著者

山家 敏彦 張 光哲 赤池 真 露木 和夫 野村 正征 長谷 弘記 海老根 東雄

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.26, no.4, pp.399-406, 1984 (Released:2010-07-05)

参考文献数

24

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In eight chronic hemodialysis patients, the effects of 7.4±2.6 months of exercise training on hemodialysis-induced hypotension and subjective complaints during hemodialysis therapy were studied. The evaluation was obtained through (1) comparing the exercise tolerance, dry weight, cardio-thracic ratio, hematocrit level, hemoglobin level, BUN level, serum creatinine level before and after training, (2) comparing frequency of hemodialysis-induced hypotension, frequency of normal saline infusion during hemodialysis therapy, and subjective complaints during hemodiolysis therapy before and after training. Exercise training resulted in increase in maximal oxygen consumption from 19.17±4.22 ml/kg/min. to 21.52±4.94 ml/kg/min. (p<0.05), in increase in hematocrit level from 22.1±4.2 % to 25.2±4.8 % (p <0.01), and in increase in hemoglobin level from 7.7±1.0 g/dl to 8.4±1.5 g/dl (p<0.05). With exercise training, the frequency of hemodialysis-induced hypotension decreased from 30.5 % to 12.9 % (p<0.05), frequency of normal saline infusion during hemodialysis therapy decreased from 34.5 % to 14.3 % (p<0.05), and frequency of complaining palpitation decreased from 5.2 % to 0.0 % (p <0.05). The decreased frequency of hemodialysis-induced hypotension, normal saline infusion, and complaining palpitation through exercise training may be due to improvement of peripheral circulation and/or increased hematocrit level. These findings suggest that subjective complaints, which are caused by hemodialysis-induced hypotension, will be decreased by exercise training.

著者

SUMIKO HOMMA NAOKI MURAYAMA TATSUHIKO KODAMA NOBUHIRO YAMADA KEIICHI TAKAHASHI YASUSHI ASANO SAICHI HOSODA TOSHIO MURASE YASUO AKANUMA

出版者

Japanese Society of Nephrology

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.35, no.8, pp.999-1006, 1993-08-25 (Released:2010-07-05)

参考文献数

30

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To study the metabolic abnormalities in familial lecithin-cholesterol acyltransferase (LCAT) deficiency, the effects of a long-term, low-fat diet and LCAT replacement therapy on plasma lipids and apolipoproteins were investigated in a patient with LCAT deficiency. The patient had elevated triglycerides (TG, 543.7 mg/dl) and phospholipids (PL, 350.3 mg/dl) and normal total cholesterol (TC, 206.9 mg/dl). Change to a low-fat diet reduced TC and TG by 20% and 75%, respectively. These reductions occurred mainly in the d<1.006 fraction. At baseline, the patient had normal apolipoprotein B (apo B), low apolipoprotein A-I (apoA-I) and apolipoprotein A-II (apoAII) and elevated apolipoprotein E (apo E). Long-term treatment with a low-fat diet increased plasma apoA-I and decreased apo E. However, urinary protein excretion did not change throughout the observed period. LCAT replacement with fresh frozen plasma (FFP) after the low-fat diet further reduced plasma apo E to the normal range. These results indicate that the elevated plasma apo E in LCAT deficiency was related not only to the lack of LCAT in the plasma, but also to fat intake. A low-fat diet may be effective in correcting lipid abnormalities. Moreover, plasma apo E may be a good indicator of the efficacy of diet therapy.

著者

小田 寿 高木 信嘉 常田 康夫 矢花 真知子 金子 好宏

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.30, no.2, pp.221-225, 1988-02-25 (Released:2010-07-05)

参考文献数

20

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It has been reported that rifampicin attenuates an effect of corticosteroid. We observed nonresponsiveness to prednisolone treatment during rifampicin administration in a case of adult nephrotic syndrome. A 21 years old man had the onset of facial edema and ascites in and was diagnosed as nephrotic syndrome (minimal change) at a certain hospital. He was treated with prednisolone and obtained complete remission. He had the complaint of chest pain in May 1984, and was transfered to our hospital. We diagnosed him as nephrotic syndrome and tuberculous pleuritis. We administered him isoniazid 300 mg/day, rifampicin 450 mg/ day, streptomycin 3 g/week and prednisolone 30 mg/day. His urinary protein was not decreased. Subsequently, we administered him predonisolone 60 mg/day. But his urinary protein was not changed. We thought that rifampicin might attenuate the effect of pre-dnisolone. After rifampicin was discontinued, urinary protein was decreased rapidly. He obtained complete remission and was discharged from our hospital. It was reported that a patient with Addison's disease required increased corticosteroid dosage whilst receiving rifampicin and had cortisol catabolism following hepatic microzomal enzyme induction by rifampicin. Our case of nephrotic syndrome showed the nonresponsi-veness to prednisolone treatment during rifampicin administration. The corticosteroid is essential to treatment of nephrotic syndrome and collagen disease, and rifampicin is an important drug in treatment of tuberculosis. We should pay attension to drug interac-tion between corticosteroid and rifampicin in the cases with combination of these drugs.

著者

武田 朝美 両角 國男 打田 和治

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.46, no.7, pp.661-666, 2004 (Released:2010-05-18)

参考文献数

10

著者

椿原 美治 飯田 喜俊 湯浅 繁一 河島 利広 中西 功 横川 朋子 友渕 基

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.24, no.10, pp.1127-1136, 1982-10-25 (Released:2010-07-05)

参考文献数

30

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Borah, et al, demonstrated that HD is a severe catabolic stress to N-metabolism. EAA loss during HD has been speculated as a stress. In order to study this mechanism, AMIYU® (contained 8 EAA and His. 7% solution, Morishita Pharm. Co. Ltd., ) was infused into venous line throughout 5 hrs. HD with the speed of 40 ml/hr. (study A) and during the last 1 hr. of 5 hrs. HD with the speed of 200 ml/hr. (study B) . The time courses of urea generation rate (Gu.), aminogram and N-balance were compared among control, study A and study B-HD. There were no significant changes in EAA level during control HD suggesting that EAA loss was replacedd by protein catabolism. Gu. (mg/min) during 4 hrs, after control HD (20.1±1.2) was significantly higher than predialysis value (4.7±0.1), indicating the catabolic stress due to HD. Gu. after study A-HD (17.3±1.3) was significantly lower than that after control HD. But Gu. after study B-HD (23.0±0.9) was significantly higher than that after control. HD. This shows that the high dose of EAA administered during the last 1 hr. of HD is not lost into dialysate but is degradated to urea about a half because the last 1 hr, in 5 hrs. HD may be already the catabolic phase. N-balance was -3.6±0.8 (g/day) on control HD day and improved by EAA supplementation throughout HD (-2, 1±0.8). Plasma total. EAA and nonEAA levels significantly increased during 4 hrs. after control HD, suggesting that amino acids were supplied through protein degradation. But in study A, plasma total nonEAA level significantly decreased during HD, indicating that protein catabolism was suppressed by EAA supplementation throughut HD. From these results, HD itself is shown to be the strong catabolic stress to N-metabolism. The rapid decrease in plasma EA.A level due to EAA loss during HD would be one of this factor. The low dose administration of EAA throughout HD is considered to be not only replace the EAA loss, but also suppress this catabolic stress.

著者

長江 明宏 住元 巧 関谷 達人 日和田 邦男 国府 達郎

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.31, no.4, pp.379-383, 1989-04-25 (Released:2011-03-01)

参考文献数

14

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This study analyzed by high performance gel permeation chromatography (HPGC) molecular forms of atrial natriuretic peptide (ANP) in plasma from anesthetized dogs stimulated by balloon inflation at the main pulmonary artery (Group A, n=4), right atrial pacing (Group B, n=4) and low-molecular dextran injection to right atrium (Group C, n=4), Mean pulmonary arterial (PA) pressure, mean right atrial (RA) pressure, mean arterial pressure, heart rate and ECG were monitored by polygraph system Mean PA pressure in Group A, heart rate in Group B and mean RA pressure in Group C increased significantly by the stimulation (p<0.01, p<0.001 and p<0.05 respectively). Other parameters were not changed significantly in the three groups. There were significant increases in ANP concentration after the three stimulations (Group A : 52.4±5.4 (SD) pg/ml→86.4±12.2 (SD) pg/ml, Group B e 43.8±6.7 (SD) pg/ml→72.0±14.1(SD) pg/ml, Group C : 42.7±8.8 (SD) pg/ml→69.3±10.0 (SD) pg/ml; each p<0.01). Gel filtration profiles showed that the increased form of plasma ANP in the three nrouos was α-ANP. These results suggest that α-ANP may be a main molecular form in plasma from dogs stimulated by the stretch of pulmonary arterial wall and right atrial wall, and atrial pacing.

著者

森 頴太郎 荘野 忠泰 井原 元 岩崎 徹 平林 俊明 依藤 良一 宮本 孝 稲垣 王子 井上 聖士 藤田 嘉一

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.26, no.6, pp.721-731, 1984 (Released:2010-07-05)

参考文献数

25

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The ACTH-Cortisol axis was studied in chronic renal failure (12 undialysed patients, Ccr below 5 ml/min and 17 dialysed patients). Basal plasma cortisol and ACTH levels were 14.7±1.2μg/dl, 41.4±11.6 pg/ml respectively in undialysed patients and 14.3±1.3μg/dl, 48.6±7.5 pg/ml respectively in dialysed patients. Both hormone levels were within normal range except 1 dialysed patient. The cortisol levels to rapid ACTH stimulation test (250μg ACTH, iv) in both groups increased approximately 10 μg/dl or more. Therefore, we suggest that the patients with chronic renal failure have normal function of adrenal cortex. After the administration of 1 mg dexamethasone orally at midnight as the method of examining negative feedback mechanism, both patients had normal or almost normal suppression of cortisol and ACTH level. But, quarter of patients in each group demonstrated abnormal diurnal rhythm of plasma cortisol and ACTH at 900 hour, 1700 hour. Dialysed patients showed normal cortisol response (Max. ΔCortisol 12.8±1.6μg. dl) to insulin (0.1 U/kg, iv) induced hypoglycemia as a stress test compared with normal controls (Max. ΔCortisol 9.0±0.8 μg/dl). While, undialysed patients showed low cortisol response (Max. ΔCortisol 5.9±1.7μg/dl). And there were no correlation between the Max. ΔCortisol and T. P., BUN, CRN, Uric Acid, Ca and the grade of hypoglycemia. Therefore, it is certain that the failure of secretion of corticotropin releasing factor in hypothalamus or of ACTH secretion in pituitary gland exists in undialysed patients. From these results that there may be impairment of CNS-Hypothalamo-Pituitary Axis in chronic renal failure and this disturbance can be recovered considerably but not perfectly by adequate long term hemodialysis, it was considered that some uremic toxin or dialysable substance associated with uremia itself may be responsible for its abnormality of cortisol and ACTH secretion.

著者

舟生 富寿 工藤 茂宣 大野 和美 二川原 和男 人見 浩 鈴木 唯司 三国 恒靖 寺山 百合子 青木 敬治 平山 順朗 小野寺 孝夫 菅原 茂

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.17, no.9, pp.823-836, 1975-09-30 (Released:2010-07-05)

参考文献数

34

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Metabolism of adrenocortical hormone in patients with chronic impaired renal function was investigated in this study. Urinary 17-OHCS (total, free and fractions-com. F, comp. E, THF, THE) we(re measured by use of thin layer in these 12 patients, including 6 patients who were made to artificial dialysis. Three patients of them were studied on load with ACTH-Z 20 units/day for 3 days intramuscularly and 9 patients were studied on administration of cortisol (1 mg/kg of body weight) intra-venously. Moreover, blood free 11-OHCS was determined in 3 patients with treatment of artificial dialysis. Following results were obtained. 1) The excretion volume of urinary total 17-OHCS remained low coincidently with decrease in creatinine clearance on control, on load with ACTH-Z and on administration of cortisol. 2) In above mentioned patients, the rate of urinary free 17-OHCS to total 17-OHCS exhibited various values which may be influenced with glomerular and tubular lesion, being compared with certain values of normal control. 3) The fractions of urinary 17-OHCS showed small pattern similar to normal control. 4) The excretion pattern of urinary 17-OHCS fractions shifted to cortisol pathway from cortisone pathway on load with ACTH-Z as normal control. 5) In the group with non-hyper BUN, the changes of the excretion volume of urinary 17-OHCS was seemed to be similar to normal control in every 2 hours measurement on administration of cortisol, while in the group with hyper BUN, the changes was not observed. 6) In the patients with artificial dialysis free 11-OHCS remained within normal range but showed abnormal in diurnary variation.

著者

鈴木 久雄

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.37, no.10, pp.534-542, 1995 (Released:2011-07-04)

参考文献数

30

被引用文献数

1

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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 (CPAH) and inulin clearance (CIN) were measured by the continuousinfusion technique. Indicators of renal hemodynamics during exercise were the percentage of CPAH, CIN 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 %CPAH, which determined the cubic regression model and %CIN, 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 %CPAH and %CIN were 35 and 49%VO2max, respectively, while %CPAH and %CIN 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.

著者

朝倉 伸司 照喜名 重治 加藤 謙吉 瀧 滋彦 浅野 泰

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.29, no.11, pp.1443-1452, 1987

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Rats with puromycin-aminonucleoside (PAN) induced nephrosis (PAN rats) exhibit disruption of the components of the GBM, visceral epithelial glycocalyx, loss of podocyte pedicles, and degeneration of renal tubules. NAG activity and proteins in urine were assayed to evaluate the degree of renal tubular damage in PAN rats. PAN nephrosis was induced in male wistar rats weighing 150 g, with the cutaneous injection of 0, 5 mg/100 g Ba W. PAN for 7 days. The NAG activities in urine and renal tissue were assayed by MCP-NAG methods. Urinary protein was analyzed by SDS-PAGE. Urinary NAG activity significantly increased from the 5th day with its peak on the 14th day. The NAG activity was detected not only in the cortical tissue but also in iso-lated glomeruli The NAG activity in renal tissue was decreased from the 2nd to 4th weeks after PAN injection as compared with that in the normal control rats, However, the activity was recovered to the normal control level by the 9th week, The major component in the urinary proteins of PAN rats was albumin in the majority of the rats, but in several rats, low molecular weight proteins (37 K, 52 K daltons) were detected as the major components in the early stage after PAN injection, Chemical analysis of these low molecular weight proteins were performed, Immunoblotting indicated that these proteins were also found in the serum, However, the following evidence indicates that these proteins are apparently derived from renal tissue: 1) Very small amounts of these proteins are found in the blood. 2) In the urine of some rats, these proteins were found at higher levels than albumin. 3) These proteins are also found in renal tissue.Further investigation is necessary to characterize these proteins.

著者

河合 浩

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.28, no.8, pp.1151-1160, 1986 (Released:2010-07-05)

参考文献数

26

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It is known that renal blood flow is reduced after clamping of the renal artery. But there are few studies of renal blood distribution after ischemia and its mechanisms are still poorly understood. Changes of renal blood distribution were studied in dogs using a four channel hydrogen gas electrode before and after one hour ischemiao In the same experiment alternation of catecholamine content (noradrenaline, adenaline and dopamine) in the renal tissue were examined electrochemically with a high-pressure liquid chromatographic technique. In each expriment the renal tissue was divided into four areas: cortex, juxtamedullary cortex, outer medulla and inner medulla.1) Before ischemia, blood flow was high in the cortex, juxtamedullary cortex and outer medulla as compared with the inner medulla.2) After ischemia, blood flow was decreased significantly in the cortex and juxtamedullary cortex, but only moderately in the outer medulla and inner medulla3) Before ischemia, the noradrenaline concentration was high in the cortex, juxtamedullary cortex and outer medullae But the inner medulla contained very little noradrenaline. The adrenaline and dopamine concentrations were low as compared with the noradrenaline except in the inner medulla.4) After ischemia, the noradrenaline concentration was elevated significantly in the cortex, juxtamedullary cortex and outer medulla. The adrenaline and dopamine concentrations were not altered in any regions.5) It is concluded that noradrenaline may have an effect on the intrarenal hemodynamic changes after ischemia as a causative factor.

著者

伊藤 貞嘉 阿部 圭志 尾股 健 保嶋 実 吉永 馨

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.30, no.1, pp.85-90, 1988

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To examine the role of prostaglandins (PGs) in the macula densa mechanism of renin release, rabbit afferent arteriole (Af) alone and afferent arteriole with macula densa attached (Af+MD) were microdissected and incubated consecutively. Hourly renin release rate from a single Af (or Af+MD) was calculated and expressed as ngAI&middot;h<SUP>-1</SUP>&middot;Af<SUP>-1</SUP> (or Af+MD<SUP>-1</SUP>)/h (where AI is angiotensin I). Basal renin release rate from Af was 0.84&plusmn;0.14ngAI&middot;h<SUP>-1</SUP>&middot;Af<SUP>-1</SUP>/h (X&plusmn;SEM, n=23) and remained stable throughout the incubations. Basal renin release rate from Af+MD was 0.33&plusmn;0.04ngAI&middot;h<SUP>-1</SUP>Af+MD<SUP>-1</SUP>/h (n=17), which was significantly lower (p<0.01) than that from Af. When furosemide (1.5 mM) was added to Af, no significant change in renin release rate was observed. However, when furosemide was added to Af+MD, renin release rate increased from 0.40&plusmn;0.05 to 1.59&plusmn;0.15ngAI&middot;h<SUP>-1</SUP>&middot;Af+MD<SUP>-1</SUP>/h (n=10, p<0.01). After the pretreatment with indomethacin, a cyclooxygenase inhibitor, furosemide still increased renin release rate from 0.17&plusmn;0.02 to 0.56&plusmn;0.09 ng AI&middot;h<SUP>-1</SUP>&middot;Af+MD<SUP>-1</SUP>/h (n=5, p<0.05) ; however, indomethacin pretreatment reduced both basal and furosemide-stimulated renin release rate (p<0.05). In the presence of PGI<SUB>2</SUB> (10 &mu;M), renin release rate from Af increased from 0.45&plusmn;0.14 to 1.49&plusmn;0.53 ng AI&middot;h<SUP>-1</SUP>&middot;AN/h (n=9, p<0.05), and further increased to 4.50&plusmn;1.24 ng AI&middot;h<SUP>-1</SUP>&middot;Af<SUP>-1</SUP>/h (p<0.02) after removal from PGI<SUB>2</SUB>. When PGE<SUB>2</SUB> (10 &mu;M) was added to Af+MD, renin release rate increased from 0.54&plusmn;0.09 to 1.26&plusmn;0.24ng AI&middot;h<SUP>-1</SUP>Af+MD<SUP>-1</SUP>/h (n=8, p< 0.05). However PGE<SUB>2</SUB> had no effect on renin release rate from Af alone. We concluded that (1) the prostaglandin system may be a modulating factor of response in the macula densa mechanism of renin release, (2) PGI<SUB>2</SUB> has direct action on renin release from affer-ent arteriole, and (3) PGE<SUB>2</SUB> may participate in the control of renin release through the action on the macula densa.

著者

主代 昇 阿部 圭志 伊藤 貞嘉 三沢 誠一 吉永 馨

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.34, no.10, pp.1107-1111, 1992

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Tissue renin content within the kidney decreases from outer to inner cortex. However, it is not known whether this gradient is due to a decrease in the number of afferent arterioles from the outer to inner cortex or the decrease in renin content per afferent arteriole. Furthermore, it is still controversial whether sodium depletion increases or decreases this gradient. According to Taugner et al., sodium depletion induces the extension of renin positive part of afferent arterioles from vascular pole toward interlobular artery. Since the length of extension may differ among superficial, midcortical, and juxtamedullary afferent arterioles, the observed gradient may vary depending on whether the entire afferent arteriole or only the vascular pole is examined. In the present study, we microdissected the entire afferent arterioles from superficial, middle, and juxtamedullary cortex of rabbit kidney, and examined tissue renin content. We studied: 1. whether tissue renin content per afferent arteriole decreases from the outer to inner cortex. 2. whether sodium depletion affects the gradient of tissue renin content within the cortex. In result, we reached the conclusions, as follows: 1. Tissue renin content per afferent arteriole decreases steeply from superficial to midcortical to juxtamedullary afferent arterioles. 2. The absolute difference in renin content among the three types of afferent arterioles becomes greater during sodium depletion. The internephron heterogeneity of tissue renin content may contribute to functional heterogeneity.

著者

伊藤 貞嘉

出版者

社団法人 日本腎臓学会

雑誌

The Japanese journal of nephrology = / 日本腎臓学会 [編集] (ISSN:03852385)

巻号頁・発行日

vol.49, no.5, pp.485-490, 2007-07-25

参考文献数

26

著者

森 建文 伊藤 貞嘉

出版者

日本腎臓学会

雑誌

The Japanese journal of nephrology (ISSN:03852385)

巻号頁・発行日

vol.52, no.2, pp.114-119, 2010-03-25

参考文献数

30

著者

矢尾板 啓 伊藤 修 有馬 秀二 遠藤 好美 竹内 和久 尾股 健 伊藤 貞嘉

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.41, no.7, pp.697-703, 1999

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We investigated the direct effect of adenosine on afferent arterioles (Af-Arts) and the receptor subtype that mediates the constrictor or dilator action of adenosine . Af-Arts were isolated from the superficial cortex of rabbit kidney and perfused in vitro. Adenosine added to either the lumen or bath constricted the Af-Arts in a dose dependent manner. This constriction was blocked by the A1 receptor antagonist, 6-oxo-3- (2-phenylpyrazole (1, 5-a) pyridin-3-yl) -1(6H) -pyridazinebutyric acid (FK838) or 8-cyclopentyl-1, 3 - dipropylxanthine (DPCPX). We also examined the effect of adenosine on preconstricted Af-Arts with norepinephrine. Adenosine added to either the lumen or bath further constricted the preconstricted Af-Arts. In the presence of FK838, adenosine added to either the lumen or bath dilated the preconstricted Af-Arts, but in a different dose dependent manner. Adenosine induced dilation was inhibited by the A<SUB>2</SUB> receptor antagonist, 3, 7-dimetyl-1- propargylxanthine (DMPX). These data indicate that adenosine constricts Af-Arts via A<SUB>1</SUB> receptors and that adenosine dilates preconstricted Af-Arts via A<SUB>2</SUB> receptors when A<SUB>1</SUB> receptors are blocked.

著者

本庶 佑

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.26, no.7, pp.831-833, 1984

著者

富野 康日己

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.45, no.4, pp.355, 2003-05-25 (Released:2010-07-05)

著者

佐々木 信博 安藤 康弘 大友 貴史 石原島 繁彦 草野 英二 浅野 泰

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.41, no.8, pp.818-824, 1999 (Released:2010-07-05)

参考文献数

14

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We report a case whose renal failure was due to malignant hypertension and in whom steroid facilitated the recovery of renal function. The patient, a 41-year-old man, was admitted to our hospital because of malaise and macrohematuria. On admission, his blood pressure was 270/160 mmHg. The plasma renin activity (PRA) and aldosterone were markedly elevated. Chest X-ray, echo cardiography and electrocardiogram revealed marked hypertrophy. Hypertensive retinopathy and arteriosclerotic change were noted on ophthalmoscopy. Because of renal dysfunction (blood urea nitrogen 45.6 mg/dl, serum creatinine 4.9 mg/dl with massive proteinuria and increased FENa, renal biopsy was performed on the 8th clinical day. The specimens showed slight proliferation of mesangial cells with mesangiolysis and inter stitial cell infiltration, in addition to marked arteriosclerosis and partial collapse of the glomerular tuft. After the administration of a Ca antagonist and angiotensin converting enzyme inhibitor (ACE-I), his mean blood pressure decreased to 100-130 mmHg, and urinary protein decreased as well. Nevertheless, renal dysfunction remained unchanged during the following 3 weeks. Thus, prednisolone (PSL, 30 mg/day) was administered on the 22nd clinical day and renal function improved thereafter without a significant change in blood pressure. The improved renal function was maintained after PSL tapered off on the 184th clinical day. It is suggested that PSL might be the therapy of choice in malignant hypertension, when the renalfunction has not been improved by anti-hypertensive treatment alone.

著者

中島 英明 宮崎 睦雄 今井 信行 横川 朋子 山本 茂生

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.43, no.4, pp.351-356, 2001-05-25 (Released:2010-07-05)

参考文献数

11

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A 63-year-old man was referred to our hospital for rapid deterioration of his renal function. He had worked as a metal founder for more than 40 years, and had been diagnosed as having silicosis. Laboratory data on admission showed severe anemia, thrombocytopenia, and end-stage renal failure (BUN 88.8 mg/ dl, serum creatinine 9.0mg/dl). Myeloperoxidase anti-neutrophil cytoplasmic antibody (MPO-ANCA) was also detected in his sera. On the next day after admission, he complained of sudden dyspnea and hemoptysis. Mechanical ventilation with pure oxygen was insufficient to improve hypoxia without concomitant use of percutaneous cardio-pulmonary support (POPS) and continuous hemofiltration (CHF). We diagnosed his condition as MPO-ANCA-associated rapidly progressive glomerulonephritis with diffuse alveolar hemorrhage. Treat ment with plasmapheresis, pulse methylprednisolone and pulse cyclophosphamide effectively improved his hemoptysis as well as chest X-ray findings and blood gas analysis. However on his later clinical course, he was complicated with superimposed complex infection and passed away. Autopsy findings showed crescentic glomerulonephritis in the kidneys and silica nodules in the lungs. Recently it has been postulated that some relationship exists between ANCA-associated (especially MPO-ANCA-associated) glomerulonephritis and silica exposure. The reported cases of glomerulonephritisin the patients with silica exposure showed a rapidly progressive clinical course and pauci-immune necrotizing crescentic glomerulonephritis in their histology. Gregorini et al, reported that 12 of 37 (32%) male patients with RPGN had either silicosis or significant silica exposure, and 7 of 8 patients examined were ANCA-positive (6 of 7 were MPO-ANCA-positive). Therefore silica seems to cause glomerulonephritis by disrupting the immune response. Including this case mentioned above, we have experienced 10 cases of MPO-ANCA-associated glomerulonephritis, at least 3 cases out of which had suffered from silicosis in the past (30%) . These results indicate that silicosis should be considered a relevant pathogen of MPO-ANCA-associated glomerulonephritis beyond the race.