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the 18th letter of the Roman alphabet (同)r

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resistance / 17歳以下父兄同伴映画の表示 / rook
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/07/03 14:36:50」(JST)

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腎血管性高血圧症（じんけっかんせいこうけつあつしょう）は、腎臓の血管障害に起因する高血圧症。

病態

腎血流が何らかの原因で低下した結果、全身が低血圧状態にあると勘違いした腎臓の傍糸球体装置が血圧上昇ホルモンであるレニンを分泌して、レニン-アンジオテンシン系が亢進して高血圧になる。

原因

内因性
- 線維筋性異形成
- 大動脈炎症候群
- 動脈硬化症 : 腎動脈が厚くなる。厚くなることを肥厚すると言う。腎動脈が肥厚して血管腔を狭窄する。
外因性
- 腎細胞癌 : 腫瘍による腎動脈の圧迫。
- 解離性大動脈瘤 : 偽腔の血腫が腎動脈を圧迫狭窄する。

統計

原因
- 線維筋性異形成 : 40%
- 動脈硬化症 : 25%
- 大動脈炎症候群20%
原因の約九割を、線維筋性異形成、動脈硬化症、大動脈炎症候群、で占める。

症状

血圧高値: 若年高血圧、高齢者で急速な血圧上昇をきたすもの、降圧薬によるコントロールが困難なものは、腎動脈狭窄に限らず二次性高血圧を疑い精査が必要。
頭痛

検査

基本的身体検査

腎血管障害による血流雑音が心窩部、腹部で聴取される。腎動脈以外の動脈狭窄を合併していないか注意すること。
血清生化学検査

高レニン血症、高アルドステロン血症、高ナトリウム血症、低カリウム血症、等が認められる。
カプトプリル負荷試験

カプトプリル内服によるレニンの過大反応を認める。両側に高度の腎動脈狭窄がある場合、ACE阻害薬投与によりショックとなる可能性もあるので注意。
画像検査

3D-CT：多列CTの登場により、狭窄部位を鮮明に画像化できるようになってきている。

腹部超音波検査：ドップラー検査により腎動脈の血流を計測する。

シンチグラフィー（レノグラム）：カプトプリル負荷レノグラム。

診断

レニン、アルドステロンの上昇確認。最終的に腎動脈造影による腎動脈の狭窄の確認。

治療

薬物療法

対症療法として各種降圧薬を用いて血圧コントロールを行う。特にレニン-アンジオテンシン系を遮断するために、アンジオテンシン変換酵素阻害薬やアンジオテンシンII受容体拮抗薬、等を用いる。
手術療法

狭窄した腎血管に対して腎動脈形成術、等を行う。腎動脈形成術は、バルーンやステントを用いる。バルーンやステントを用いる腎動脈形成術を経皮経管的腎血管形成術(PTRA)と言う。PTRAが治療の第一選択となることも多い。^[1]

予後

診療科

腎臓内科 - 循環器内科

脚注

^ Zeller T, te al: Predictors of improved renal function after percutaneous stent-supported angioplasty of severe atherosclerotic ostial renal artery stenosis. Circulation 108 2244-2249, 2003.

参考文献

外部リンク

この項目は、医学に関連した書きかけの項目です。この項目を加筆・訂正などしてくださる協力者を求めています（プロジェクト:医学／Portal:医学と医療）。

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UpToDate Contents

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1. 心電図チュートリアル：心室拡大および心室肥大 ecg tutorial chamber enlargement and hypertrophy
2. 幼児および小児における孤立性心室中隔欠損の病態生理および臨床的特徴 pathophysiology and clinical features of isolated ventricular septal defects in infants and children
3. 左脚ブロック left bundle branch block

English Journal

Left atrial enlargement and right ventricular hypertrophy in essential hypertension.

Cuspidi C1, Negri F, Tadic MV, Sala C, Parati G.Author information 1Department of Health Science, University of Milano-Bicocca , Milano , Italy.AbstractAbstract Aim. Diastolic dysfunction related to hypertensive left ventricular hypertrophy (LVH) has been shown to affect right-sided cardiac morphology and haemodynamics. As left atrial enlargement (LAE) is a marker of chronically elevated left ventricular (LV) filling pressure and diastolic dysfunction, we investigated the relationship between LAE and right ventricular hypertrophy (RVH) in systemic hypertension. Methods. A total of 330 essential hypertensives, categorized according to tertiles of left atrial (LA) diameter indexed to body surface area were considered for the analysis. All subjects underwent a quantitative echocardiographic examination as well as extensive clinical and laboratory investigations. RVH was defined as anterior right ventricular (RV) wall thickness ≥ 6.0/5.5 mm in men and women, respectively, and LVH as LV mass index ≥ 51/47 g/m(2.7) in men and women, respectively. Results. The prevalence of LVH increased across LA diameter tertiles from 21.0% to 50% and that of RVH from 26.3% to 41.8% (p < 0.01for both). This was also the case for biventricular hypertrophy (from 10.0% to 26.0%, p < 0.01). Differences in both LV and RV structure across LA diameter tertiles remained significant after adjusting for age, office systolic/diastolic blood pressure and duration of hypertension. Similar results were obtained when study population was divided according to absolute LA diameter tertiles. Conclusions. Our findings provide further evidence of an interaction between left and right chambers in systemic hypertension by showing that LAE is associated with RVH. The clinical and prognostic implications of such observation remain be evaluated in future prospective studies.
Blood pressure.Blood Press.2014 Apr;23(2):89-95. doi: 10.3109/08037051.2013.803312. Epub 2013 Jun 13.
Abstract Aim. Diastolic dysfunction related to hypertensive left ventricular hypertrophy (LVH) has been shown to affect right-sided cardiac morphology and haemodynamics. As left atrial enlargement (LAE) is a marker of chronically elevated left ventricular (LV) filling pressure and diastolic dysfunct
PMID 23763624

Combination therapy with fasudil and sildenafil ameliorates monocrotaline-induced pulmonary hypertension and survival in rats.

Elias-Al-Mamun M1, Satoh K, Tanaka S, Shimizu T, Nergui S, Miyata S, Fukumoto Y, Shimokawa H.Author information 1Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine.AbstractBackground: Pulmonary hypertension (PH) is a fatal disease characterized by pulmonary artery (PA) remodeling, elevated PA pressure and right ventricular (RV) failure. It has been previously demonstrated that treatment with a Rho-kinase inhibitor, fasudil, ameliorates PH in animal models. Here, whether combination therapy with fasudil and sildenafil further ameliorates PH in rats was examined. Methods and Results: PH was induced in Sprague-Dawley rats by the use of a single subcutaneous monocrotaline (MCT) injection, which caused PA remodeling, elevated RV systolic pressure (RVSP), and RV hypertrophy (RVH). While fasudil and sildenafil monotherapy inhibited the development of MCT-induced PH in the prevention and treatment protocols, their combination therapy further improved RVSP and RVH. Moreover, a histological examination demonstrated significant improvements of PA remodeling in the combination group compared with the monotherapy groups. An echocardiographic examination also revealed significant reduction in RV diameter in the combination group compared with the monotherapy groups. Mechanistic experiments revealed significant inhibition of Rho-kinase activity in PA trunk, lung and RV tissues in the combination group as well as in the monotherapy groups. Finally, the combination therapy markedly improved the long-term survival compared with the monotherapy groups. Conclusions: These results indicate that the combination therapy with fasudil and sildenafil shows the synergistic effects through the inhibition of Rho-kinase activity for the treatment of PH. (Circ J 2014; 78: 967-976).
Circulation journal : official journal of the Japanese Circulation Society.Circ J.2014 Mar 25;78(4):967-76. Epub 2014 Feb 18.
Background: Pulmonary hypertension (PH) is a fatal disease characterized by pulmonary artery (PA) remodeling, elevated PA pressure and right ventricular (RV) failure. It has been previously demonstrated that treatment with a Rho-kinase inhibitor, fasudil, ameliorates PH in animal models. Here, whe
PMID 24553194

Genetic Deletion of TLR4 on Platelets Attenuates Experimental Pulmonary Hypertension.

Bauer E1, Chanthaphavong RS, Sodhi CP, Hackam DJ, Billiar TR, Bauer PM.Author information 1Surgery, University of Pittsburgh School of Medicine.AbstractRATIONALE: Recent studies demonstrate a role for TLR4 in the pathogenesis of pulmonary hypertension (PH), however, the cell types involved in mediating the effects of TLR4 remain unknown.
Circulation research.Circ Res.2014 Mar 17. [Epub ahead of print]
RATIONALE: Recent studies demonstrate a role for TLR4 in the pathogenesis of pulmonary hypertension (PH), however, the cell types involved in mediating the effects of TLR4 remain unknown.OBJECTIVE: The objective of this study was to determine the contribution of TLR4 expressed on nonparenchymal cell
PMID 24637196