This study investigated the effects of exercise intensity on renal hemodynamics. Three healthy male subjects underwent exercise tests on a bicycle ergometer at 7 different work loads for 15 min. The indicators of exercise intensity employed in this study were the percentage of maximal oxygen uptake (%VO₂max) and percentage of ventilatory threshold (%VT). As renal clearence parameters, para-aminohippurate clearance (C_PAH) and inulin clearance (C_IN) were measured by the continuousinfusion technique. Indicators of renal hemodynamics during exercise were the percentage of C_PAH, C_IN and filtration fraction (FF) at rest. Plasma norepinephrine (NE), plasma epinephrine (E) and plasma renin activity (PRA) were measured. The best regression models between renal clearance parameters and exercise intensity were selected using Akaike's information criterion (AIC). 1) The renal clearance parameters used during exercise were %C_PAH, which determined the cubic regression model and %C_IN, which determined the quadratic regression model as the exercise intensity increased using AIC. 2) The percentage of maximal oxygen uptake at the onset of decrease in %C_PAH and %C_IN were 35 and 49%VO₂max, respectively, while %C_PAH and %C_IN began to decrease at 75 and 105% VT, respectively. Intensity of exercise at the onset of increase in %FF was 49%V0₂max or 106%VT. 3) The renal clearance parameters during exercise decreased linearly as NE, E and PRA increased. The increase in NE contributed mainly to a change in renal clearances shown by multiple regression analysis. The above results suggest that the relationship among renal plasma flow (RPF), glomerular filtration rate (GFR) and exercise intensity were demonstrated by the cubic regression model and quadratic regression model using AIC, respectively. Glomerular filtration rate and FF were main tained at the resting levels during aerobic exercise.

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Although disorders of renal calcitriol synthesis play an important role in the pathogenesis of secondary hyperparathyroidism in the early and moderate phase of chronic renal failure, the treat ment of secondary hyperparathyroidism with vitamin D metabolite has not attained consensus from the view point that is accelerates the progression of renal disease. The aim of this study was to evaluate the efficacy and adverse effect of low-dose daily oral treatment of 1.25 vitamin D for patients with mild to moderate renal failure. Fifteen chronic renal failure patients with serum creatinine ranging from 2.5 to 6.1 mg/dl and serum intact parathyroid hormone ranging from 100 to 450 pg/ml, were treated with oral 0.25-0.5μ g of 1.25 vitamin D for six months, after a six month control periods. In the six months control periods, serum intact parathyroid hormone, alkaline phosphatase activity, and bone gla protein increased significantly, however after the treatment of 1.25 vitamin D, serum intact parathyroid hormone, alkaline phosphatase activity, and bone gla protein decreased signifi cantly. Serum calcium concentration increased significantly after the initiation of 1.25 vitamin Dtreatment, so it could not be ascertained whether or not 1.25 vitamin D directly suppressed parathyroid hormone synthesis. Bone mineral densities did not change within one year. Renal function was evaluated from the slopes of the reciprocal serum creatinine concentration versus time. The slopes did not change after the administration of 1.25 vitamin D In conclusion, 1.25 vitamin D treatment of secondary hyperparathyroidism in patients with mild to moderate renal failure had beneficial therapeutic effect on humoral bone parameters, and did not show any adverse effect on renal function.

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In order to clarify the relationship betweeen vasoactive substances and changes in blood pressure (BP) during hemodialysis (HD) in patients with end-stage renal disease, we measured plasma renin activity (PRA), plasma concentration of aldosterone (PAC), and the plasma concentrations of epi nephrine (E), norepinephrine (NE), dopamine (DA), and atrial natriuretic peptide (ANP) in patients on HD. Fourty-eight patients, consisting of 24 males and 24 females, were included in this study. Their mean age was 63.8 years, and their mean HD duration was 55.9 months. In 9 patients without diabetes mellitus (DM) and whose BP was stable during HD, PRA and plasma concentrations of E and NE increased significantly during HD, and that of DA decreased during HD. In 9 patients without DM and whose BP fell during HD, PRA and plasma concentrations of E and NE showed no significant response to the decrease in body weight during HD. In spite of the increase in NE concentration during HD in 8 patients without DM and whose BP was usually hypotensive, BP remained low. This might be due to the decrease in sensitivity of their peripheral autonomic receptors to NE. In the 9 patients with DM whose BP was stable and 13 patients with DM whose BP fell during HD, vasoactive substances made almost no effective response to the decrease in body weight during HD. In conclusion, we must take into consideration the fact that both hypotensive patients during HD and diabetic patients on HD might exhibit an abnormal response of their vasoactive substances.

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IgA 1 is an exceptional serum glycoprotein because it has O-glycans in the hinge region . It has been observed that the monocyte/macrophages infiltrarte within the glomeruli in IgA-N . On the other hand, it is well established that the carbohydrate side chains (N-glycans) of the IgG molecule play a role in the binding of IgG to Fc receptors. Therefore, the binding of IgAl to monocyte/macrophage cell lines was observed with the aim of clarifying the role of the O-glycan side chains in IgA-N in the initial mechanism of glomerular damage due to the interaction between the O-glycan chains on the IgA 1 molecule and infiltrating monocyte / macrophages. Two human myelomonocytic cell lines, THP-1 and U-937, were activated and incubated with separated IgA 1 (IgA-N, n =16; other glomerulonephritides (other GN), n=15; healthy controls, n=9). The binding attitude of IgAl to the cell lines was observed by flow immunofluorometry using a FACScan. FACScan showed that the binding of IgA 1 to both of the stimulated monocyte/ macrophage cell lines was increased in IgA-N compared to the normal controls and other GN. The binding of IgAl to THP-1 was partially, but definitely inhibited by adding 100 mM melibiose (19.6±7.7%) and galactose (13 .1±2.9%), but not glucose (2.9±2.2%), lactose (4.7±4.7%) and mannose (3.3±3.3%). These results suggested that THP-1 had a receptor that recognized the O-glycan in the IgA 1 hinge region. To establish that the binding between monocyte/macrophage cell lines and the IgA 1 molecule is a specific phenomenon that occurs through IgA receptors, the change of [Ca²⁺] i level of stimulated THP-1 cells on addition of IgAl was observed. The [Ca²⁺] i level of stimulated THP-1 was distinctly increased 10 to 20 seconds after the addition of IgAl. This indicated that the binding of IgA 1 to the cells observed by FACScan was specific, and that the calcium-mediated intracellular signal transduction was definitely evoked due to the binding of IgA 1 to the cells. These observations may explain the possible role of O-glycans in the IgAl hinge region for mediating the binding of the IgAI molecule to infiltrating monocyte/macrophages, resulting in the initiation of the mechanism (s) causing glomerular damage .

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It is well known that blood access is essential for long-term hemodialysis treatment. Arteriovenouos fistula (AVF) is the most widely used method. However, this method of access frequently fails (access failure) as a result of stenosis. We attempt simple femoral vein puncture (FV-method) instead of AVF in such patients and have experienced 12 patients who were undergoing hemodialysis treatment using the FV-method, three times a week for more than one year. We devised special needles (18- and 19-gauge) for the FV-method. Generally, we use a 19-gauge needle with 4 side holes. We discuss here the results of 12 patients consisting of 4 males and 8 females with a mean age of 57.9 years, a mean duration of dialysis of 10.0 years, and a mean duration of FV-method of 3.5 years. Their underlying diseases were chronic glomerulonephritis (9 patients), diabetic nephropathy (2 patients) and nephrosclerosis (1 patient). Before the use of the FV-method, AVFs were attempted a mean of 3.8times and an artificial graft, 4 times in 3 patients. Ten patients were outpatients and 2 were inpatients. As for the indications of the FV-method, 11 patients had access failure and another had suffered from heart failure resulting from an over flow of blood through AVF. KT/V, PCR and TACBUN were measured monthly and were within the normal range in almost all of the patients. Concerning complications of the FV-method, hematoma formation after detachment of the needle at the end of dialysis and pain at needle puncture were sometimes noted. Furthermore, the clinical course of a dialysis patient using the FV-method for about 10 years without any problems is presented. From these results, it is obvious that the FV-method for blood access is nearly equivalent to AVF for performing long-term hemodialysis treatment.

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We investigated the clinical features and outcome of 14 patients with anti-myeloperoxidase antibody (MPO-ANCA) positive rapidly progressive glomerulonephritic syndrome. Underlying disaeses included microscopic polyarteritis in 6 patients, idiopathic crescentic glomerulonephritis with lung hemorrhage in 2 patients, idiopathic glomerulonephritic in 3 patients, rapidly progressive glomerulonephritic syndrome without renal biopsy in 1 patient, crescentic glomerulonephritis associatedwith Sjogren syndrome and progressive systemic sclerosis in 1 patient and crescentic glomerulonephritic associated with sarcoidosis in 1 patient. Five patients were male (mean age, 59.2 years) and 9 were female (mean age, 54.0 years). On admission, most patients had anemia, leukocytophilia, and marked elevation of C-reactive protein (CRP). Average hemoglobin, white blood cell count and CRP levels on admission were 8.1 mg/dl, 11, 500 / mm³ and 14.7 mg/dl, respectively. Average serum creatinine was 4.0 mg/dl. All patients were treated with steroids either with or without cyclophosphamide. As the patients recovered clinically, the MPO-ANCA titers declined. Although most patients responded well to immunosuppressive therapy, some died of serious complications (such as acute respiratory distress syndrome, fungal infection, and pneumocystis pneumonia). The prognosis of patients with severe renal failure was especially poor. We conclude that early diagnosis, treatment and intensive care during immunosuppressive therapy are very important in the managment of MPO-ANCA-positive rapidly progressive glomerulonephritis.

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In order to clarify endocrinological changes before and after living-related renal transplantation in a patient of Bartter's syndrome involving chronic renal failure, serial quantitative determinations of the renin-angiotensin-aldosterone system and 24-hour urinary excretion of 6-keto-prostaglandin F_lα and kallikrein were performed. A male patient was admitted to hospital because of a pale face and short stature at the age of 13 years. He was 126 cm in height (M-3.8SD). Blood pressure was 110/60 mmHg and edema was not observed. Laboratory findings showed that his hematocrit was 22.1%, serum potassium 2.9 mEq/ 1, creatinine clearance was 30.7 ml/min/ 1.73m² and, β₂-microgobulin was elevated to 39.9 mg/l in urinalysis. Plasma renin activity and aldosterone were remarkably elevated to 24.23 ng / ml / hr and 738 pg / ml, respectively. The kidney biopsy specimen showed diffuse glomerulosclerosis and hypertrophic change of the juxtaglomerular apparatus was also demonstrated. He was diagnosed as Bartter's syndrome with short stature and chronic renal failure. At the age of 18, he was introduced on hemodialysis and the living-related renal transplantation was performed the next year. Two weeks after the transplantation, plasma renin activity, angiotensin, I, II and aldosterone were markedly changed from 37.8 to 2.3 ng/ml/hr, 2400 to 220 pg/ml, 256 to 17 pg/ml and 3700 to 110 pg / ml, respectively. Urine prostaglandin F _1α was improved from 860 to 321 ng / day and kallikrein was also changed from 400 to 25.2 μg/day. These results indicated that abnormalities of several hormones in Bartter's syndrome could be normalized by living-related renal transplantation. It can be deduced that the kidney plays an important role in endocrinological pathogenesis of this syndrome.

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We report here two cases of mixed cryoglobulinemia showing renal involvement associated with hepatitis C virus (HCV) infection. The subjects were 62-and 63-year-old males. Both patients presented with purpura on the legs, which was diagnosed as allergic vasculitis by skin biopsy. Case 1 followed a clinical course of progressive nephrotic syndrome with mild hematuria. He also had diabetes mellitus and hypertension. In contrast, case 2 showed only mild hematuria without proteinuria at the time of the renal biopsy. Both cases had immunological disarrangements, such as severe hypocomplimentemia and seropositive rheumatic factor. Recently, it was reported that patients with type II mixed cryoglobulinemia had HCV seropositivity, and revealed membranoproliferative glomerulonephritis. These facts strongly suggested that renal lesions are the result of direct damage mediated by cryoglobulinemia and an activated complement pathway through an immune complex mechanism related to HCV.

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A 68-year-old male patient with renovascular hypertension (RVHT) and nephrotic syndrome (NS) is described. He was admitted to our hospial for detailed investigation of severe hypertension and massive proteinuria. After asmission, a diagnosis of RVHT with a right nonfunctional kidney and NS was made. Nephrectomy and contralateral renal biopsy were performed for refractory hyperten sion and detailed investigation of the NS, respectively. The renal biopsy showed focal segmental glornerulosclerosis (FGS) in the left kidney, whereas the nephrectomised kidney exhibited only ischemic change. After the operation, his blood pressure became stable without anti-hypertensive agents, but proteinuria remained in the nephrotic range. Six months later, proteinuria had disappeared and his renal function was stable. These findings suggest that NS and FGS might have resulted from an activated renin-angiotensin-axis and that the prolonged NS was due to severe glomerular injury. Although there have been many reports describing the relationship between RVHT and FGS in an experimental environment, this relationship is very rare in clinical cases. Therefore we present this case to increase understanding of the cause of FGS.

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