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

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.

著者

井関 邦敏 藤見 惺 川崎 晃一 尾前 照雄

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.21, no.2, pp.157-163, 1979 (Released:2010-07-05)

参考文献数

14

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A case of pseudo Bartter syndrome in furosemide abuse was described. The case was 24 year-old female, a nurse, who was admitted because of persistent hypokalemia on, she noted pretibial edema for which furosemide was prescribed by a local doctor. Since then, she had taken about 80 mg of furosemide daily until, when transient cardiac and respiratory arrest developed and serum potassium was found to be 2.0 mEq per liter. The patient was advised to discontinue furosemide. Serum potassium, however, remained inn hypokalemic range in spite of potassium supplementation. At admission she appeared healthy and denied using furosemide, diuretics and laxatives. Serum potassium was 2.4, sodium 143, chloride 90 mEq per liter. Arterial blood pH was 7.477 and plasma bicarbonate 31.3 mEq per liter. Diagnosis of pseudo Bartter syndrome was suspected because of 1) persistent hypokalemia with increases in potassium clearance, plasma renin activity, plasma aldosterone concentration 2) low response of blood pressure to angiotensin II 3) minimal to moderate hyperplasia of J-G apparatus 4) no improvement of clinical condition with indomethacin. After discharge, the patient had been well with persistent hypokalemia until, when she became unconscious abruptly followed by generalized convulsion. Serum potassium was 1.5 mEq per liter. Incidentally it was discovered that she had obtained a lot of furosemide from pharmacy without doctor's prescription. At first she insisted not to take furosemide but finally admitted taking furosemide 280 mg daily. It was quite surprising that she had been taking furosemide continuously even though having episodes of cardiac and respiratory arrest, generalized convulsion which, she should know, might be deeply related to f urosemide usage. It is strongly suggested that furosemide abuse would be one another etiologic condition for pseudo Bartter syndrome and furosemide should not be prescribed without careful supervision.

著者

北浦 圭介 浅野 健一郎

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.47, no.8, pp.887-892, 2005-11-25 (Released:2010-05-18)

参考文献数

14

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抗糸球体基底膜 (GBM) 病は急速進行性糸球体腎炎の経過を辿り, 治療開始時から透析療法を必要とする場合は予後不良とされている.症例は29歳, 男性。 平成15年6月末から38度以上の発熱, 倦怠感を認め近医を受診した。 尿中白血球3+, 尿蛋白2+, 尿潜血3+を示し, 急性腎盂腎炎を疑い当院泌尿器科に紹介入院となった。 入院時CRP 18.9mg/dl, BUN 20mg/dl, Cr 2.9mg/dlを示し抗生剤の投与を行うも, 第11病日にはBUN 78mg/dl, Cr 9.2mg/dlと悪化したため当科転科となった。 細菌培養は陰性であり, 急速進行性糸球体腎炎を疑いソルメドロールパルスを含むステロイド療法, シクロフォスファミドを開始し, 同時に血液透析を行った. 胸部CTでは肺病変は認められず, 腎組織では4個中2個に細胞性半月体を認めた。 MPO-ANCA, PR-3-ANCA陰性, 抗GBM抗体169Uを認め, 抗GBM抗体型糸球体腎炎と診断した。 第30病日からアルブミンを置換液とした血漿交換を6回施行した。 血漿交換後, 抗GBM抗体は28Uまで低下し, それまで乏尿であったが1カ月後には尿量1,000~1,200ml/日を認め, また, 腎機能も徐々に改善し10月末にはBUN40mg/dl, Cr 4.1mg/dlまで低下したため血液透析を離脱した。 その後腎機能障害は悪化せず■に退院した。 後日再度腎生検を施行したが, 20個中18個が糸球体硬化に至っていた。 本例は臨床的に高度腎機能障害を有し, かつ発症から血漿交換開始まで約40日と期間が長かったにも関わらず透析を離脱し得た。 本例では透析を離脱できた原因として血漿交換療法の追加・併用療法が有用であったと考えた。

著者

木戸 千元

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.9, no.2, pp.221-234, 1967-03-30 (Released:2010-07-05)

参考文献数

50

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In order to investigate patho-physiology of the nephrotic syndrome, the author made on examination of lipid, energy and carbohydrate metabolism, with priority to liver, by using the experimental nephrotic rats induced by aminonucleoside (AN). The resalts were as follows 1) In the AN nephrotic rats, the significant increase in serum cholesterol, esterified fatty acid, and phospholipid were observed, although these lipid concentration in the livers were nearly unchanged. The incorporation with acetate-1-C14 into cholesterol, glucose-U-C14 into fatty acid, and NaHP32O4 into phospholipid respectively, in the liver slices, increased in the nephrotic rats injected nine times with AN, and the synthesis of these lipids in the liver was considered highly increasing. 2) O2 Consumpsion of the substrates in the liver slices generally increased in the nephrotic rats and the result suggested increasing energy metabolism in the nephrotic syndrome. 3) The content of glycogen in the livers and muscles decreased in the nephrotic rats at the time of taking food freely as well as after five hours fasting, and showed a tendency to decrease even after the administration of a certain quantitative of glucose, and the similar decreasing tendency was also seen in the blood sager. In the nephrotic rats, hypoglycemic state was clearly observed. The ratio yields of C14O2 from glucose-6-C14 to that from glucose-1-C14 in the slice of liver showed a tendency to decreased in the nephrotic rats and the above-mentioned fact suggested the possibility of increasing lipogenesis. By investigating the activity of glycolytic enzymes, the author observed that G-6-ease and MDH significantly decreased in the nephrotic group, while LDH strikingly increased. There were no significant differences in PG iso, PG mut, ALD, G6PD, and ICD. From the enzymological level, the existence of lipogenic pattern could not be concluded.

著者

杉山 敏

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.667-675, 2004 (Released:2010-05-18)

参考文献数

59

著者

血尿診断ガイドライン検討委員会

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.48, no.Supplement, pp.1-34, 2006-10-25 (Released:2010-05-18)

著者

岡田 満 吉岡 加寿夫 磯川 貞之 竹村 司 木下 智弘 赤野 則久 牧 淳

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.11, pp.1195-1199, 1992

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This paper describes a case report of acute interstitial nephritis associated with Bufferin(R). A 15-year-old girl were referred to our hospital due to fever and renal dysfunction. Laboratory findings showed elevation of serum BUN and creatinine, and increased urinary &beta;2-MG excreation. Light microscopic findings of her renal biopsy specimen revealed edema and numerous inflammatory cells in the interstitium, and minor alterations in glomeruli. The interstitial infiltrates consisted mainly of T cells and also monocytes/macrophages. Interstitial cells were labelled with antibodies to interleukin (IL)-1 and tumor necrose factor (TNF). Bufferin(R) was positive by lymphocyte stimulation test . Thus, we considered that this drug was causative in this case. This observation suggests the participation of cell -mediated immune injury in drug induced acute interstitial nephritis .