今日の臨床サポート

腎硬化症

著者: 小井手裕一1) いすゞ病院 内科

著者: 田村功一2) 横浜市立大学医学部 循環器・腎臓内科学教室

監修: 岡田浩一 埼玉医科大学 腎臓内科

著者校正/監修レビュー済:2020/03/12
参考ガイドライン:
  1. 日本腎臓学会編:エビデンスに基づくCKD診療ガイドライン2018
患者向け説明資料

概要・推奨   

  1. 高血圧歴を有し、尿蛋白が少なく、慢性糸球体腎炎や糖尿病などの基礎疾患のない腎機能障害患者は、腎硬化症である可能性が高い(推奨度2)
  1. 適切な降圧療法は、腎硬化症の進展を抑制する(推奨度1)
  1. 尿蛋白症例では、RAS系阻害薬を中心として、尿蛋白減少を意識した降圧療法を選択すべきである(推奨度2)
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  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契
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薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
小井手裕一 : 特に申告事項無し[2021年]
田村功一 : 未申告[2021年]
監修:岡田浩一 : 講演料(協和キリン,中外製薬,田辺三菱,第一三共),研究費・助成金など(協和キリン),奨学(奨励)寄付など(協和キリン,中外製薬,田辺三菱,第一三共,アステラス,MSD,武田薬品,鳥居薬品,ファイザー,ノバルティス,日本ベーリンガーインゲルハイム,大塚製薬,塩野義,大日本住友)[2021年]

改訂のポイント:
  1. CKD GL2018の記載を踏まえ、75歳以上の高齢者、ステージG4、5などのハイリスク者、A1区分の過剰な降圧の注意などが、今回のポイントです。

病態・疫学・診察

疾患情報(疫学・病態)  
  1. 腎硬化症とは、高血圧(参照: 本態性高血圧症 )にある期間曝露されることにより生じる、腎内の動脈硬化性血管病変(小動脈の内膜肥厚と細動脈の硝子化)に基づく腎障害の総称である。
  1. 末期腎不全患者の透析導入における原疾患として腎硬化症の占める割合は、現在、わが国では16%であり、年々増加傾向にある。
  1. その背景として、約4,000万人ともいわれる高血圧患者が存在しており、特に65歳以上の高齢者では2~3人に1人が罹患している。(参照: 本態性高血圧症 )
  1. 高齢化の進んでいる日本では、今後高血圧患者がさらに増加することが予測され、それは腎硬化症から透析へと至る患者が増加することを意味する。透析患者の増加をくい止めるためにも、的確な降圧治療が重要である。
  1. 病理学的変化は、腎内の小動脈、細動脈での動脈硬化が進展することによる腎血流低下からの糸球体虚血性変化(糸球体硬化)が主体であり、二次的な腎間質障害も加わり腎不全に至る。
  1. 腎硬化症は、臨床的には発症形式により分類される。
  1. 良性腎硬化症では、加齢や持続する高血圧を背景に緩やかに進行する腎機能障害と、比較的軽度な臨床症状を呈する。
  1. 悪性腎硬化症では、高度の高血圧とともに急速に進行する腎機能障害や、高血圧性網膜症、脳血管障害、心不全などの急速な臨床症状を呈する。
  1. 良性腎硬化症と悪性腎硬化症の病態はまったく異なり、一般的に「腎硬化症」と呼ぶ場合は良性腎硬化症を指す。
 
  1. 高血圧歴を有し、尿蛋白が少なく、慢性糸球体腎炎や糖尿病などの基礎疾患のない腎機能障害患者は、腎硬化症である可能性が高い(推奨度2)
  1. まとめ:腎硬化症の大規模臨床試験はアフリカ系アメリカ人を対象としたAASK試験のみであるが、腎硬化症の診断基準について検証されている[1]
  1. 代表事例:AASK試験においては、(二次性および悪性高血圧を除く)高血圧歴を有し、高度な蛋白尿(2.5g/日以上)および糖尿病や慢性糸球体腎炎などの基礎疾患を伴わないという腎硬化症の診断基準が用いられた。39例に対し腎生検を施行したところ、28例に動脈硬化の所見が認められた。また間質の線維化と血清Crの間には強い相関が認められた。
  1. 結論:著明な尿蛋白がなく、軽度から中等度の腎機能障害を示した非糖尿病性アフリカ系アメリカ人に対する高血圧性腎症(=腎硬化症)との臨床的診断は、組織学的にも一致していることが明らかにされた。
  1. 追記:腎硬化症の唯一の大規模臨床試験であるAASK研究において、高血圧に起因する腎硬化症患者が適切に対象とされていることが本論文により証明されている。
問診・診察のポイント  
  1. 軽~中等症の本態性高血圧に長期間曝露されることにより腎硬化症へと進展することが多く、高血圧性腎症とも呼ばれる。(参照: 本態性高血圧症 )

これより先の閲覧には個人契約のトライアルまたはお申込みが必要です。

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文献 

著者: A Fogo, J A Breyer, M C Smith, W H Cleveland, L Agodoa, K A Kirk, R Glassock
雑誌名: Kidney Int. 1997 Jan;51(1):244-52.
Abstract/Text African Americans have excess hypertension and end-stage renal disease presumed due to hypertension compared to Caucasians. The AASK was designed to examine the impact of antihypertensive therapies and two levels of blood pressure control on the rate of decline of GFR in African Americans with presumed hypertensive renal disease. During the pilot phase of the trial, eligible participants were requested to undergo renal biopsy to assess the underlying lesions in this population. Eighty-eight hypertensive (diastolic BP > 95 mm Hg) non-diabetic African American patients between the ages of 18 to 70 years, with GFR between 25 to 70 ml/min/1.73 m2 and without marked proteinuria were assessed for possible renal biopsy. Forty-three patients did not undergo renal biopsy due to refusal or contraindications. Adequate renal biopsies were obtained in 39 of the remaining 46 patients. Biopsy findings were analyzed and then compared to clinical parameters. The 39 patients studied, 29 men and 10 women, were on average 53.0 +/- 11.0 years old, and had a MAP of 109 +/- 15 mm Hg and GFR 51.7 +/- 13.6 ml/min/1.73 m2 (not significantly different from nonbiopsied patients). Thirty-eight of these 39 biopsies showed arteriosclerosis and/or arteriolosclerosis, severity on average 1.5 +/- 0.9 and 1.5 +/- 0.8, respectively on a 0 to 3+ scale. Interstitial fibrosis was moderate, 1.3 +/- 0.9 (0 to 3+ scale). Segmental glomerulosclerosis was present in five biopsies, and in one patient, biopsy and clinical findings were consistent with idiopathic focal segmental glomerulosclerosis. Additional lesions included mesangiopathic glomerulonephritis in one patient, basement membrane thickening suggestive of diabetic nephropathy in one, and cholesterol emboli in two cases. Arteriolar and arterial sclerosis were tightly linked, and correlated with interstitial fibrosis and the reciprocal of serum creatinine. Global glomerulosclerosis was extensive, involving on average 43 +/- 26% of glomeruli. The extent of this lesion did not correlate with degree of arteriolar or arterial thickening, but did correlate with systolic blood pressure (P = 0.0174), the reciprocal of serum creatinine (P = 0.0009), serum cholesterol (P = 0.0129) and interstitial fibrosis (P < 0.0001). These data underscore that renal biopsies in non-diabetic hypertensive African-Americans with mild to moderate renal insufficiency in the absence of marked proteinuria are overwhelmingly likely to show renal vascular lesions consistent with the clinical diagnosis of hypertensive nephrosclerosis.

PMID 8995739  Kidney Int. 1997 Jan;51(1):244-52.
著者: Janice Lea, Tom Greene, Lee Hebert, Michael Lipkowitz, Shaul Massry, John Middleton, Stephen G Rostand, Edgar Miller, Winifred Smith, George L Bakris
雑誌名: Arch Intern Med. 2005 Apr 25;165(8):947-53. doi: 10.1001/archinte.165.8.947.
Abstract/Text BACKGROUND: The magnitude of proteinuria is associated with a graded increase in the risk of progression to end-stage renal disease and cardiovascular events. The objective of this study was to relate baseline and early changes in proteinuria and glomerular filtration rate (GFR) to long-term progression of hypertensive nondiabetic kidney disease.
METHODS: Post hoc analysis of a randomized 3 x 2 factorial trial. A total of 1094 African Americans with hypertensive renal disease (GFR, 20-65 mL/min per 1.73 m(2)) were followed up for a median of 3.8 years. Participants were randomized to a mean arterial pressure goal of 102 to 107 mm Hg (usual) or 92 mm Hg or less (lower) and to initial treatment with a beta-blocker (metoprolol), an angiotensin-converting enzyme inhibitor (ramipril), or a dihydropyridine calcium channel blocker (amlodipine)
RESULTS: Baseline proteinuria and GFR predicted the rgate of GFR decline. For each 10-mL/min per 1.73 m(2) lower baseline GFR, an associated mean +/- SE 0.38 +/- 0.08-mL/min per 1.73 m(2) per year greater mean GFR decline occurred, and for each 2-fold higher proteinuria level, a mean +/- SE 0.54 +/- 0.05-mL/min per 1.73 m(2) per year faster GFR decline was observed (P < .001 for both). In multivariate analysis, the effect of baseline proteinuria GFR decline persisted. Initial change in proteinuria from baseline to 6 months predicted subsequent progression, with this relationship extending to participants with baseline urinary protein levels less than 300 mg/d.
CONCLUSIONS: The change in the level of proteinuria is a predictor of subsequent progression of hypertensive kidney disease at a given GFR. A prospective trial is needed to confirm this observation.

PMID 15851648  Arch Intern Med. 2005 Apr 25;165(8):947-53. doi: 10.100・・・
著者: L Y Agodoa, L Appel, G L Bakris, G Beck, J Bourgoignie, J P Briggs, J Charleston, D Cheek, W Cleveland, J G Douglas, M Douglas, D Dowie, M Faulkner, A Gabriel, J Gassman, T Greene, Y Hall, L Hebert, L Hiremath, K Jamerson, C J Johnson, J Kopple, J Kusek, J Lash, J Lea, J B Lewis, M Lipkowitz, S Massry, J Middleton, E R Miller, K Norris, D O'Connor, A Ojo, R A Phillips, V Pogue, M Rahman, O S Randall, S Rostand, G Schulman, W Smith, D Thornley-Brown, C C Tisher, R D Toto, J T Wright, S Xu, African American Study of Kidney Disease and Hypertension (AASK) Study Group
雑誌名: JAMA. 2001 Jun 6;285(21):2719-28.
Abstract/Text CONTEXT: Incidence of end-stage renal disease due to hypertension has increased in recent decades, but the optimal strategy for treatment of hypertension to prevent renal failure is unknown, especially among African Americans.
OBJECTIVE: To compare the effects of an angiotensin-converting enzyme (ACE) inhibitor (ramipril), a dihydropyridine calcium channel blocker (amlodipine), and a beta-blocker (metoprolol) on hypertensive renal disease progression.
DESIGN, SETTING, AND PARTICIPANTS: Interim analysis of a randomized, double-blind, 3 x 2 factorial trial conducted in 1094 African Americans aged 18 to 70 years with hypertensive renal disease (glomerular filtration rate [GFR] of 20-65 mL/min per 1.73 m(2)) enrolled between February 1995 and September 1998. This report compares the ramipril and amlodipine groups following discontinuation of the amlodipine intervention in September 2000.
INTERVENTIONS: Participants were randomly assigned to receive amlodipine, 5 to 10 mg/d (n = 217), ramipril, 2.5 to 10 mg/d (n = 436), or metoprolol, 50 to 200 mg/d (n = 441), with other agents added to achieve 1 of 2 blood pressure goals.
MAIN OUTCOME MEASURES: The primary outcome measure was the rate of change in GFR; the main secondary outcome was a composite index of the clinical end points of reduction in GFR of more than 50% or 25 mL/min per 1.73 m(2), end-stage renal disease, or death.
RESULTS: Among participants with a urinary protein to creatinine ratio of >0.22 (corresponding approximately to proteinuria of more than 300 mg/d), the ramipril group had a 36% (2.02 [SE, 0.74] mL/min per 1.73 m(2)/y) slower mean decline in GFR over 3 years (P =.006) and a 48% reduced risk of the clinical end points vs the amlodipine group (95% confidence interval [CI], 20%-66%). In the entire cohort, there was no significant difference in mean GFR decline from baseline to 3 years between treatment groups (P =.38). However, compared with the amlodipine group, after adjustment for baseline covariates the ramipril group had a 38% reduced risk of clinical end points (95% CI, 13%-56%), a 36% slower mean decline in GFR after 3 months (P =.002), and less proteinuria (P<.001).
CONCLUSION: Ramipril, compared with amlodipine, retards renal disease progression in patients with hypertensive renal disease and proteinuria and may offer benefit to patients without proteinuria.

PMID 11386927  JAMA. 2001 Jun 6;285(21):2719-28.
著者: Jackson T Wright, George Bakris, Tom Greene, Larry Y Agodoa, Lawrence J Appel, Jeanne Charleston, DeAnna Cheek, Janice G Douglas-Baltimore, Jennifer Gassman, Richard Glassock, Lee Hebert, Kenneth Jamerson, Julia Lewis, Robert A Phillips, Robert D Toto, John P Middleton, Stephen G Rostand, African American Study of Kidney Disease and Hypertension Study Group
雑誌名: JAMA. 2002 Nov 20;288(19):2421-31.
Abstract/Text CONTEXT: Hypertension is a leading cause of end-stage renal disease (ESRD) in the United States, with no known treatment to prevent progressive declines leading to ESRD.
OBJECTIVE: To compare the effects of 2 levels of blood pressure (BP) control and 3 antihypertensive drug classes on glomerular filtration rate (GFR) decline in hypertension.
DESIGN: Randomized 3 x 2 factorial trial with enrollment from February 1995 to September 1998.
SETTING AND PARTICIPANTS: A total of 1094 African Americans aged 18 to 70 years with hypertensive renal disease (GFR, 20-65 mL/min per 1.73 m(2)) were recruited from 21 clinical centers throughout the United States and followed up for 3 to 6.4 years.
INTERVENTIONS: Participants were randomly assigned to 1 of 2 mean arterial pressure goals, 102 to 107 mm Hg (usual; n = 554) or 92 mm Hg or less (lower; n = 540), and to initial treatment with either a beta-blocker (metoprolol 50-200 mg/d; n = 441), an angiotensin-converting enzyme inhibitor (ramipril 2.5-10 mg/d; n = 436) or a dihydropyridine calcium channel blocker, (amlodipine 5-10 mg/d; n = 217). Open-label agents were added to achieve the assigned BP goals.
MAIN OUTCOME MEASURES: Rate of change in GFR (GFR slope); clinical composite outcome of reduction in GFR by 50% or more (or > or =25 mL/min per 1.73 m2) from baseline, ESRD, or death. Three primary treatment comparisons were specified: lower vs usual BP goal; ramipril vs metoprolol; and amlodipine vs metoprolol.
RESULTS: Achieved BP averaged (SD) 128/78 (12/8) mm Hg in the lower BP group and 141/85 (12/7) mm Hg in the usual BP group. The mean (SE) GFR slope from baseline through 4 years did not differ significantly between the lower BP group (-2.21 [0.17] mL/min per 1.73 m2 per year) and the usual BP group (-1.95 [0.17] mL/min per 1.73 m2 per year; P =.24), and the lower BP goal did not significantly reduce the rate of the clinical composite outcome (risk reduction for lower BP group = 2%; 95% confidence interval [CI], -22% to 21%; P =.85). None of the drug group comparisons showed consistent significant differences in the GFR slope. However, compared with the metoprolol and amlodipine groups, the ramipril group manifested risk reductions in the clinical composite outcome of 22% (95% CI, 1%-38%; P =.04) and 38% (95% CI, 14%-56%; P =.004), respectively. There was no significant difference in the clinical composite outcome between the amlodipine and metoprolol groups.
CONCLUSIONS: No additional benefit of slowing progression of hypertensive nephrosclerosis was observed with the lower BP goal. Angiotensin-converting enzyme inhibitors appear to be more effective than beta-blockers or dihydropyridine calcium channel blockers in slowing GFR decline.

PMID 12435255  JAMA. 2002 Nov 20;288(19):2421-31.
著者: Gabriel Contreras, Tom Greene, Lawrence Y Agodoa, DeAnna Cheek, George Junco, Donna Dowie, James Lash, Michael Lipkowitz, Edgar R Miller, Akinlou Ojo, Mohammed Sika, Beth Wilkening, Robert D Toto, African American Study of Kidney Disease and Hypertension Study Group Investigators
雑誌名: Hypertension. 2005 Jul;46(1):44-50. doi: 10.1161/01.HYP.0000166746.04472.60. Epub 2005 May 16.
Abstract/Text The African American Study of Kidney Disease and Hypertension examined the effect on renal function decline of 2 blood pressure (BP) goals (low mean arterial pressure [MAP] < or =92 versus usual MAP 102 to 107 mm Hg) and 3 antihypertensives (ramipril versus amlodipine versus metoprolol). We previously reported that in all drug groups combined the BP intervention had similar effects on the primary outcome of glomerular filtration rate (GFR) slope or the main secondary clinical composite outcome of end-stage renal disease (ESRD), death, or GFR decline by 50% or 25 mL/min per 1.73 m2. This report examines the effect of the BP intervention separately in the 3 drug groups. The BP effect was similar among the drug groups for either GFR slope or the main clinical composite. However, the BP effect differed significantly among the drug groups for the composite of ESRD or death (P=0.035) and ESRD alone (P=0.021). Higher event rates for amlodipine patients assigned to the usual BP goal (0.087 per patient-year for ESRD or death and 0.064 per patient-year for ESRD) were seen compared with the remaining groups of the factorial design (range, 0.041 to 0.050 for ESRD or death; and range, 0.027 to 0.036 for ESRD). The low BP goal was associated with reduced risk of ESRD or death (risk reduction 51%; 95% confidence interval, 13% to 73%) and ESRD (54%; 8% to 77%) for amlodipine patients, but not for patients assigned to the other drug groups. These secondary analyses suggest a benefit of the low BP goal among patients assigned to amlodipine, but they must be interpreted cautiously.

PMID 15897360  Hypertension. 2005 Jul;46(1):44-50. doi: 10.1161/01.HYP・・・
著者: Lawrence J Appel, Jackson T Wright, Tom Greene, John W Kusek, Julia B Lewis, Xuelei Wang, Michael S Lipkowitz, Keith C Norris, George L Bakris, Mahboob Rahman, Gabriel Contreras, Stephen G Rostand, Joel D Kopple, Francis B Gabbai, Gerald I Schulman, Jennifer J Gassman, Jeanne Charleston, Lawrence Y Agodoa, African American Study of Kidney Disease and Hypertension Collaborative Research Group
雑誌名: Arch Intern Med. 2008 Apr 28;168(8):832-9. doi: 10.1001/archinte.168.8.832.
Abstract/Text BACKGROUND: Antihypertensive drugs that block the renin-angiotensin system (angiotensin-converting enzyme inhibitors [ACEIs] or angiotensin receptor blockers) are recommended for patients with chronic kidney disease (CKD). A low blood pressure (BP) goal (BP, <130/80 mm Hg) is also recommended. The objective of this study was to determine the long-term effects of currently recommended BP therapy in 1094 African Americans with hypertensive CKD.
METHODS: Multicenter cohort study following a randomized trial. Participants were 1094 African Americans with hypertensive renal disease (glomerular filtration rate, 20-65 mL/min/1.73 m2). Following a 3x2-factorial trial (1995-2001) that tested 3 drugs used as initial antihypertensive therapy (ACEIs, calcium channel blockers, and beta-blockers) and 2 levels of BP control (usual and low), we conducted a cohort study (2002-2007) in which participants were treated with ACEIs to a BP lower than 130/80 mm Hg. The outcome measures were a composite of doubling of the serum creatinine level, end-stage renal disease, or death.
RESULTS: During each year of the cohort study, the annual use of an ACEI or an angiotensin receptor blocker ranged from 83.7% to 89.0% (vs 38.5% to 49.8% during the trial). The mean BP in the cohort study was 133/78 mm Hg (vs 136/82 mm Hg in the trial). Overall, 567 participants experienced the primary outcome; the 10-year cumulative incidence rate was 53.9%. Of 576 participants with at least 7 years of follow-up, 33.5% experienced a slow decline in kidney function (mean annual decline in the estimated glomerular filtration rate, <1 mL/min/1.73 m2).
CONCLUSION: Despite the benefits of renin-angiotensin system-blocking therapy on CKD progression, most African Americans with hypertensive CKD who are treated with currently recommended BP therapy continue to progress during the long term.

PMID 18443258  Arch Intern Med. 2008 Apr 28;168(8):832-9. doi: 10.1001・・・
著者: Lawrence J Appel, Jackson T Wright, Tom Greene, Lawrence Y Agodoa, Brad C Astor, George L Bakris, William H Cleveland, Jeanne Charleston, Gabriel Contreras, Marquetta L Faulkner, Francis B Gabbai, Jennifer J Gassman, Lee A Hebert, Kenneth A Jamerson, Joel D Kopple, John W Kusek, James P Lash, Janice P Lea, Julia B Lewis, Michael S Lipkowitz, Shaul G Massry, Edgar R Miller, Keith Norris, Robert A Phillips, Velvie A Pogue, Otelio S Randall, Stephen G Rostand, Miroslaw J Smogorzewski, Robert D Toto, Xuelei Wang, AASK Collaborative Research Group
雑誌名: N Engl J Med. 2010 Sep 2;363(10):918-29. doi: 10.1056/NEJMoa0910975.
Abstract/Text BACKGROUND: In observational studies, the relationship between blood pressure and end-stage renal disease (ESRD) is direct and progressive. The burden of hypertension-related chronic kidney disease and ESRD is especially high among black patients. Yet few trials have tested whether intensive blood-pressure control retards the progression of chronic kidney disease among black patients.
METHODS: We randomly assigned 1094 black patients with hypertensive chronic kidney disease to receive either intensive or standard blood-pressure control. After completing the trial phase, patients were invited to enroll in a cohort phase in which the blood-pressure target was less than 130/80 mm Hg. The primary clinical outcome in the cohort phase was the progression of chronic kidney disease, which was defined as a doubling of the serum creatinine level, a diagnosis of ESRD, or death. Follow-up ranged from 8.8 to 12.2 years.
RESULTS: During the trial phase, the mean blood pressure was 130/78 mm Hg in the intensive-control group and 141/86 mm Hg in the standard-control group. During the cohort phase, corresponding mean blood pressures were 131/78 mm Hg and 134/78 mm Hg. In both phases, there was no significant between-group difference in the risk of the primary outcome (hazard ratio in the intensive-control group, 0.91; P=0.27). However, the effects differed according to the baseline level of proteinuria (P=0.02 for interaction), with a potential benefit in patients with a protein-to-creatinine ratio of more than 0.22 (hazard ratio, 0.73; P=0.01).
CONCLUSIONS: In overall analyses, intensive blood-pressure control had no effect on kidney disease progression. However, there may be differential effects of intensive blood-pressure control in patients with and those without baseline proteinuria. (Funded by the National Institute of Diabetes and Digestive and Kidney Diseases, the National Center on Minority Health and Health Disparities, and others.)

PMID 20818902  N Engl J Med. 2010 Sep 2;363(10):918-29. doi: 10.1056/N・・・
著者: Ashish Upadhyay, Amy Earley, Shana M Haynes, Katrin Uhlig
雑誌名: Ann Intern Med. 2011 Apr 19;154(8):541-8. doi: 10.7326/0003-4819-154-8-201104190-00335. Epub 2011 Mar 14.
Abstract/Text BACKGROUND: The optimal blood pressure target in patients with chronic kidney disease (CKD) is unclear.
PURPOSE: To summarize trials comparing lower versus higher blood pressure targets in adult patients with CKD and focus on proteinuria as an effect modifier.
DATA SOURCES: MEDLINE and the Cochrane Central Register of Controlled Trials (July 2001 through January 2011) were searched for reports from randomized, controlled trials with no language restriction.
STUDY SELECTION: Authors screened abstracts to identify reports from trials comparing blood pressure targets in adults with CKD that had more than 50 participants per group; at least 1-year follow-up; and outcomes of death, kidney failure, cardiovascular events, change in kidney function, number of antihypertensive agents, and adverse events.
DATA EXTRACTION: Reviewers extracted data on study design, methods, sample characteristics, interventions, comparators, outcomes, number of medications, and adverse events and rated study quality and quality of analyses for proteinuria subgroups.
DATA SYNTHESIS: Three trials with a total of 2272 participants were included. Overall, trials did not show that a blood pressure target of less than 125/75 to 130/80 mm Hg is more beneficial than a target of less than 140/90 mm Hg. Lower-quality evidence suggests that a low target may be beneficial in subgroups with proteinuria greater than 300 to 1000 mg/d. Participants in the low target groups needed more antihypertensive medications and had a slightly higher rate of adverse events.
LIMITATIONS: No study included patients with diabetes. Trial duration may have been too short to detect differences in clinically important outcomes, such as death and kidney failure. Ascertainment and reporting of adverse events was not uniform.
CONCLUSION: Available evidence is inconclusive but does not prove that a blood pressure target of less than 130/80 mm Hg improves clinical outcomes more than a target of less than 140/90 mm Hg in adults with CKD. Whether a lower target benefits patients with proteinuria greater than 300 to 1000 mg/d requires further study.

PMID 21403055  Ann Intern Med. 2011 Apr 19;154(8):541-8. doi: 10.7326/・・・
著者: R D Toto, H C Mitchell, R D Smith, H C Lee, D McIntire, W A Pettinger
雑誌名: Kidney Int. 1995 Sep;48(3):851-9.
Abstract/Text Hypertensive nephrosclerosis is a progressive renal disease and the leading cause of end-stage renal disease (ESRD) in blacks in the United States. It is generally believed that hypertensive renal injury is responsible for progressive renal failure; however, it is not known whether pharmacologic lowering of blood pressure to any level prevents progression of renal disease. Accordingly, we performed a long-term prospective randomized trial to determine whether "strict" [diastolic blood pressure (DBP) 65 to 80 mm Hg] versus "conventional" (DBP 85 to 95 mm Hg) blood pressure control is associated with a slower rate of decline in glomerular filtration rate. Eighty-seven non-diabetic patients (age 25 to 73; 68 black, 58 male) with long-standing hypertension (DBP > or = 95 mm Hg), chronic renal insufficiency (GFR < or = 70 m/min/1.73 m2) and a normal urine sediment were studied. DBP was pharmacologically lowered to < or = 80 mm Hg (3 of 4 consecutive measurements at 1 to 4 weeks intervals) after which patients were randomized. DBP and GFR (renal clearance of 125I-iothalamate) were measured at baseline, at three months and every six months post-randomization. The rate of decline in GFR (GFR slope, in ml/min/1.73 m2/year), estimated by the method of maximum likelihood in a mixed effects model, was the primary outcome variable. In a secondary analysis, 50% reduction in GFR (or a doubling of serum creatinine) from baseline, ESRD and death were combined.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID 7474675  Kidney Int. 1995 Sep;48(3):851-9.

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