A 38 year-old man complained of headache visited a physician Hypertension, 160/90 mmHg, was pointed ont, and no findings were revealed in urinalysis at that time. The blood pressure was decreased to 130/80 mmHg with 3-month administration of hydrochlo-romethiazide (50 mg/day)., proteinuria was first mentioned, and the blood pressure was 180/120mmHg. He was referred to the Hospital on, with chief complaints of severe headache and edema on lower extremities. Hypertension ranged 240/150 to 160/120 mmHg. Laboratory findings showed urine protein 10-50g/day, plasma albumin 2.4g/100ml, plasma cholesterol 356mg/100ml, plasma potassium 3.1mEq/L, plasma renin activity 14.0ng/ml/h and plasma aldosterone concentration 58ng/100m1. Intravenous pyelogram, renogram and renoscintigram showed that the right kidney was working poorly, and retrograde transfemoral aortogram revealed stenosis of right main renal artery. Hypertension could not be improved with α-methyldopa, spinorolactone, hydralazine, pindolol and trichloromethiazide, so that right nephrectomy was performed. About three weeks post operatively, the blood pressure fell to 146/90 mmHg and proteinuria decreased to 1.0-2.5 g/day. Plasma renin activity and plasma aldosterone concentration fell to 1.2 ng/ml/h and 6.0 ng/100 ml, respectively. Hypercholesteremia, hypoalbuminemia and hypokalemia were improved. Microscopic examination of the right kidney revealed that most glomeruli were completely hyalinized, arterioles showed a great increase in medial width and neither infiltration of small round cells nor necrosis was found around the arterioles. The pathologic diagnosis was renal atrophy followed by artery stenosis due to arteriosclerosis. It is suspected that the nephrotic syndrome was induced by hypertension and high renin-angiotensin-aldosterone.

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A 51 year old male with features typical of Bartter's syndrome is described. Several theories have been proposed to explain the pathogenesis of this disorder. Lataly, loss of sodium at the proximal tubule or ascending limb of Henle's loop was disclosed These tubular defect led to extracellular fluid volume depletion and consequent stimulation of the renin-angiotensin-aldosterone (RAA) axis. On the other hand, it is well known that prostaglandins have a potent natriuretic action. We therefore investigated the response of this patient to β-adrenergic blockade with propranolol, and indomethacin, potent inhibitor of prostaglandin biosynthesis. Prostaglandin E₁(PGE₁), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured by radioi mmunoassay. Measured PGE₁ ranged from 10.1 to 25.4 ng/ml and clearly exceeded the normal range for adults of 1. 56 ±0.98ng/ml. Treatment with indomethacin, which decreased plasma PGE₁ level by 73.5 per cent, did not affect blood pressure, significantly. And PRA decreased from 10.1 to 1.8 ng/ml/hr and PAC, from 44.0 to 10.2ng/dl. Serum potassium level and angiotensin sensitivity recovered to normal level with the treatment of indomethacin. Angiotensin II analogue which acted antagonistically before treatment, acted agonistically after treatment as in normal adults. Propranolol suppressed the elevation of PRA and PGE₁, but they remained still over the normal range, and serum potassium level stayed within normal range. These results suggest that the renal salt wasting caused by excessive prostaglandins in this disorder, stimulates the RAA axis and results in secondary hyperaldosteronism. Suppresed prostaglandin synthesis by indomethacin may have a important role on dramatic improvement of clinical features of Eartter's syndrome.

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Blood sugar, serum immunoreative insuliu (IRI), serum C-peptide immunoreactivity (CPR) and plasma pancreatic glucagon (IRG) were determined on intravenous glucose tolerance test and arginine test (infusion of l-arginine (0.5g/kg) for 30 minutes) in 58 patients with chronic renal disorders, whose creatininoe clearance rates (Ccr) ranged from 6.0 to 118.5ml/min. 1) Fasting blood sugar levels were 66 to 102mg/100ml, K values were 0.87 to 5.30%/min, and those were correlated to Ccr (r=-0.355 p<0.01, r=0.467 p<0.001) respectively. 2) Fasting levels of serum IRI, serum CPR and plasma IRG were respectively 3 to 31μU/ml, 1.8 to 9.4ng/ml and 75 to 333pg/ml. CPR and IRG showed remarkably high levels in patients with Ccr below 50ml/min. CPR and IRG were correlated to Ccr (r=-0.606 p<0.001, r=-0.631 p<0.001), though IRI was not correlated to Ccr (r= -0.139) 3) As Ccr decreased, serum IRI showed high response, serum CPR showed delayed and high response, and plasma IRG showed high levels, to the intravenous administration of glucose. XJIRI (60 min) was correlated to Ccr (r=-0.378 p<0.01). 4) As Ccr decreased, plasma IRG showed high response to the infusion of arginine. ΣΔIRG (120min) was correlated to Ccr (r= -0.570 p<0.001) These data suggest that kidney plays a major role in the metabolism of C-peptide and pancreatic glucagon. And it is concluded that function of pancreatic α and β cells is not deteriorated in the patients with severe chronic renal dysfunction, whereas glucose tolerance becomes impaired with the fall of renal function. Furthermore, hyperglucagonemia has an influence on the impaired glucose tolerance in chronic renal dysfunction.

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Serum antibody titers to common enterobacterial antigen (CA) and specific 0-antigen (OA), immunofluorescent localization of CA and histological changes of renal tissues were studied in rats with experimental retrograde E, coli 01 pyelonephritis. Antibody titers to OA (OA-titer) rapidly increased (mean 1 : 80) within the first three weeks after the bacterial injection, followed to decrease to mean level of 1 : 20 in the 4th week, 1 : 8 in the 6th week and 1 : 6 in the 14th week. On the other hand, antibody titers to CA (CA-titers) almost never rose within the first five weeks (mean 1 : 4), and increased to mean level of 1 : 7 in the 6th week, 1 : 11 in the 10th week and 1 : 13 in the 12th week. In the increasing stage of OA-titers, acute pyelonephritis with infiltration of neutrophils and phagocytes in the interstitium and with a large amount of immunofluorescent whole bacterial CA in the renal tissues were found in most of the animals. In a stage when CA titers had not increased yet after the peak of OA-titers, active chronic pyelonephritis with plasmocytic and lymphocytic infiltraion and with whole bacterial or amorphous CA in the interstitial phagocytes, were displayed in most of involved kidneys. In the stage of a decrease of OA-titers and an increase of CA-titers, chronic pyelonephritis was found with PAS-positive epithelioid-like cells, surrounded by plasmocytic and lymphocytic infiltration and contained a large amount of the amorphous antigens. In the stage of reduction of the titers to both OA and CA, chronic pyelonephritis with weak PAS-reactivity and a small amount of amorphous CA was noted. In rats without increase of CA-titers, minimal lesions such as pyelitis, with little or no CA were found in the kidneys. It is concluded that the determination of common antibody titer is significant to the diagnosis of chronic pyelonephritis.

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To clarify the significance of resting PRA as an index of sodium balance in patients under chronic hemopialysis, we studied the resting PRA, sodium balance of the body and the clinical symptoms in 45 hemodialysis patients. Hypotensive drugs were discontinued at least for three months before the test. PRA was measured before (pre-dialysis PRA) and after the dialysis (postdialysis PRA) once a month, Hemodlalysls is performed in a recirculating dialysate supply system of 50 liter capacity, so the sampling of dialysate is easy at the end of the dialysis. “R” is calculatedd as an index of releasability of renin as follows:
(R=post-dialysis PRA/pre-dialysis PRA/removed sodium/removed water×100)
Patients were divided into three groups according to the mean value of resting PRA measured 3 times at monthly intervals: low renin group, 1-9 ng/ml ; normal renin group, 10-29 ng/ml, highh renin group, more than 30 ng/ml. 1) Resting PRA was decreased in accordance with the duration of dialysis and age. 2) R was also decreased in accordance with the duration of dialysis but not with age. 3) The incidence of low, normal and high renin groups were 35.6%, 42.2 and 22. 2, respectively. 4) The systolic blood pressure was not different among the three groups, while the diastolic blood pressure tended to be high in parallel with the renin levels. 5) The characteristics of low renin group was as follows; Both the amounts and concentrations of sodium removed by the preceding dialysis were low, R was low. Intake of sodium was high, age was advanced, long duration of dialysis, and slight degree of organ damage. 6) The characteristics of normal renih group was as follows; All parameters are intermediate between those of low and high renin groups. 7) The characteristics of high renin group was as follows ; Both the amounts and concentrations of rmoved sodium by the preceding dialysis were high, R was highs Intake of sodium was low, young age, short duration of dialysis, advanced organ damage, and hyponatremia. From these results, it seems likely that the resting levels of PRA in chronic dialysis patients are reflecting the state of sodium balance in the body, and renin is contributing to the hypertension, especially to the elevation in diastolic blood pressure in patients belonging to thee high renin group.

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In order to induce chronic renal lesions with secondary hyperparathyroidism, Sodium sulfacetyl thiazole (SAT, 0.15g/kg⋅ body weight) was admihistered intraperitoneally to Wistar male rats, twice a week for four weeks. Renal lesions consisted of interstitial nephritis, dilateted tubular Iumens with atrophied epitheliums and tubular obstructions by sulfocrystals. The SAT-administered rats showed increased levels of BUN and serum phosphate, decresed level of serum calcium and a mild anemic state. Average values of inulin clearance (±S.D.) was 0.37±0.35m1/min which was comparable to one fifth of that of control rats. Fractional excretion of Phosphate was increased and parathyroid glands showed histologically hyperplasia of chief cells. Calcium contents were also increased in the lung, heart, stomach and kidneys. Taken all together, the data suggest that the SAT-induced uremic rats provide an oppropriate model of investigating disturbances of calcium and phosphate in chronic renal disease.

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Renal microinjection experiment was performed to clarify the mechanism of various segments of rat nephron with respect to regulation of urinary potassium excretion. Wister rats were divided into the following four groups. (A) control group (B) high-potassium diet group (G) low-potassium diet group (D) nephron population reduction (N.P.R, ) group. Microinjection of the artificial solutions containing both ⁸⁶Rb and ³H-inulin were performed into the proximal and distal convoluted tubules as well as cortical peritubular capillaries in rats undergoing mannitol diuresis, Excretory patterns of tese substances were analyzed in successive urine sampl-es. ³H-inulin is entirely recovered in the urine of the experimental kidney following the injection into the proximal and distal tubules. 86Rb is an adequate tracer for potassium and is absorbed into the potassium pool from either proximal tubular injections or peritubular capillaries. 86Rb excreted with a time course similar to thar of ³H-inulin is termed as 'direct recovery' and that excreted more slowly, 'delayed recovery', The ⁸⁶Rb recoveries which were obtained after pro-ximal injections were independent of the injection site and averaged 9%. Secretion of ⁸⁶Rb into the urine was stimulated during enhanced K secretion and decreased during reduced K secretion along the distal nephron. Distal tubular injections gave 100% direct recovery in control, high-K diet, and N. P. R. rats. It was apparent that the ⁸⁶Rb recovery was significantly reduced, although not delayed, in animals deprived of dietary potassium for several weeks. At the collecting duct, the extensive net potassium reabsorption is observed in potassium depleted rats, whereas K absorption might be reduced or even secretion is seemingly taking place in potassium loading rats. In conclution, distal convolution and collecting duct play the major role in the regulation of urinary potassium excretion.

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