Effects of a new amino acids granule (AMI-U G®), consisting 8 essential amino acids and histidine, on rats with ischemic chronic renal failure (uremic rats) were investigated. 1) The time course of changes in SUN, creatinine clearance and urinary osmolality of uremic rats produced by the methods of Avioli et al., were similar to those in patients with chronic renal failure. 2) In the uremic rats fed with 24, 12, 6, 3 and 1% protein diets, the body weight, N-balance and biological findings (SUN, serum total protein, albumin, hematocrit, serum Mg, Ca, Na and K) were observed for 4 weeks. In the group fed with 3 % protein diet, both the change of body weight and N-balance were maintained nearly at zero level throughout the experime ntal period and this group seemed to be the most suitable for the observation of the effect of AMI-U G on the uremic rat. 3) In the uremic rats fed with 3 % protein diets containing AMI-U G (0, 0. 1, 0.5 and 1.5%. respectively), serum and urine biochemical examinations were done weekly till the 4 th week. Increase in the body weight, positive N-balance and decrease in SUN were observed in the groups fed with diets containing 0.5% and L 5% AMI-U G. 4) In addition, serum methylguanidine and aminogram of the uremic rats fed with 3 % protein diet containing 1.5% AMI-U G (G-A) or 1.5% Ref G (G-B) were observed on the 4th week and weekly for 4 weeks, respectively. Comparing to the result with the G-E group, in the G-A group serum methylguanidine level was decreased and aminogram became to be in normal range. It is concluded that AMI-U G® is one of the most excellet amino acids granules for essential amino acids therapy for renal failure.

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A 23-year old hypertensive woman with Ask-Upmark kidney is described. She have had a four years' duration of hypertension and no history of urinary tract infection. DIP showed a hypoplas is left kidney with thinning of the cortex in the area form upper pole to middle portion. The right kidney was large in size and normal in appearance. Aortography demonstrated a small left renal artery without the stenotic findings. The right main renal artery was normal. Plasma renin activity was normal and the angiotensin II analogue (Sar¹, Ile⁸ AII) infusion showed a rise in blood pressure on a normal sodium diet and no change in blood pressure on a low sodium diet. The renal vein renin ratio on furosemide administration was 1.8, suggesting the increased renin release from hypopiastic left kidney. A rapid normalization of blood pressure was observed after left nephrectomy. Histological examination of the kidney revealed the characteristic features of Ask-Upmark kidney which consisted of thyroid-like tubules devoid of glomeruli, thick-walled arterioles and fibrosis in the deppressed areas.

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Three patients with saccular aneurysms arising from unilaterl renal arteries or their distal tribut-aries were presented together with a review of reports from the Japanese Literatures. One hundred and eleven patients (51 males, 59 females and 1 unspecified), 1 to 71 year in age, displayed 127 renal artery aneurysms. Seventy-four patients had hypertension. The blood pressures of the males and females were 177±6/107±5 and 171±6/105±5 mmHg (mean±S.E.), respectively. Solitary aneurysms affected 50 patients and multiple ones occurred in 15 subjects. The blood pressures of the former and the latter group were 171±5/103±4 and 185±8/113±5mmHg (mean±S.E.), respectively. These differences were not statistically significant. The blood pressures of the patients with jet-type aneurysms were considerably higher than those of the subjects with saccular type aneuryms (197±5/113±3s/161±6/99±5, mmHg, mean±S.E., respectively). Of the 53 patients with hypertension, high blood pressure was improved in 42 patients following the treatment. Subsequently, the necessity for curative measures, either surgical or nonsurgical, can be emphasized in patients with renal aneurysms.

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The effect of free chlorine (hypochlorous acid) which is widely used as bacterial agent, on human red blood cells was investigated. Our in vitro study has shown that, 1. Free chlorine caused marked hemolysis but no detectable methemoglobin formation.2. Combined chlorine (chloramines) induced marked methemoglobin formation but no direct hemolysis. As free chlorine is an oxidant that causes hemolytic anemia in dialyzed patients, we neutralized it by addition of ascorbic acid in physiological amounts to dialysate.3. Ascorbic acid added to dialysate produced a great improvement in anemia of dialyzed patients, with haematocrit values averaging 3.53.6 % higher. On the other hand, the ascorbate cyanide test suggessed that the reducing power of uremic red bloodd cells might be diminished.4. The degree of abnormality in the ascorbate cyanide test was found to be well correlated with the severity of hemolysis induced by free chlorine contained in dialysis water.

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The effects of ubiquinone (Coenzyme Q₁₀) on plasma renin activity (PRA) and plasma aldosterone (PAL) were studied during the acute respiratory acidosis in the dogs. Our previous studies showed that PRA was increased and. PAL was slightly increased, during the acute respiratory acidosis in the dogs. In the present experiment, PRA was increased in both control group and ubiquinone group, and PAL was increased in control group, but decreased in ubiquinone group, during the acute respiratory acidosis. And also the NaK ratio in urine was decreased in control group but increased in ubiquinone group. We concluded that:(1) Ubiquinone had no direct effect on renin-angiotensin system(2) Ubiquinone suppressed the biosynthesis and release of aldosterone in the adrenal gland.

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Thirteen anesthetized dogs weighing 8.0 to 15.0 kg (mean of 12.0±0.7 kg) were used. Urinary sodium excretion was 6.5±1.9 μEq/min., suggesting relative sodium depleted state. Intrarenal infusion of angiotensin II (Hypertensin, Ciba, 60 ng/min.) elicited the decreases in effective renal plasma flow (CPAx) and glomerular filtration rate (Ccr), the increases in filtration fraction. (FF) and renal vascular resistance (RVR), and no change in extraction ratio of PAH (EPAH) and mean blood pressure (MBP). Intrarenal infusion of competitive antagonist [Sar¹, Ile⁸]-angiotensin II (20 ng/min) elicited the increase in C_PAH, the decreases in FF and RVR, and no change in Ccr and MBP. The time course of the renal function was observed in 4 dogs. It was stable throughout the experiment except the minor reduction of C_PAH 20 min. after the first control clearance period. These suggest that exogenous and endogenous angiotensin II in the sodium depleted dog induce vasoconstriction, which is much marked in the efferent arteriole than in the afferent arteriole. These also suggest that the distribution of Intrarenal blood flow will not be changed markedly by exogenous angiotensin II of the dose used in this experiment and endogenous angiotensin II. The changes in renal function due to [Sar¹, Ile⁸]-angiotensin II (20 ng/min) disappeared during the following infusing of large dose of[Sar¹, Ile⁸]-angiotensin II (100 ng/min), suggesting the agonistic activity of [Sar¹, Ile⁸]-angiotensin II with increasing doses.

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Plasma aldosterone concentration (PAC) in 8 patients with terminal renal failure was investigated before and after hemodialysis. Plasma renin activity, Na and K were measured together with the PAC during the study. There was a significant correlation between plasma aldosterone and plasma potassium concentration after hemodialysis ; but not before hemodialysis. There was no correlation among PAC, PRA and plasma sodium during hemodialysis. These results demonstrate that aldosterone secretion on the patients with terminal renal failure could be stimulated by plasma potassium more than by renin-angiotensin system. And it seems that aldosterone secretion is not significantly interfered by administration of heparin in dosages used during long-term hemodialysis.

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Baroreflex sensitivity (BS) was evaluated in 22 nondialyzed patients with endstage chronic glomerulonephritis (Serum creatinine concentration ≥ 3 mg 100 ml) in order to investigate the mechanism of hypertension in chronic renal failure (CRF). BS was judged by the slope of the linear regression of the R-R interval of the electrocardiogram on the drug-induced blood pressure elevation with injection of phenylephrine or blood pressure reduction with amyl nitrite inhalation. Plasma renin activity (PRA) was measured in 17 patients by Haber's method. Plasma volume (PV) was measured with dye dilution method. (1) BS was reduced in CRF as compared with normal controls. Serum creatinine concentration, anemia, age, duration of renal failure, and arteriosclerosis were not correlated with BS, but a significant positive correlation was found between BS and motor nerve conduction velocity measured on ulnar nerve, indicating that uremic neuropathy including autonomic neuropathy might be involved in barorecep-tor dysfunction in CRF. (2) Plasma renin activity was not correlated with BS. Reduction of BS was considered to have no enhancing effect on renin secretion. (3) BS was significantly lower in 9 hypertensioe than 13 normotensive patients. (4) Saline was given to 7 normotensive patients for 2 or 5 days in order to determine whether the greater reduction of BS can be an initiating factor of hypertension. Blood pressure was raised to hyper. tensive levels with increase of PV only in 2 patients in whom BS was as nearly low as that of hyper tensives, but not in other 5 cases whose BS was mildly depressed. Plasma volume increased to the same degree in both groups. From these results, it can be concluded that baroreceptor dysfunction may be one of the pathoge-netic factors initiating hypertension in CRF.

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In order to investigate the sodium excretory capacity in patients with biopsy-proven primary glomerulonephritis, two-hours' static upright position was loaded after two-hours supine position. In all of the patients and of healthy control subjects, the change from supine to upright position was followed by decreases in creatinine clearance (C_Cr), fractional sodium excretion (FE_Na), and thus sodium excretion (U_NaV) . However, the decreases in these values were significantly greater in the patients than in healthy subjects, suggesting that both glomerular and tubular responses to orthostasis in the patients were abnormal. In those patients with mesangial proliferatioe glomerulonephritis whose glomerular and tubular functions during supine position were normal (NP), orthostasis induced significantly greater decreases in C_Cr, FE_Na and U_NaV than in healthy subjects, indicating that renal lesion such as mesangial proliferation played an important role in the abnormal postural response. In addition, it was suggested that no abnormality in renal function in NP might be disclosed unless some stress such as a postural change would be loaded. Among the factors affecting glomerular filtration and tubular sodium reabsorption, serum total protein concentration, plasma renin activity and plasma aldosterone concentration were increased after orthostasis in both NP and healthy subjects, the increases in these values being significantly greater in NP than in healthy subjects. From these results, it was concluded that: (1) In patients with glomerulonephritis, whether their renal function during supine position was impaired or not, orthostasis resulted in more sodium retention than in healthy subjects. (2) The causal sequence leading to the abnormal orthostasic antinatriuresis in NP was greater decrease in glomerular filtration which might result from the existence of the renal lesion, and greater increase in tubular sodium reabsorption mainly caused by hyperreaction of renin-angiotensin. aldosterone system, than in healthy subjects.

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