Changes of plasma renin activity (PRA), blood pressure and heart rate were observed for 2 hours of physical exercise loaded on normal subjects. The PRA was significantly decreased in comparison with the basal value both 1 and 3 minutes after the initiation of the exercise, but returned to the basal value 5 minutes after the initiation of the exercise followed by a significant elevation from 30 minutes to the end of the exercise. The mean blood pressure was elevated significantly 1 minute after the initiation of the exercise and remained elevated throughout the period of exercise.
In order to clarify causes of the above-mentioned transient decrease in PRA observed immediately after the initiation of the exercise, the same experiment was performed in patients with hyperthyroidism, who were considered to be sympaticotonic, with or without the pretreatment of propranolol. The PRA in the patients with hyperthyroidism remained unchanged for initial 1 minute after the onset of the exercise, but a rapid elevation observed 3 minutes after the initiation of the exercise lasted throughout the experiment. Little alterations were observed both 1 and 3 minutes after the initiation of the exercise in the patients with hyperthyroidism pretreated by propranoloh.
The PRA of the renal venous blood (RPRA) in dogs whose blood pressure in renal arteries was lowered by constricting the abdominal aorta just above the branching portion of the renal arteries showed 3-fold increase compared to the control value. The RPRA was decreased transi-ently at 30 seconds, then increased slightly one minute after the release of the constriction, and returned gradually to the control value afterwards. These results may suggest that a transient decrease in PRA immediately after the initiation of the exercise in normal subjects is resulted from the sympathicGtonia that has been brougnt about just after the exercise, and is related to the concomitant rapid elevation of blood pressure.

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Twentyfour patients with various forms of renal diseases were treated with urokinase (U.K.). Of these patients, twelve had chronic glomerulonephritis (G.N.), three had membranoproliferative G. N., two had rapidly progressive G. N., one had membranous nephropathy and six had chronic renal failure. Daily dosis of U.K. was 6000 internatinal units. Laboratory data listed below were compared before and after U.K. treatment; urinary output (U.V.), urinary protein (U-P), urinary erythrocyte (U-RBC), blood pressure (B.P.), blood urea nitrogen (BUN), serum creatinine (Scr), creatinine clearance (Ccr), fibrin/fibrinogen degradation products in urine and in blood (U-FDP, B-FDP) and serial renal biopsies. These patients divided into two groups depend on effectiveness of U.K. treatment. Ten of these were responded well, however others were not. In regard to t.ne clinical course, rapid progression or acute exacerbation was found just before treatment in all cases of effective group (Group I) as compared with five cases of not effective group (Group II). The mean period from rapid progression or acute exacerbation to start the therapy was 2.6±1. 3 months (M.) in Group I and 6.3±1.6 M. in another. All patients in Group I had histologicaly marked proliferation, crescents formation and less frequently fibrin thorombi. Immunof luorescent study of these revealed deposition of fibrin/fibrinogen and positive immunoglobulins and complements. In Group I, the administration of U.K. was associated with statistically significant improvement of U.V., U-RBC, BUN, Ccr and B-FDP and remarkably improvement of B.P., Scr, U-FDP and serial renal biopsy findings. But U-P was increased except three cases in Group I.
The indication of fibrinolytic therapy with U.K. was thought to be as follows ; 1) rapid progression or acute exacerbation in clinical course, 2) rapid deteriolation of renal function, rapid increase of BUN, B.P. and U-RBC and continuous abnormality of U-FDP in laboratory examination and 3) diffuse prolif erative G. N. with crescents formation and/or fibrin thorombi and glomerular deposition of fibrin or fibrinoid material in renal biopsy findings. The time of start to therapy was thought to be suitable within three M. from acute exacerbation or rapid progression. The criteria of effect was able to be judged as follows ; 1) serial renal biopsy findings and serial renal function tests in absolute condition, 2) Scr, U-RBC and B.P. in relative condition and 3) BUN, U.V., U-P and U-FDP in additional condition. According to the criteria, all the patients of Group I are possible to be judged effectively and all of Group II to be judged not effectively. The fibrinolytic therapy is effectively as same as anticoagulant therapy in G.N., if the patient will be selected well.

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For the purpose of elucidating the uric acid metabolism of rats, a kinetic study was made using ₁₅N-labelled uric acid. The male Sprague Dowley (230g) rats were used in which uricase activity was inhibited by administering potassium oxonate. Then the uric acid metabolism was confirmed to be in steady state under this enzyme inhibition,
Within 20 hours after intravenous injection of 1.0mg labelled uric acid, atom % excess of ₁₅N of plasma uric acid was determined at several time intervals,
Thus a disappearance curve was obtained and expressed as sum of two exponential curves; Q(t)=4.40e_-0.729t+0.91e_-0.077t from which equation, it was revealed that two compartment model could be applied for the uric acid metabolism.
Also from this equation, the daily synthesis, pool size, turnover rate and metabolic clearance rate of uric acid in rats, were calculated as 18.3 mg/day, 165.5 mg, 0.077 and 3.99%/hr, respectively.

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Infection of urinary tract in early period after renal transplantation is observed relatively often and is responsive usually to medical tretment. Sometimes, it causes depression of the graft function or sepsis.
Therefore, we should make every effort on its prevention. From March. 1975, we proposed to prevent it. We changed urinary drainage method from open system to closed system within 3 days on postoperative course. Furthermore, the irrigation of urethra and bladder before and after catheterization with 0.05% gluconate hibiten solution was added.
In our series the incidence of early infection of urinary tract after renal transplantation had been reduced from 43% (3 out of 7 transplants) in old open system to 0% (9 transplants) in closed system within 3 days postoperatively.
In our series, 33 patients received 34 renal allografts from 33 living related donors and one cadaver donor between July. 1970 and December. 1976. We reviewed 9 cases of the early infection of urinary tract after renal transplantation.
Incidence of the infection were higher in transplants which were drained by urethral catheter over 4 days and those with the urologioal complication.
The infection in the cases with the urological complication had a tendency to become chronic.
The infection occured almost within 2 weeks after transplantation.
The infection had no relation with the urine volume during the drainage.
Pseudomonas was the most frequent pathogen in the infections.

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Peripheral nerve dysfunction is one of the most common symptoms in uremia and its degree has been in use as an indicator of well-being in regular dialysis treatment patients. In search of a preciser approach to the identification and the management of uremic neuropathy, the Heckmann's technique for the measurement of nerve excitability has been used to study patients with chronic renal failure. Degree of peripheral nerve dysfunction was determined on the basis of hypoexcitability. Experimental materials were 23 patients with chronic renal failure; 21 untreated patients whose creatinine clearance were under 50 ml/min (A-group), 2 patients with conservative treatment whose creatinine clearance were under 10 ml/min (B-group). In A-group, ulnar nerve excitability (UNE) of patients over 20 ml/min of creatinine clearance was normal and they showed little symptoms of uremia. In the patients under 20 ml/min, UNE decreased and they definitely showed uremic symptoms. Moreover, in the patients under 10 ml/min, dialysis treatment was almost always necessary, since the UNE and uremic symptoms were not improved with conservative treatment. On the other hand, in the patients under 10 ml/min of creatinine clearance in B-group who had been doing favorably with conservative treatment, did not show hypoexcitability or uremic symptoms. From these data on UNE, it can be concluded that a relationship exists between the lowering of UNE and residuary nephron and that the improvement of UNE and uremic symptoms is poss sible with conservative treatment only. Thus, we suggest that the measurement of UNE will be useful as an indicator of inducing patients with chronic renal failure to dialysis treatment, and as a judgment of effects of dialysis treatment.

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With hand of an autopsy case (NA-5728), 28 years old male, an interpretation is given of the relationship between cardiocascular anomalies, sclerotic Lohlein nephritis and terminal membrano-proliferative glomerulonephritis in pathogenetic view. The cardiovascular anomalies are consisting of aorto-pulmonary window, VSD and a left side pulmonary artery delivered from the aorta, not from the pulmonary artery. There was also an endocarditis, still active locally, at the aortic valve which delivered emboli to give a splenic infarction and Lohlein focal nephritis. The cardiovascular anomalies of this type caused secondry pulmonary hypertension to form a plexiform lesion of the pulmonary artery and also severe hypoxgenemia. The serum level of Na ranged at 142 mE/l.It has been proven that 3 times positive blood cultures for viridans steeptococci were given at the age of 6 years old, though negative blood culture intensively done at terminal seriod. Serum com-plement level at the terminal was proven to be normal in which severe nephrotic syndrome was ensuing.
As to the pathogenesis of renal lesions; sclerotic focal nephritis and membrano-proliferative glom erulonephritis it would be suggested that some alteration of immunological background occure in the past history. First positive viridans in culture turned negative in the later part of history. There are also causative processes of hemodynamic alteration involving hypoxia attributable to nephritic lesions. In case of congestive heart failure membranous nephritis was described to occur. Hypernatremia developed at the terminal period, though blood pressure ranged at the level 104/70 mmHg.
Summerizing these congestive heart failure would play some role for triggering the membrano-proliferative glomerulonephritis at the end coinciding alteration of immunological state.

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