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Mae BP yn targedu ●clefyd cronig yn yr arennau ●gorbwysedd

Mae'r nodau pwysedd gwaed gorau posibl (BP) ar gyfer cleifion â gorbwysedd a chlefyd cronig yn yr arennau (CKD) yn parhau i gael eu trafod. Addasodd canllawiau Cymdeithas y Galon America / Coleg Cardioleg America (AHA / ACC) 2017 y diffiniad / dosbarthiad gorbwysedd a chyflwyno targed BP dwys o<130/80 mmHg for most individuals at high risk of cardiovascular disease, including patients with CKD [1]. The 2021 Kidney Disease: Improving Global Outcomes (KDIGO) guidelines recommended an even tighter systolic BP target of <120 mmHg for the management of hypertension in CKD [2]. Which, therefore, is the BP threshold that indicates a therapeutic benefit in this high-risk patient population?

Yn ôl astudiaethau perthnasol, mae cistanche yn berlysiau Tsieineaidd traddodiadol sydd wedi'i ddefnyddio ers canrifoedd i drin afiechydon amrywiol. Mae wedi'i brofi'n wyddonol i feddu ar briodweddau gwrthlidiol, gwrth-heneiddio a gwrthocsidiol. Mae astudiaethau wedi dangos bod cistanche yn fuddiol i gleifion sy'n dioddef o glefyd yr arennau. Mae'n hysbys bod cynhwysion actif cistanche yn lleihau llid, yn gwella gweithrediad yr arennau ac yn adfer celloedd yr arennau â nam arnynt. Felly, gall integreiddio cistanche o fewn cynllun trin clefyd yr arennau gynnig manteision mawr i gleifion wrth reoli eu cyflwr. Mae Cistanche yn helpu i leihau proteinwria, yn gostwng lefelau BUN a creatinin, ac yn lleihau'r risg o niwed pellach i'r arennau. Yn ogystal, mae cistanche hefyd yn helpu i leihau lefelau colesterol a thriglyserid a all fod yn beryglus i gleifion sy'n dioddef o glefyd yr arennau.

Cliciwch Ar Cistanche Tubulosa Ar gyfer Clefyd yr Arennau

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david.deng@wecistanche.com WhatApp:86 13632399501

In this issue of Hypertension Research, Suzuki et al. [3] reported the results of a large retrospective observational study that aimed to explore the association of BP with the risk of developing cardiovascular disease in 188,837 Japanese adults with dipstick proteinuria and an estimated glomerular filtration rate (eGFR) >60 ml/min/1.73 m2. These individuals were categorized into 4 groups following the classification of hypertension that was introduced in the 2017 AHA/ACC guidelines. During a mean follow-up period of 1050 days, 7039 individuals reached the prespecified primary cardiovascular outcome, defined as the composite of myocardial infarction, angina pectoris, stroke, and heart failure. The analysis was conducted separately for individuals who were not taking BP-lowering medications (n = 173,833) and those who were receiving anti-hypertensive treatment (n = 15,004) [3]. Among drug-naive individuals, compared with the category of normal BP, the multivariable-adjusted hazard ratio (HR) for the primary cardiovascular outcome was 1.07 [95% confidence interval (CI): 0.97–1.17] in the category of elevated BP, 1.30 (95% CI: 1.21–1.40) in stage 1 hypertension and 2.17 (95% CI: 2.01–2.34) in stage 2 hypertension [3]. Among drug-treated individuals, compared with the reference category of patients with a normal BP range, the multivariate-adjusted HR for the composite cardiovascular outcome was 1.00 (95% CI: 0.82–1.23), 0.97 (95% CI: 0.83–1.14) and 1.19 (95% CI: 1.02–1.38) in those with elevated BP, stage 1 and stage 2 hypertension, respectively [3]. This dose-response relationship was consistent in the restricted cubic spline analysis. In the subgroup of drug-naive individuals, the cardiovascular risk was progressively increased after the cutoff point of 120/80 mmHg. Among individuals taking BP-lowering medications, an indication of increased cardiovascular risk was observed only when the BP levels were >140% 2f90 mmHg [3].

Un dull o ddiffinio gorbwysedd a nodi'r targedau therapiwtig gorau posibl yw gwerthuso lefelau BP am y risg o ganlyniadau iechyd andwyol, fel y gwnaed yn yr astudiaeth arsylwadol fawr o Suzuki et al. [3]. Ymhlith unigolion sy'n cymryd meddyginiaethau gostwng BP, dangosodd y dadansoddiad hwn nad yw'r categori gorbwysedd cam 1, fel y'i diffinnir yng nghanllaw 2017 AHA / ACC, yn nodi cleifion sydd â risg uwch o ddatblygu clefyd cardiofasgwlaidd [3]. Os tybiwn fod y cysylltiad risg hwn yn achosol, yna efallai na fydd y targed BP dwys o 130/80 mmHg a sefydlwyd yng nghanllaw 2017 AHA/ACC yn addas ar gyfer trin gorbwysedd mewn cleifion â CKD proteinwrig. Gan gymryd i ystyriaeth mai cyfyngiad cynhenid ​​​​ar astudiaethau arsylwi yw eu hanallu i ddarparu cysylltiadau risg achos-ac-effaith uniongyrchol, dull mwy dibynadwy o ddiffinio'r trothwy BP o fudd therapiwtig yw gwerthuso data o hap-dreialon sy'n dangos gostyngiadau yn y risg o canlyniadau iechyd andwyol gyda phrotocolau lleihau pwysedd gwaed dwys.

Compelling clinical trial evidence to demonstrate nephroprotection with lower BP targets is lacking. The Modification of Diet in Renal Disease (MDRD) [4] and the African American Study of Kidney Disease and Hypertension (AASK) [5] were 2 landmark trials that randomly assigned nondiabetic patients with CKD to achieve an intensive (approximately 125/75 mmHg) versus a standard (140/90 mmHg) BP goal. Until the completion of their randomized phase, neither of these 2 trials demonstrated an overall improvement in kidney outcomes with the achievement of tighter BP control [4;5]. However, a sub-group analysis of the MDRD suggested that intensive BP-lowering results were associated with a slower rate of decline in the GFR in patients who had more severe proteinuria (>1 g/diwrnod) ar y llinell sylfaen [4]. Cefnogwyd y syniad bod proteinwria yn addasu effeithiau triniaeth gostwng BP dwys hefyd gan ddadansoddiad post hoc o'r AASK [6]. Ar ôl i'r cyfnod prawf ddod i ben, gwahoddwyd cyfranogwyr AASK i gymryd rhan mewn astudiaeth carfan ôl-dreial. Yn y dadansoddiad cyffredinol o gamau prawf a charfan yr AASK, nid oedd unrhyw wahaniaeth rhwng y breichiau triniaeth ddwys a thriniaeth safonol yn y risg o ddilyniant CKD [6]. Fodd bynnag, gwelwyd gostyngiad risg cymharol sylweddol o 27 y cant yn y canlyniad arennau cyfansawdd yn yr is-grŵp o gyfranogwyr AASK a oedd â chymhareb protein-i-creatinin wrinol o> 0.22 g/g ar y llinell sylfaen [6]. Er mai dim ond mewn dadansoddiadau is-grŵp y gwelwyd arwydd o nephroprotection gyda rheolaeth BP dwys, dylanwadodd y data ansawdd isel hyn ar ganllaw 2012 KDIGO i ddarparu argymhelliad Lefel 2D gwan ar gyfer targed BP llymach o<130/80 mmHg in proteinuric CKD and a standard BP target of <140/90 mmHg for patients without proteinuric CKD [7].

Wedi'i gyhoeddi yn 2015, dangosodd Treial Ymyrraeth Pwysedd Gwaed Systolig (SPRINT) fod ymhlith 9361 o gleifion nad ydynt yn diabetig â phroffil risg cardiofasgwlaidd uchel, gan dargedu BP systolig o<120 mmHg compared with < 140 mmHg provoked a 25% relative risk reduction in fatal and nonfatal cardiovascular events as well as a 27% relative risk reduction in all-cause mortality [8]. A prespecified subgroup analysis that included 2624 SPRINT participants with an eGFR of <60 ml/min/1.73 m2 at baseline showed that the cardioprotective benefit of intensive BP-lowering did not differ between patients with or without CKD [9]. A subsequent subgroup analysis of 1723 SPRINT participants with a urinary albumin-to-creatinine ratio of ≥30 mg/g at baseline also showed that the beneficial effects of intensive BP control on cardiovascular events and all-cause death were similar irrespective of the presence of albuminuria [10]. A slower progression of CKD was not associated with the lower systolic BP target in SPRINT [9]. It must be noted, however, that the prespecified kidney outcome, defined as the composite of sustained ≥ 50% decline in eGFR from baseline or end-stage kidney disease, occurred in only 15 patients in the intensive-treatment arm versus 16 patients in the standard-treatment arm [9]. Therefore, SPRINT was not adequately powered to detect the kidney protective effects of intensive BP-lowering.

Er bod SPRINT wedi dangos budd cardioprotective sylweddol pan dargedwyd BP systolig i lefelau<120 mmHg compared with <140 mmHg, the 2017 AHA/ ACC guideline set the systolic BP target at 130 mmHg [1]. Most likely, this algebraic adjustment by 10 mmHg was performed in an attempt to counteract the expected mean difference between routine office BP recordings that are widely used in daily clinical practice and research-grade BP measurement methodology that guided the intensifies- cation of antihypertensive treatment throughout the SPRINT trial. In SPRINT, office BP was measured under standardized conditions: multiple automated BP recordings were taken after a prespecified 5-minute rest period in a quiet room and without the presence of an observer in the room [8]. In a diagnostic test study that included 275 patients with CKD, office BP was measured with the research-grade technique that was used in SPRINT [11]. On the same day, office BP was also recorded without the specification of a 5-minute seated rest [11]. The mean difference between research-grade and routine office systolic BP was −12.7 mmHg, but the 95% limits of agreement were wide, ranging from −46.1 mmHg to 20.7 mmHg [11]. These data indicate that algebraic manipulation of routine office BP of any degree is probably insufficient to counteract the large variability in BP levels from patient to patient. Perhaps the 2021 KDIGO guidelines take a clearer and more straightforward position on this crucial issue, recommending a systolic BP target of <120 mmHg (as in the intensive-treatment arm of SPRINT) with the use of standardized BP measurement methodology in the office environment [2].

Have the results of SPRINT conclusively answered the question of the optimal BP target for the management of hypertension in the entire spectrum of patients with CKD? The answer is probably no. The results of SPRINT are generalizable to patients with clinical characteristics similar to those of the patients who participated in that landmark trial. Notably, SPRINT excluded patients with diabetic kidney disease, polycystic kidney disease, proteinuria >1 g/ dydd, ac eGFR<20 ml/min/1.73 m2 [8–10]. Future research is needed to investigate the benefit/risk ratio of intensive BP-lowering protocols in these large subgroups of patients with CKD.

Cydymffurfio â safonau moesegol

Cyfeiriadau

1. Whelton PK, Carey RM, Aronow WS, Casey DE, Collins KJ, Dennison HC, et al. 2017 ACC / AHA / AAPA / ABC / ACPM / AGS / APhA / ASH / ASPC / NMA / PCNA Canllaw ar gyfer Atal, Canfod, Gwerthuso a Rheoli Pwysedd Gwaed Uchel mewn Oedolion: Adroddiad o Goleg Cardioleg America / America Tasglu Cymdeithas y Galon ar Ganllawiau Ymarfer Clinigol. Gorbwysedd 2018; 71: 1269-324.

2. Canllaw Ymarfer Clinigol KDIGO 2021 ar gyfer Rheoli Pwysedd Gwaed mewn Clefyd Cronig yr Arennau. Arennau Int. 2021; 99:S1-S87.

3. Suzuki Y, Kaneko H, Yano Y, Okada A, Fujio K, Matsuoka S, et al. Y cysylltiad rhwng BP a chanlyniadau cardiofasgwlaidd mewn cleifion â phroteinwria dipstick a gweithrediad yr arennau wedi'i gadw. Hypertens Res. 2022.

4. Klahr S, Levey AS, Beck GJ, Caggiula AW, Hunsicker L, Kusek JW, et al. Effeithiau cyfyngu ar broteinau dietegol a rheoli pwysedd gwaed ar ddatblygiad clefyd arennol cronig. Grŵp Astudio Addasu Diet mewn Clefyd Arennol. N. Eng J Med. 1994;330:877–84.

5. Wright JT, Bakris G, Greene T, Agodoa LY, Appel LJ, Charleston J, et al. Effaith gostwng pwysedd gwaed a dosbarth cyffuriau gwrthhypertensive ar ddatblygiad clefyd gorbwysedd yr arennau: canlyniadau treial AASK. JAMA 2002; 288: 2421-31.

6. Appel LJ, Wright JT, Greene T, Agodoa LY, Astor BC, Bakris GL, et al. Rheolaeth ddwys ar bwysedd gwaed mewn clefyd cronig yn yr arennau gorbwysedd. N. Eng J Med. 2010; 363:918-29.

7. Clefyd yr Arennau: Grŵp Gwaith Pwysedd Gwaed Gwella Canlyniadau Byd-eang (KDIGO). Canllaw ymarfer clinigol KDIGO ar gyfer rheoli pwysedd gwaed mewn clefyd cronig yn yr arennau. Suppl Int Arennau. 2012; 2: 337-414.

8. Wright JT Jr, Williamson JD, Whelton PK, Snyder JK, Sink KM, Rocco MV, et al. Treial ar hap o reolaeth pwysedd gwaed dwys yn erbyn safonol. N. Eng J Med. 2015; 373: 2103-16.

9. Cheung AK, Rahman M, Reboussin DM, Craven TE, Greene T, Kimmel PL, et al. Effeithiau rheolaeth BP ddwys mewn CKD. J Am Soc Nephrol. 2017; 28: 2812-23.

10. Chang AR, Kramer H, Wei G, Boucher R, Grams ME, Berlowitz D, et al. Effeithiau rheoli pwysedd gwaed yn ddwys mewn cleifion ag Albuminuria a hebddynt: Dadansoddiadau Post Hoc o SPRINT. Clin J Am Soc Nephrol. 2020; 15: 1121-8.

11. Agarwal R. Goblygiadau techneg mesur pwysedd gwaed ar gyfer gweithredu treial ymyrraeth pwysedd gwaed systolig (SPRINT). J Am Heart Assoc. 2017;6:e004536.

Am ragor o wybodaeth: david.deng@wecistanche.com WhatApp:86 13632399501