Eighty cases of renovascular hypertension including 47 with unilateral main renal arterial stenosis (UMRAS), 16 bilateral main renal arterial stenoses (BMRAS), 15 renal arterial branch stenosis (RABS) and 2 unilateral main renal arterial stenoses with contralateral renal arterial branch stenoses were studied. Abnormal findings were observed in 84% of UMRAS, 73% of BMRAS and 74% of RABS by rapid sequence pyelographic study, and in 84% of UMRAS, 63% of BMRAS and 54% of RABS by radioisotope renographic study. The ischemic pattern was obtained in 69% of UMRAS, 50% of BMRAS and 40% of RABS in split renal function test. High resting peripheral vein blood plasma renin activity values were obtained in 67% of UMRAS, but in only 33% of BMRAS and RABS. Hyperresponsiveness of renin secretion was found in 80% of BMRAS and 56% of RABS. A significant elevation of PRA in the stenotic kidney was found in 78% of UMRAS and 50% of unilateral RABS. Angiographic study revealed unilateral vascular lesion in 60 cases and bilateral in 19 cases. Development of collateral circulation was found in 73% of cases. Forty-nine cases underwent a surgical treatment and 40 cases of them were cured or improved. The most reliable diagnostic and prognostic criteria for surgical curability were to demonstrate collateral circulation and elevated peripheral vein PRA levels with increased renin secretion from the affected kidney. The postoperative course of blood pressure was examined with regard to the PRA in 18 nephrectomized and in 12 revascularized patients. The normalization of blood pressure was quicker in the latter than in the former, while the normalization of PRA was quicker in the former than in the latter.

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Based on the evidence of a rapid removal of prostaglandins (PGs) in the lung, inhibition of the pulmonary removal of PGE₁ and PGF_2α, was studied with isolated guinea-pig lungs. 1) In normal lungs, the average percent inactivation of PGE₁ and PGF_2α (5ng/ml) were 83.67±8.73% and 80.92±8.49%, respectively. 2) The percent inactivation of PGF₁ and PGF_2α decreased with increasing doses. 3) In normal lungs, the average percent inactivations of PGE₁ and PGF_2α, were 20.52±5.33% and 23.31±8.27%, respectively, with continuous infusion of indomethacin. 4) In sensitized lungs, the average percent inactivations of PGE₁ and PG_2α (5ng/ml) were 37.44±13.13% and 35.12±13.44%, respectively. 5) These results demonstrate that indomethacin has an inhibitory activity on PG inactivation, in addition to its already established activity on PG biosynthesis and that sensitization of lungs also inhibits inactivation of PGs per fused through the pulmonary vasculature.

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Hematological and cytogenetic studies on bone marrow cells were performed on 101 adults with acute leukemia, 58(57.4%) of whom had abnormal karyotypes in their leukemic cells prior to treatment. In myelocytic leukemia, nonrandom distribution of chromosomal abnormalities was observed, C-, D+, E+, G- abnormalities, which were probably due to translocation of C group chromosome to the long arm of G chromosome, t (Cq- ; Gq+). This translocation occurred significantly more often than expected. All patients with these translocations had low neutrophil alkaline phosphatase activity and characteristic findings in blood pictures and survival time. Serial cytogenetic examinations were also performed on 32 patients. When the condition of these patients with abnormal karyotypes turned to complete or incomplete remission by effective treatment, most of the bone marrow metaphases were replaced by normal karyotypes, and sometimes, co-existence with a small percentage of abnormal karyotypes was observed. It seems that chromosome analyses during the course of the disease gave some information about the judgement of remission and guide for the leukemia therapy. The discussion was made on the frequency of chromosome abnormalities in acute leukemia, possible nonrandom abnormalities of chromosomes in acute myelocytic leukemia, and a fairly weak relationship between chromosome aberrations and survival time.

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During the 3-year period ending in 1974, 3 cases of documented septicemia due to Clostridium perfringens of the type A food-poisoning variety were observed in our clinic. It was a complication of acute myelogenous leukemia, chloroma, and aplastic anemia. It developed with the sudden onset of clinical manifestations of acute gastroenteritis, but not of acute hemolysis nor of gas gangrene. The strains isolated from the blood were all heat-sensitive and produced both α- and θ-toxins. Moreover, they did not correspond to any of Hobbs' types 1-17. It was suggested that in patients with depressed resistance acute gastroenteritis due to C. perfringens, probably preexisting among the indigenous intestinal flora, can be a source of septicemia.

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31-year-old female. During her first pregnancy, she was found to have hypertension, proteinuria and anemia. These symptoms subsided after intrauterine death of fetus at the 3rd trimester, but redeveloped in her 2nd pregnancy. Thirst and polydipsia developed during pregnancy and persisted following the delivery. She first visited our Clinic because of nausea, vomiting, abdominal pain and anemia. These symptoms improved with ambulant therapy. She complained of right ulnar pain due to a right ulnar cyst. Amass in the right neck was found, and laboratory tests revealed marked hypercalcemia, hypophosphatemia, increased alkaline phosphatase and renal dysfunction. Cystic fibrous ostitis, nephrocalcinosis and gastric ulcer were confirmed. Marked elevation of plasma renin activity associated with hyperaldosteronism and proximal renal tubular acidosis were demonstrated. After removal of parathyroid tumor, hypercalcemia and hyperreninemia definitely improved. She died of hypercalcemic crisis due to recidivation of hyperparathyroidism. Postmorten examination : Recidivation of the right parathyroid cancer with metastases to adjacent fatty tissue and right lobe of the thyroid and periparathyroid lymph nodes. Extensive fibrous ostitis, bilateral nephrocalcinosis, calcification of alveolar walls and heart muscle, pyelonephritis, gastric ulcer, cystitis and mild pulmonary edema.
The authors assumed that hyperreninemia associated with hyperaldosteronism in this case was secondary to proximal renal tubular acidosis and hypercalcemia.

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