Serum immunoreactive parathyroid hormone (iPTH) was measured in 33 patients with end-stage renal failure and 36 under hemodialysis, and its relationship to calcium metabolism was studied. 1. A significant positive regression line was obtained in relationship between serum iPTH con-centration and converse of creatinine clearance in patients with end-stage chronic renal failure. 2. In relationship between serum iPTH concentration and the duration of dialysis, two different type of regression line were observed. One group of patients (Group A, iPTH <3. 8) showed im-provement of serum iPTH concentration depending on the increase of the duration of dialysis, and the other showed increase of serum iPTH concentration (Group B, iPTH >3.8). 3. In comparison of serum iPTH concentration with both serum calcium and AlPase activity, highly significant regression lines were obtained in each case in either non-dialysed or dialysis patients. 4. Four out of 36 dialysis patients showed the typical roentgenologic changes of hyperparathy-roidism. All of these patients belonged to Group B and were under 30 in age. They showed high serum iPTH concentration and AlPase activity. From these results, it was suggested that repeated measurements of serum iPTH concentration in dialysis patients are profitable to detect the extent of bone lesion and judge the prognosis of it.

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To identify patients with low-plasma renin activity (PRA) hypertension, we measured PRA and plasma aldosterone (PA) in recumbent before and in upright posture after 30 and 120 minutes of the intravenous infusion of furosemide in 39 patients with labile hypertension on low sodium diet. This test was again repeated on high sodium diet in 22 of them. Urine was collected during 120 minutes after furosemide infusion and sodium and potassium in urine were measured. After one week of low sodium diet (NaCI 5 g per day), 8 (36.8 per cent) in 22 patients showed low PRA less than 1 ng per ml per hour. 11 (50.0 per cent) in 22 patients showed normal PRA between 1 and 3 ng per ml per hour. 3 (13.6 per cent) in 22 patients showed high PRA more than 3 ng per ml per hour. After furosemide infusion, 3 (13.6 per cent) in 8 patients with low PRA did not show the re-sponse of PRA. After 3 days of high sodium diet (NaCI 10 g and NaHCO310 g), patients with low PRA increased to 17 (77.3 per cent) from 8 cases and non-responder to furosemide increased also to 9 (40.9 per cent) from 3 cases. In these cases, no patient showed high PRA more than 3 ng per ml per hour. Before and after 30 and 120 minutes of furosemide infusion, mean PRA was 1. 9, 3.7, and 4.4 ng per ml per hour and mean PA was 10, 8, 15. 4, and 18.8 ng per 100 ml in low sodium diet. In high sodium diet, mean PRA was 0.59, 2.0 and 2.2 ng per ml per hour and mean PA was 6.3, 9.1 and 10.7 ng per 100 ml. In the former, both PRA and PA increased progressively but in the latter, they showed plateau in 30 minutes. The increase rate of PA per 1 ng PRA elevation was 3.20 ng per 100 ml in low sodium diet but 2.75 ng per 100 ml in high sodium diet. This means the difference of sensitibity to angiotensin II of adrenal cortex in low or high sodium load. During 120 minutes after furosemide infusion, sodium in urine of low PRA hypertensive group was much more than other groups but potassium in urine of this group was less than other groups. Potassium sodium ratio in urine was 0.098, 0.111 and 0.137 in low, normal and high PRA hyper-tensive groups respectively. In 4 patients of primary aldosteronism, potassium in urine was markedly higher and potassium sodium ratio was such a higher value as 0.26 compared with other low PRA hypertensive groups. If this low PRA hypertensive group should be caused by an unknown mineralocorticoid, potassium in urine and potassium sodium ratio of this group must be high value due to the influence of this hormone. In all of these patients in three groups excepting primary aldosteronism, basal PRA and PA value showed a good correlation with potassium sodium ratio in urine. From these results, all of the low PRA hypertension will not be always caused by an unknown mineralocorticoid. Excessive mineralocorticoid hypertension should be in such patients not only with low PRA but also with increased potassium excretion in urine after furosemide infusion.

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The authors reported that urine of healthy or sick people always involves platelets or cell elements originated from platelets. These small bodies can be termed as "platelet-like bodies in urine" (U-PLB). The purpose of this study is to examine the U-PLE obtained from the urine of patients with renal diseases. Platelets were found in mechanical renal hematuria caused immediately after percutaneous renal biopsy and in the urine of patient with a suspicuous renal tumor. Transmission electron microscopy (TEM) and scanning electron microscopy (SEM) revealed that the urine ob-tained from a patient with so-called idiopathic renal bleeding, a patient with chronic glomerulone-phritis (CGN) and a patient on the following day of renal allo-transplantation all contained platelets. Platelet-like cells were shown by TENT and SEM in the urine obtained from two patients with acute glomerulonephritis, a patient with CGN and a patient with chronic renal failure. The urine of patients with various renal diseases always contained platelets or platelet-like cells, and cell elements originated from platelets. The urine, in which many disc-shaped U-PLB were found by phase contrast microscopy, contained many platelets or U-PLB, which were shown by TEM.

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Fifty nine cases (31 children and 28 adults) presenting chance proteinuria and/or hematuria were selected in this study out of 192 renal biopsy cases examined light and immunofluorescent microscopy. Fourty four cases (21 children and 23 adults) out of these 59 were diagnosed to be Ig-A nephropathy (Ig-A NP). Other 14 cases out of 15 cases showed no deposition of immuno-globulines and complements (Ig-G, Ig-M, Ig-E, Ig-D, C3 and Clq), while the remaining 1 case re-vealed fibrin deposits along glomerular capillary loops. The levels of serum Ig-A in those with Ig-A NP ranged between 92-880 mg/dl, with the mean value 275.2 mg/dl. On the other hand, those without Ig-A deposit ranged between 150-430 mg/dl, with the mean value 223.0 mg/dl. Of the 44 cases with Ig-A NP (7-60 yrs. average age: 19 yrs.), 21 cases (15 children and 6 adults) showed Ig-A deposition alone in the mesangial area. The other 23 cases (6 children and 17 adults) exhibited mesangial Ig-A deposition accompanied with Ig-G and/or C3. It is posturated that Ig-A NP accompanied with the glomerular deposition of other immunoglobulins and C-components tends to be much more frequent in adults than in children. Regarding to histopathological findings, minimal change (MC) or focal prolif erative glomerulonephritis (FPGN) were often seen in children, whereas generalized prolif erative glomerulonephritis (GPGN) were more commonly seen in adults. Although the common features of the clinical findings were microscopic hematuria, the proteinuria were also identified in 27 cases (7 children and 20 adults). GPGN was commonly observed as com-pared to MC or FPGN in those who presented proteinuria in addition to microhematuria. Although Ccr determinations at biopsy were within normal range in the majority of our Ig-A NP cases, 2 cases out of 44 cases followed up showed the decrease in Ccr levels. Those evidences suggest that although Ig-A NP has a very prolonged clinical course but is not always a benign evolution.

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Studies of immunological and clinicopathological aspects have been carried out in four patients with membranoproliferative glomerulonephritis (MPGN). Nine renal biopsy specimens were obtained from them during three years. Immunoserological findings were studied by examining serum immunoglobulins (Img), RA, ASLO, Wasserman reaction, anti-nuclear antibody (ab), Au antigen, anti-glomerular basement mem-brane (GMB) ab., anti-tubular BM ab., anti-mesangial ab. and others. One of the patients had positive anti-GBM ab. and his renal immunofluorescence (FAT) showed in a fashion of linear pat-tern along GBM for anti-human IgG serum. Serum Img, especially IgG, were decreased in nephrotic state. In coagulation system, fibrinogen/fibrin degradation products (FDP) in blood were normal, but urinary FDP were increased during active nephritic state, in which renal FAT showed glomerular fibrin deposition and renal histology revealed glomerular fibrin thorombi. At these state, fibrinolytic therapy with urokinase was associated with remarkable improvement of renal function tests. Serum complement studies were measured by examining CH50, alternative CH50 (ASCH50), C3, C4 and C3PA. These data suggested that complement system was activated via the classical and alternative pathway at the maximal active nephritic state. Correlation between ACH50, CH50 and complements in total and indivisual serial measurements suggested dominant complement activation via alternative pathway, but one of these cases dominant via classical pathway. C3NeF was mea-sured by using immunolectrophoresis and ACH50, but none of cases were detected. Renal histological findings showed type I in three and type ii in one. These typical histolog-ical features were fairy reversible with irreversible sclerotic changes. Renal FAT for glomerular deposits were examined by using anti-human serum for IgG, IgA, IgM, IgE, secretary piece, fibrinogen/fibrin, GBM, C3, Clq, C4, C3PA and properdin. The observa-tions indicated that deposition of complements were more dominant than that of Img and comple-ment system was more dominant via alternative pathway or Cl bypass. Correlation between renal histology, renal FAT and serum complements were relatively better. According to these data, etiology and pathogenesis were discussed in MPGN.

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In order to study the influence of haemodialysis on dopamine-β-hydroxylase (DBH) activity in plasma, we measured plasma DBH, total plasma protein and blood pressure before and after hae-modialysis in fourteen patients with chronic uremias. DBH activity was determined by modified method of Creveling et al. As Co-enzyme A, cystein and other -SH compounds are known to inhibit DBH, the level of endogenous DBH inhibitors in Plasma was also examined by using purified beef adrenal DBH preparation which is free from endogenous inhibitors. The DBH activity per ml of plasma was significantly elevated after haemodialysis. Although plasma total protein also in-creased following the dialysis, DBH activity per mg plasma protein was also higher after the dialysis than that before the dialysis. On the other hand, inhibition of purified DBH by the plasma obtained after haemodialysis was more marked than by the plasma before dialysis, suggesting that endogen-ous DBH inhibitors increased after haemodialysis. These results indicate that absolute DBH activity in plasma obtained after haemodialysis is virtually higher than the estimated activity and elevation of plasma DBH after haemodialysis was neither due to the decrease in endogenous inhibitor nor the increase in the activators. Haemodialysis produced the reduction of systolic and diastolic blood pressure which may be caused by the reduction of extracellular fluid after the dialysis. Several explanations are possible for the increase in plasma DBH activity after haemodialysis as follow; 1) The reduction of extracellular fluid by haemodialysis may stimulate the secretion of DBH from sympathetic nerve terminals and 2) Treatment of the patient with haemodialysis itself stimulate the secretion of DBH, because the treatment itsely is associated with a great stress.

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Several proline derivatives were synthesized and converting-enzyme inhibiting action of these compounds was evaluated by assessing the depressor action to angiotensin I-induced pressor re-sponses in anesthetized rats. Of all derivatives synthesized, D, L-2-methyl-3-mercaptopropanoyl-L-proline (D, L-m-m-p) was shown to have the most potent inhibiting action of converting-enzyme. Intra-venous administration of 0.1, 0.2 and 1.0 mg/kg of D, L-m-m-p showed 68%, 75%, and 80% suppression of the pressor action of angiotensin I, 0.15-0.6 μg/kg iv bolus. This inhibiting action was about ten times potent compared with Bradykinin Potentiator B indentified from snake venom of Agkistrodon halt's blomhoffii. Its converting-enzyme inhibiting action was effective in any routes of administration tested, i.e., intra-venous, subcutaneous and per Os. Effect on blood pressure of D, L-m-m-p (0.5 mg/kg, S.C.) was examined in rats having experi-mental models of renovascular hypertension. In one-kidney Goldblatt type rat, blood pressure reduction was observed in acute phase, but not observed in chronic phase. In two-kidney Goldblatt type rat, blood pressure reduction was observed in chronic phase. On the contrary, in normal rats no consistent blood pressure changes were observed. Thus, D, L-m-m-p is an active inhibitor of converting-enzyme by any routes of administration, it is a useful agent for investigation of renin-angiotensin system in animal experiment and also promising agent for diagnosis and treatment of renin dependent hypertension in human.

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