCA and salt treated dogs with hyporeninaemia, but plasma renin activity was not increased higher than the upper limit of control level, and this limited increase of plasma renin activity were maximum on the next day after nephrectomy and gradually returned to control level within one week (Fig. 5-A, B). 4) Degree of experimental renal hypertension in DOCA and salt treated dogs and untreated control dogs did not show significant difference (Fig. 6). 5) The present results raise the following possiblity ; vascular hyperresponsivility to a small amount of endogenous angiotensin in DOCA and salt treated dogs with hyporeninaemia might have develop experi-mental renal hypertension.

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The effects of angiotensin I upon synthesis of aldosterone, corticosterone and cortisol were examined by incubation of beef adrenal tissue slices under the three different conditions. In the first experiment adrenal tissue slices were incubated with 2 and 10μg/g tissue of angiotensin I. Both 2 and 10μg/g tissue of angiotensin I stimulated the synthesis of aldosterone, corticosterone and cortisol significantly. However, during the incubation 70 to 75% of angiotensin I was converted to angiotensin II. In the second experiment 2.6 mM of EDTA and 3.4 mM of 8 hydroxyquinoline were added to prevent the conversion of angiotensin I to angiotensin II. Although the conversion was prevented, EDTA and 8 hydroxyquinoline made adrenal cells inactive to the stimulation of angiotensin I and II. In the third experiment adrenal slices were incubated with angiotensin I for 15 minutes and after then EDTA and 8 hydroxyquinoline were added. Ten ag/g tissue of angiotensin I stimulated aldosterone and corticosterone significantly. During the incubation about 25% of angiotensin I was converted to angiotensin II, but this converted amount of angiotensin II was not effective to stimulate the synthesis of aldosterone and corticosterone. From these results we can conclude that angiotensin I directly stimulates the synthesis of adreriocor-tical steroidogenesis as well as angiotensin II.

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Between January 1951 and November 1971, 323 patients of electrical burns were addmitted to the. Among them only one patient was complicated by acute renal failure.A search of the Japanese literature failed to reveal a report of a similar patient. PATIENT-, a 42 year old man, touched an electric wire carrying 20, 000 volts with both hands while the patient was working near a circuit breaker on. He was taken to a near-by practitioner and transferred to the on the following day. Urinary outputt fell on the second day after the electric injuries. The patient had been on peritoneal dialysis and thenn began on regular hemodialysis. Nineteen days after electric shock, the 24-hour urine output exceeded, 600 ml. but fell again three days later. Paralytic ileus and jaundice developed. He died 26 days fol-lowing electrical burn. Postmortem examination demonstrated acute tubular necrosis, bile peritonitis, gangrenous cholecystitis and pulmonary congestion and edema. The peritoneal irrigation or artificial kidney should be employed early in the treatment of acute renal failure. However, in electrical burns the extensive thrombosis in the venules and patent arterioles cause widespread edema and exudate, which make artificial dialysis more difficult and are likely to necessitate the use of balance-bed. We agreed that early excision of electrical burn injury might be preferable and secondary bleeding from the devitalized tissue should be watched.

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