A 17-year-old girl complained of a headache and pain in the chest and back. The blood pressure on her right leg was 230/110 mmHg and there was a difference in blood pressure among the four extremities. Vasular murmur was audible on the neck, chest and abdomen. Erythrocyte sedimentation rate was 140 mm per hour. The leucocyte count was 9000. CRP test was 6 plus and ASLO was 333 T. u. Serum electrophoresis showed hypergammagl obulinemia (25.3%). Urinalysis showed 30mg/100ml of protein and numerous erythrocytes in the high-power field. Creatinine clearance was 79.3ml per minute, a PSP test showed 38.5% excretion in 15 minutes. Intravenous pyelography revealed that the right kidney was small and faint, Aortography demonstrated the stenotic orifice of the brachiocephalic, the left common carotid, the subclavian, the superior mesenteric and the bilateral renal arteries. Plasma renin activity of the right renal vein was 7.0ng/ml/h and the left 6.8ng/ml/h. The case was diagnosed as renal vascular hypertention due to aortitis syndrome. The right kidney was autotransplanted and at the same time a renal biopsy was performed. On light microscopic study, eight of 13 glomeruli showed a slight and segmental increase of mesangial matrix and five of these also had slight cellular droliferation. Immunohistologic study showed granular deposition of IgA, IgM, fibrinogen, C₃, C₄ and C₁q in the mesangial area and along the glomerular basement membrane in 13 out of the 16 glomeruli observed. Blood pressure had fallen to the normal range by the 133rd day after the operation. It might be possible to speculate that infectection by streptococus hemolyticus triggered the production of anti-aortic antibody, which in turn caused aortitis syndrome, and the immune complex deposited in the kidney induced focal glomerulonephritis.

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Methylguanidine (MG) was determined by modifying the methods of Baker et al. and Menichini et al.. MG was measured by ion exchange column-chromatography using Dowex 50 W, and MG movement of serum and urine in uremia was examined. 1. According to the reduced renal function, viz, chronic renal failure, serum and urine MG levels increase, and it is probable that dialysis treatment is insufficient to remove MG from the body fluid. 2. When the ratio of MG to creatinine clearance is higher than 1. 0, patients are found to suffer from various symptoms of uremia and require dialysis treatment. 3. The daily urinary excretion of MG was found to be much higher immediately after a successful renal transplantation than in a single performance of hemodialysis. In such a case, uremic symptoms disappeared rapidly. Therefore, it is postulated that MG plays an important role in the symptoms of uremia.

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A 36 years old female patient with renal staghorn caluculus associated with renal sarcoidosis was reported. Diagnosis for sarcoidosis was based on the findings such as epitheloid granuloma without caseous degeneration in the biopsy specimen from her right kidney, positive for Kveimm test, hypergammaglobulinemia, bilateral renal stones, granulomatous inflammation with foreign body reaction in the biopsy specimen from her operation scar, and conjunctival follicle. Our case is the first one in Japan, which was discovered by renal biopsy.

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Serum carcinoembryonie antigen (CEA) of 133 uremic patients on hemodialysis was assayed by sandwich method of Nishi and Hirai, and moderate increase of serum CEA (2.57 ± 0.11 ng/ml, [mean ± standard error]) was found. Among those patients, significant increase of serum CEA levels was found in cigarette smokers and aged groups. High serum CEA was significantly more frequent in blood group O and B than in blood group A. In 67 of them, their serum CEA levels were compared with the history of hemodialysis, 24-hour urinary volume and various laboratory data. No significant relations were found between those and serum CEA levels. The general increase of serum CEA in uremic patients was not explainable solely by smoking, age and blood groups. It may be due to inability to excrete CEA-like substances into urine in these patients.

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The activity of urinary kallikrein was measured by using tosyl-arginine methyl ester as a substrate and was expressed as an esterase activity. The examinees were 25 normal persons and 94 patients consisting of 56 cases with nephrotic syndrome (19 in the acute atage, 37 in the latent stage), 17 cases with chronic glomerulonephritis and 21 with chronic renal failure (9 with and 12 without hemodialysis). The results obtained are as follows : 1) This method modified by the author is suitable for estimating kallikrein activity in human urine. 2) The urine esterase activity estimated according to the author's method can be regarded as the urine kallikrein activity, as the esterase activity can not be detected by the author's method in the standard solutions of urokinase which is contained in human urine and has an esterase activity smiilar to the urine kallikrein. 3) The daily urinary kallikrein excretion (KE) is less in chronic glomerulonephritis and outstandingly less in chronic renal failure than in the normal controls. 4) KE shows a close positive correlation to 15.min PSP excretion, and a faint one to creatinine clearance, that is KE shows a positive correlation to renal functon. 5) The KE of six cases with various renal diseases were observed, continuously from the acute stage to the convalescent stage. No definite tendency was found in the course of KE. 6) There is no relation between the kallikrein activity and the concentration of urine protein, even though observed by 15-min PSP in 3 excretion groups. 7) The kallikrein activity is parallel, in general, to the urokinase activity. 8) In nephrotic syndrome, the kallikrein activity is apt to show a negative correlation to the urine α1-antitrypsin ; α₁-antitrypsin being an inhibitor to blood kallikrein. It is suggested that the urine α₁-antitrypsin can function as an inhibitor to the urine kallikrein. (Autoabstract)

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The factors of blood coagulation and f ibrinolysis were measured in patients with renal diseases to evaluate the pathophysiological feature of the coagulation and fibrinolysis in renal diseases. The subjects consisted of 28 cases with nephrotic syndrome (9 in acute stage, 19 in latent stage), 20 with chronic glomerulonephritis, 25 with chronic renal failure (11 with and 14 without hemodialysis) and 30 normal controls The results are as follows 1) Prothrombin time shows no difference among disease groups, and also in comparision with control group, Partial thromboplastin time is shorter, fibrinogen is more abundant, and platelet count is more numerous in the acute stage of nephrotic syndrome than in others. 2) In thrombelastogram, normal r, short k and broad ma are found in the acute stage of nephrotic syndrome, and also in chronic renal failure. 3) Plasma plasminogen is lower in the acute stage of nephrotic syndrome, Euglobulin lysis time is generally longer in nephrotic syndrome. Antiplasmin activity is higher in nephrotic syndrome, especially in the acute stage. 4) α₂-macroglobulin level is higher and α₁-antitrypsin level is lower in the acute stage of nephrotic syndrome. Antiplasmin activity shows a positive correlation to α₂-macroglobulin, but no correlation to α₁-antitrypsin in nephrotic syndrome. 5) Positive correlations of antiplasmin activity to β-lipoprotein and triglyceride are found in nephrotic syndrome. 6) In 4 cases with nephrotic syndrome, fibrinogen was abundant, plasminogen was low, antipasmin high and α₂-macroglobulin high in the acute stage, and these factors tended to be normal with the remission. It is concluded, as a whole, that a hypercoagulability exists in the acute stage of nephrotic syndrome and chronic renal failure, and a low fibrinolytic activity which may be due to the high levels of serum α₂-macroglobulin and serum lipids exists in nephrotic syndrome.

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To examine the role of intrarenal vascular coagulation(IVC) in chronic glomerulonephritis, hemostatic parameters of renal vein blood (RVB), urine FDP and renal histology were examined in 70 cases withh chronic glomerulonephritis. RVB was sampled by Seldinger's technique. Fibrin /fibrinogen degradationn products (FDP) were measured by hemagglutination inhibition immunoassay and soluble fibrin monomer complexes (SFMC) by Lipinski's method. Correlation was obtained between an increase of fibrinogen, FDP' and SFMC in RVB and the degree of intraglomerular fibrin deposits seen by immunofluorescence. The increase in fibrinogen was significantly higher in RVB than systemic vein blood (inferior vena cava blood), in active or progressive renal disease. Therefore, FDP and other coagulation parameters in RVB are thought to be a reliable way of estimating intrarenal hemostatic abnormalities resulting in deposit and lysis of fibrin within the kidney. An increase of FDP, SFMC and fibrinogen and a slight decrease of f ibrinolytic activity in RVB were observed in chronic glomerulonephritis with decreased renal function or with the nophrotic syndrome. Daily excretion of FDP in the urine and the extent of intraglomerular fibrin deposition were greater in nephrotics than in nomnephrotics. In contrast, no increase of FDP in. RVB was found in non-nephrotics. We conclude that RVB sampling for coagulation parameters is a reliable and sensitive method for assessing IVC, and IVC plays an important role in aggravation of chronic glomerulonephritis, especially when nephrotic syndrome is present.

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