To investigate the influences of guanine nucleotides on hormone action, effect of guanosine triphosphate (GTP) and its analog, guanylylimidodiphophate [Gpp (NH) p] on the vasopressin-induced osmotic water flow of the toad bladder were studied. The urinary bladders of the toad, Bufo japonicus, were used. Each hemibladder was mounted in a glass chamber. To measure the osmotic water flow volumetrically, Ringer's solution diluted to 1/5 of normal was applied to the mucosal chamber. To make substrate and hormone depletion, the bladders were incubated 14 hours in glucose-free Ringer's solution. GTP enhanced vasopressin-induced osmotic water flow of the toad bladder to 132% the control at the concentration of 1×10^-4M while failed it at 1×10^-5M. Gpp (NH) p could also increase vasopressin-induced water flow at the concentration of 3×10^-4M and Km was 2×10^-6M. However, Gpp (NH) p could not enhance cyclic AMP-induced osmotic water flow. While Gpp (NH) p added to the serosal chamber without vasopressin, no significant change of the osmotic water flow was observed. Adenylylimidodiphosphate [App (NH) p] could not affect vasopressin-induced osmotic water flow. These findings indicate GTP and GTP analog can enhance the vasopressin-induced water flow across the toad bladder membrane, but ATP or ATP analog cannot. Gpp (NH) p could not affect the vasopressin-induced osmotic water flow of the bladder without 14 hours pre-incubation. The present study suggests that guanine nucleotides can stimulate vasopressin-mediated increment of adenylate cyclase activity of the toad bladder in the presence of substrate and hormone depletion.

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Urinary β-D-N-acetylglucosaminidase (NAG) was investigated.I. Analysis of the enzymatic property of the urinary NAG. Urinary NAG was stable at room temperature for about a week, not correlated with the urinary protein or serum NAG concentration, and larger than serum albumin in molecular weight. Its isozyme was different between the serum and urine.II. Investigation of the urinary NAG in various renal diseases in childhood. In nephrotic syndrome, urinary NAG activity was increased higher than 5-10 folds of the normal controls. In acute glomerulonephritis, urinary NAG activity was also increased, but lower than in nephrotic syndrome. Normal NAG activity in orthostatic proteinuria and acute cystitis suggested no existence of pathological lesion in the kidney. In congenital renal tubular disorders, such as hydronephrosis, Fanconi syndrome, bilateral renall hypoplasia or Lowe syndrome, urinary NAG activity was in normal range, but urinary low-molecular proteins, such as lysozyme or β-2-micro globulin were increased. In acquired renal tubular injury, such as Wilson's disease, galactosemia or patients administered with aminoglycosides, urinary NAG was highly increased without urinary protein. These results suggested that urinary NAG did not reflect damaged renal function, but newly added injury to renal tissue, like GOT or GPT in hepatic diseases. In chronic glomerulonephritis, the patients were divided to two groups, those having increased urinary NAG activity, and the others having normal urinary NAG activity. 60% of the former group had improved urinary findings after 20 months, but none of the latter group. So, urinary NAG activity was thought as a good indicator of the prognosis in renal diseases.

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Herein are reported on two cases of renal artery aneurysms in congenital solitary kidneys treated by the different surgical methods; namely in situ and ex situ aneurysmectomy. The first case, 33 year old housewife, survived after rupture of a large non-calcified aneurysm locating at the main artery of her congenital solitary kidney and was transferred to our facility. In situ aneurysmectomy and end-to-end anastomosis of the renal artery was tried but was troubled by dense hematoma embedding the renal hilar region and resulted in mild stenosis of the anastomosic site. However, the patient has been keeping normal renal function and normotension two years postoperatively. The second case; 55 year old housewife had multiple calcified and non-calcified aneurysms locating at the main, first, second and third bifurcation of her congenital solitary kidney with maximum non-calcified one measuring 30 mm in diameter. Besides renal artery aneurysms in solitary kidney, she had other congenital abnormality as uterus bicornus, absent left iliac vein andd two small aneurysms in cerebral artery region. Due to aggravating right backache suggesting urgent rupture of her aneurysms, ex situ aneurysmectomy was performed. After flushing by icecold hyperosmolar intracellular electrolyte solution, five aneurysms were excised and renal arterial tree was reconstructed by angioplastic technique including patchgraft and pair-of-pants anastomosis. Without dividing her ureter, the kidney was transplanted to her right iliac fossa in upsidedown fashion after 6 hours' ischemia. She recovered from transient postoperative acute renal failure and has been doing fairly well one year postoperatively. Several discussions regarding renal artery aneurysm in solitary kidney including associated congenital abnormality and surgical hazards were presented. Ex situ surgery and use of hyperosmolar electrolyte solution were recommended as safe methods of aneurysmectomy in these circumstances.

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This study was performed to analyse recovery process of various complications in chronic renal failure with successful renal transplantation. Twenty patients were treated renal allograft from living donors from March, 1975 to April, 1978. Sixteen patients who have good renal function with the serum creatinine less than 2.5 mg%, were examined in uremic neuropathy, uremic osteodystrophy, anemia, thyroid function test and sweating abnormality before and after renall transplantation. Motor nerve conduction velocity (NCV) was reduced in 7 cases out of 15 before transplantation. All cases expect one, recovered into the normal range in NCV within 2 months, A severely damaged patient took 3 years to normalize in NCV. Serum calcium and phosphate levels became normal within several days after transplantation. Serum alkaline phosphatase became abnormally high between 3 months and one year after transplantation. Accompaniing this finding, the bone uptake of Tc 99 m diphosphonate (Bone scan) became prominent. The recovery from the bone disease took 1 to 1.5 years by bone scan. The rentogenological improvement seems to need more time. There were no improvement of vascular calcification and atherosclerotic change under the observation up to 2 years, The levels of parathormone (PTH) which were high in 5 cases out of 11 before transplantation became normal one day to 3 months after transplantation. Anemia and uremic skin color were recovered between 1 and 3 months after transplantation. Thyroid function tests which were performed before transplantation, were compatible with subclinical hypothyroidism. Free thyroxine indices which were in the low normal range before, went up in the middle of the normal range within 1-6 months after transplantation, Disturbed perspiration became normal within one to 3 months. These data indicate that early transplantation is recommended if a patient has uremic neuropathy, osteodystrophy, vascular calcification and/or atherosclerotic changes, because of the retarded or irreversible recovery from them with successful renal transplantation.

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It was found that Masugi nephritis induced in cholesterol-fed rabbits was characterized by accumulation of foam cells in glomeruli. In order to investigate the origin of these foam cells, electron microscopic observations of glomerular lesions were performed. Prior to the experiment, 9 rabbits were fed a diet containing 0.5% cholesterol for 4 weeks. The serum cholesterol level ranged from 450 to 690 mg/dl at the beginning of the experiment. The animals were maintained on the same diet during the subsequent experiment. Masugii nephritis was induced in 7 animals by single intravenous injection of 2 ml of nephrotoxic duck serum and the remaining two were used as controls. Kidney specimens were obtained by either surgical biopsies or autopsies at different stages from 6 to 28 days after injection of nephrotoxic serum. The results obtained were as follows: 1. The number and extent of glomerular foam cells roughly paralleled the natural course of Masugi nephritis. At the peak of the disease, they were seen not only in the glomeruli but also in extracapillary portions forming crescents. They disappeared when glomerular lesions were subsided. 2. Foam cells were apparently derived from migrant blood monocytes and mesangial cells with a wide variety of intermediate forms. Monocytic foam cells were seen in the capillary lumens as well as in the subendothelial space and mesangium. They often migrated in Bowman's space at the peak of the disease. Furthermore, they transformed into multinucleate giant cells including Touton type's. 3. There was no evidence that endothelial cells underwent a transformation into foam cells. 4. Lipid deposits filling the cytoplasm of foam cells seemed to be in two forms, free cytoplasmic droplets and membrane-bounded structures containing debris. The latter developed later preferentially in the central portion of the cytoplasm and were considered to be originated from lysosomes. 5. It seemed unlikely that glomerular lesions in Masugi nephritis were aggravated by foam cell accumulation. Foam cells were most probably a reflection of systemic hyperlipemia in the kidneys with active glomerular damage.

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Renal tissue from 39 SLE patients (diagnosed as having satisfied ARA criteria for SLE) without overt clinical nephropathy before and at the time of renal biopsy were examined histologically. They were classified into 5 types including minimal change (MC), focal proliferative GN (FGN), diffuse proliferative GN (DPGN), membranous GN (MGN) and membranoproliferative GN (MPGN). Thirty SLE patients with MC or FGN were divided into two groups. They were the patients with and without the appearance of abnormal urinalysis after renal biopsy. Nine patients with DPGN, MGN or MPGN associated with no overt clinical nephropathy did not have abnormal urinalysis until the time of last observation. Comparative and follow-up studies of the clinical and immunological findings these groups were done. The SLE patients with abnormal urinalysis after renal biopsy had significantly more hypo-complementemia and high titers of anti-native DNA antibodies at the time of the appearance of abnormal urinalysis than the patients without abnormal urinalysis. The appearance of abnormal urinalysis in MC and FGN did not seem to relate the initial and maintenance dosage of steroids. The frequency of the appearance of abnormal urinalysis was 80.0% after 4 years follow-up in the patients with hypocomplementemia and 62.8% after 3 years follaw-up in the patients with high titer of anti-DNA antibodies. Continuous normalization of complement level by steroids therapy seemed to be able to prevent the appearance of abnormal urinalysis. It may connect to prevent the progression of glomerular lesion from MC or FGN to DPGN, MGN or MPGN.

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Recently, the number of casereports on "chronic polyneuropathy with skin hyperpigmentation, hypertrichosis, edema and abnormal immunoglobulins" has increased to be more than fifty in Japan. Although decreased renal functions were found in many cases, there were a few precise reports with special reference to the renal lesion. We experienced two cases of this syndrome. The renal biopsy revealed characteristic membranoproliferative glomerulonephritis in both cases.[Case 1] A 45-year-old man was admitted to the hospital because of edema and sensory distur-bance of both legs. The urine protein was 37 mg/dl, BUN 39.3 mg/dl, Cr 1.7 mg/dl, GFR 41.0 ml/ min, and RPF 312.2 ml/min. [Case 2] A 62 year-old-man was admitted to the hospital with a chief complaint of gait disturbance and numbness of upper and lower limbs. The urine protein was negative, BUN 27.9 mg/dl, Cr 1.6 mg/dl, GFR 62.0 ml/min and RPF 204.9 ml/min. There was no Bence-Jones proteinuria and immunoelectrophoresis showed a slightly increased 1gM and no M-component in both cases. [Renal histopathological findings] The glomerular changes were highly characteristic with a close similarity between the two cases. There were increases in the number of mesangial cells and the amount of mesangial matrix. The mesangial proliferation gave the impression of the lobular pattern. The capillary walls were thickened and showed a double contour with PAM stains. The circumferential mesangial interposition was confirmed by electronmicroscopy and collagen like material was observed along the thickened glomerular basement membrane. There was no specific glomerular fluorescence for lgG, A, M, E, light chain (kappa, lambda), Clq, C3, C4 and fibrinogen in either case.

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A wide varieties of patients with renal diseases characterized by clinical and pathological observations were studied for the distribution of C3b receptor: chronic proliferative glomerulonephritis (C.P.G.N.) 43 cases, acute poststreptococcal glomerulonephritis (A.G.N.) 9 cases, membranoproliferative glomerulonephritis (M.P.G.N.) 6 cases and membranous nephropathy (M. N.) 2 cases. In addition, 6 cases of systemic lupus erythematosus (S.L.E.) and 2 cases of acute renall failure (A.R.F.) were also studied. Control subjects comprised 6 healthy kidneys.The results were as follows: 1) It was found that EAC3b was specifically fixed to glomeruli in normal kidney, confirming the existence of C3b receptor in normal glomeruli. 2) In C.P.G.N. group, the staining pattern with C3 was grouped into four classes, i.e. G.B.M. pattern, mesangial pattern, combined pattern and negative on immunofluorescent microscopy. The population of C3b receptor tended to be decreased more drastically in the G.B.M. pattern than in the mesangial pattern. 3) In C.P.G.N. group, the patients were classified into three groups on light microscopy: (a) those in mild P.G.N., (b) moderate P.G.N. and (c) advanced G. N. Generally, many cases of advanced G. N. group tended to exhibit the more decreased staining of C3b receptor than those of mild P.G.N. group. 4) The number of C3b receptor was decreased especially in patients with M.P.G.N., A. G. N. and M. N. 5) The prosperity and decay of glomerular C3b receptor may play on important role in the deposition of C3 to G.B.M. and glomerular injury. Moreover, it is reasonable to consider the influences of steriod and immunosuppressive drugs on the staining of glomerular C3b receptor in our study. Further studies will be needed to establish the precise role of C3b receptor in the pathophysiolgy of renal diseases.

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