The pathogenesis of renal damage in gout is yet a controversial subject. The author investigated renal vascular impairments through renal function tests, renal biopsy and renal angiography in 13 gouty patients. And similar study as in gouty patients was performed in several other renal diseases for the sake of comparison. Renal angiographic findings in 13 cases of gouty patients were analyzed and divided into four groups, namely normal type. pyelonephritic type, glomerulonephritic type and arteriosclerotic type. Renal angiography has been evaluated as an excellent diagnostic method for surgical renal diseases. However, the author would like to emphasize that it is a method which can also offer valuable informations on medical renal diseases. Vascular changes in the kidney of collagen diseases were confirmed in broader e rtent in renal angiography than were presumed from findings of renal biopsy or renal function tests. But the definite conclusion could not be drawn as only a few cases of collagen diseases were included in this series. The concept that arteritis or arteriosclerosis develops in the kidney secondary to glomerulonephritis or pyelonephritis seems worth while to emphasize. Vascular changes in the kidney of gouty patients are supposed to derive from such systemic factors as hyperuricemia and disturbances of lipid metabolism in one hand and such local factors as urate deposition and pyelonephritis in the other hand. Therefore, vascular changes may precede renal parenchymal changes, but sooner or later the former will be promoted and lead to arteriosclerosis by local changes. Not a little portion of the etiologic factors mentioned above can be now influenced by medical control. Therefore, careful effort should be paid to avoid deterioration of renal or vascular complication to improve prognosis in gout.

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Many studies on acute renal failure caused by the transfusion of low molecular weight dextran have been reported in recent medical literature. The histological findings of the kidney on these cases are characterized by osmotic nephrosis. In the present paper, histologic examination of osmotic nephrosis from the autopsy cases at the Department of Pathology, Keio University School of Medicine was performed. In addition, the experimentally produced osmotic nephrosis in rats was investigated by light and electron microscopy and histochemical methods. The results were summarized as follows: 1) In 1000 autopsy cases of recent three years, 20 cases with osmotic nephrosis were found. Intravenous transfusion of various fluids had been performed within a week before the death on all of these 20 cases. Histologically, the intensity of osmotic nephrosis seemed to be corresponded with the amount of the dextran transfusion and the degree of oliguria and anuria. 2) The low molecular weight dextran (M. W. 40, 000) was injected intraperitoneally into 46 adult Wistar rats, 40 to 60 ml per kg. The experimental rats were deviled into three groups; group 1: dehydration for 72 hours, group 2: urinary stasis by ligation of oneside ureter for 24 hours, group 3: 48 hours after 15 minutes shut down of oneside renal artery blood flow. The intensity of hydropic changes in tubular epithelium was ranged in group 1, group 2 and group 3. In group 2 and 3, the intensity of hydropic changes was more prominent in the pretreated side. 3) Electron microscopic and histochemical observations suggested that the lysosome played an important role to the occurrence of hydropic changes of renal tubules. 4) The pathogenesis of acute renal failure related to the transfusion of dextrans was discussed.

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The effect of diuretics upon NH₃ metabolism was studied using healthy rats and hepatic cirrhosis rats produced by the penicillium islandicum insult rice.(1) Acetazolamid increases the activity of renal glutaminase I, and accelerates the discharge of NH₃ from the kidney. Hydrochlorothiozide, ethacrinic acid and chlormerodrin increase the activity of glutaminase I only when injected into peritoneal cavity every day for 2 weeks. MK 870, however, does not increases the activity. This indicates the possibility that the defect of K is an attributable factor in the cases of hydrochlorothiazide, chlormerodrin and ethacrinic acid. Hepatic cirrhosis rats feature in the intensified renal glutaminase I activity, and also in the more notable effect of diuretics than usual.(2) The activity of hepatic glutaminase I is increased by acetazolamide, while the other diuretics, such as hydrochlorothiazide, ethacrinic acid, chlormerodrin, accelerate the activity only when injected into the peritoneal cavity. The activity of hepatic glutaminase I decreases in the hepatic cirrohosis rats.(3) Urea production is accelerated by acetazolamide. Hydrochlorothiazide increased the urea production when it is given by the intraperitoneal injection. It is considered to be due to the state of being devoid of Na under the effect of diuretics, rather than the direct effect of diuretics. Chlormerodrin acts to reduce the urea production. The urea production in the cirrhosis produced by penicillium islandicum insult rice is decreased.(4) Arginase activity. Chlormerodrin decreases the arginase activity, while the other diuretics have no effect upon the arginase activity. The decrement of arginase activity is found in crrhosis rat produced by penicillium islandicum incult rice and it is still decreased by the supply of chlormerodrin.(5) Ethacrinic acid and chlormerodrin decreases the O₂ consumption of rat liver mitochondria, and inhibit the ATP production. This is assumed mainly due to the interruption of electoron transfer in mitochondria by ethacrinic acid and chlormerodrin. Cirrhosis rat liver produced by Penicillium Islandicum insult rice show low degree of ATP production, and it is still decreased by ethacrinic acid and chlormerodrin. In brief, acetazoramide possibily affects directly upon activity of glutaminase I and causes the increase of NH₃ discharge into the urine and blood. Although ethacrinic acid and hydrochlorothiazide increase the activity of glutaminase I, it is viewed as a secondary effect caused by the defect of K. Acetazolamide and hydrochlorothiazide accelerate urea production. Ethacrinic acid and chlormerodrin depress the respiration of rat liver mitochondria, and reduce the ATP production.

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Approximately 2900 chronic hemodialysis on 34 patients with chronic renal failure were performed between These results have been analysed in detail and can be summarized as follows; 1. All of 34 patients, aged 18-64, 24 males and 9 females, were "unselected" severe renal failure, including 27 chronic glomerulonephritis, 3 chronic pyelonephritis, 2 malignant hypertension, 1 polycystic kidney, 1 diabetic nephropathy, and 1 pyonephrosis with septicemia. 2. At the end of 13 of them could return to work, continuring their hemodialysis once or twice a week and 10 patients remained in hospital. Ten died of various causes such as hepatic failure, heart failure, cerebral hemorrhage, Gastrointestinal hemorrhage, sepsis, or hypoglycemic shock. 3. Average cannular duration of these cases was 11.3 months on arterial side and 8.65 months on venous side. Warf arin was effective to prevent blood clotting in cannula. 4. 610 hemodialysis were performed with regional heparinization. The heparin sensitivity and protamine-heparin neutralization ratio of each patient were determined previously. Only 10 blood clotting in dialyzer and 3 episodes of hemorrhage were observed. Anticoagulation rebound was seen in about 24 per cent. 5. When the serum osmotic pressure droped more than 30 milliosmols within 7 hours using Kiil dialyzer, disequilibrium syndrome appeared frequently. The dialysis with low concentration dialysate increased the frequency and severity of this syndrome. Slow dialysis by one layer Kiil dialyzer was effective to prevent this syndrome. 6. Transient GPT elevation was observed in 18 patients. In five patients developed icterus, and two of them died. There were no difinite correlation between frequency or severity of hepatitis and the volume of blood transfusion. 7. The most important medical factor which made rehabilitation difficalt for these patients was complications of cardiovascular system. 8. We did not find any difinitive secondary hyperparathyroidism or calcium metastasis in our cases.

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In order to study the role of the renin-angiotensin system in hypertensioe disorders and to evaluate clinical usefulness of the estimation of plasma renin activity in differentiation of various types of hypertension, plasma renin activity was measured in 25 normotensive control subjects and 81 patients with various types of hypertension under controlled conditions. Renin activity in renal venous plasma was also measured in 9 patients with benign essential hypertension and 3 patients with renovascular hypertension. The effects of posture, dietary sodium restriction and diuretic on plasma renin activity were examined in the normotensive controls and patients with benign essential hypertension. The estimation of plasma renin activity was done using the improved assay method described by Skinner in 1967. The results were as follows: 1) The mean values of plasma renin activity did not significantly differ from normal in patients with benign essential hypertension, renal artery aneurysm and chronic glomerulonephritis without renal failure. 2) There was no significant difference in plasma renin activity between the renal failure type of chronic glomerulonephritis with hypertension and without hypertension. 3) Plasma renin activity was increased in patients with entering stage of malignant hypertension, malignant hypertension and unilateral renal artery stenosis. 4) Plasma renin activity was suppressed in patients with primary aldosteronism. 5) Renal venous plasma renin activity was remarkably high on affected side in patients with unilateral renal artery stenosis. 6) Plasma renin activity was increased on upright posture, dietary sodium restriction and diuretic administration. From this study, it is proved that the estimation of plasma renin activity under various conditions is very useful in differentiation of various types of hypertension, and suggested that the renin-angiotension system played an important role in malignant hypertension and unilateral renal artery stenosis.

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To elucidate the effects of plasma sodium and water balance on renin secretion, plasma renin activity, plasma sodium concentration, hematocrit, plasma volume, and arterial blood pressure were measured in 14 patients of chronic renal failure before and after peritoneal dialysis and the amount of the water volume removed by peritoneal dialysis was also measured. Estimation of plasma renin activity was carried out using the improved assay method described by Skinner in 1967. Plasma volume was determined using 30-40 μc of RISA. Peritoneal dialysis was repeated 15 times over two days with two liter dialysate (361-472 mOsm/L) each time. The results were as follws: 1) Plasma renin activity was increased significantly after peritoneal dialysis. The mean increase was 58.1±33.3% (95% confidence limits). 2) There was no significant correlation between the amount of water removed and plasma renin activity. 3) Blool pressure rose slightly after peritoneal dialysis, but the elevation was not significant. 4) The plasma sodium concentration was increased significantly after peritoneal dialysis. There was no inverse correlation between plasma sodium concentration and renin activity. 5) Increase of hematocrit and decrease of plasma volume were significant after peritoneal dialysis. There was significant correlation between increasing rate of renin activity and decreasing rate of plasma volume. From the present study, it may be concluded that a dominant stimulus to renin secretion in peritoneal dialysis is a decrease in plasma volume, but not a decrease in plasma sodium concentration.

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The control of renin secretion in the denervated kidney with or without contralateral kidney was studied by observing the changes of renal plasma flow (RPF), glomerular filtration rate (GFR), urinary sodium excretion and renin secretion produced by the suprarenal aortic constriction. Renin secretion was calculated by the following equation: renin secretion=(renal venous renin activity-renal arterial renin activity) ×RPF and renin activity was measured by Skinner's improved assay method. The experiments were performed on 16 dogs (Five dogs: neither denervation nor contralateral nephrectomy had been performed in these dogs, which were used as a control group. Six dogs: one kidney had been denervated, but the contralateral kidney left untouched. Five dogs: one kidney had been denervated and the contralateral kidney removed). The following results were obtained. 1) The decrease of urinary sodium excretion and the increase of renin secretion in the denervated kidney with contralateral kidney were less than those in the control group by the reduction in renal perfusion pressure of the same degree, while the decrease of RPF and GRF was almost equal. 2) The decrease of urinary sodium excretion and the increase of renin secretion in the denervated kidney without contralateral kidney were more than those in the denervated kidney with contralateral kidney by the reduction in renal perfusion pressure of the same degree, while the decrease of RPF and GFR was almost equal. These findings suggest that renin secretion might be controlled indirectly by the changes of urinary sodium excretion which were produced by renal denervation or removal of contralateral kidney.

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