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來源：泰然健康網(wǎng) 時間：2024年12月11日 07:53

高鉀血癥是慢性腎臟病（chronic kidney disease，CKD）患者中常見的電解質(zhì)紊亂之一，嚴重時可危及生命。在我國，血鉀>5.5 mmol/L通常被定義為高鉀血癥，但2016年加拿大心血管協(xié)會指南[1]、2019年意大利腎臟病協(xié)會腎病患者高鉀管理指南[2]、2020改善全球腎臟病預(yù)后組織（KDIGO）腎臟病血鉀管理專家共識意見[3]等國際指南共識將高鉀血癥定義為血鉀>5.0 mmol/L。越來越多的研究數(shù)據(jù)表明，“臨床正?！毖浄秶亩x需要考量血鉀對患者的心腎事件及總體預(yù)后的影響。國外CKD生存研究表明[4-5]，血鉀水平與死亡率呈“U”形曲線，血鉀在4.0~4.5 mmol/L具有最佳生存期，而即使是輕度低鉀（血鉀<4.0 mmol/L）和輕度高鉀（血鉀>5.0 mmol/L）也與患者死亡率升高具有顯著相關(guān)性。但在我國，尚缺乏血鉀水平與CKD患者預(yù)后的相關(guān)研究數(shù)據(jù)。

根據(jù)國外相關(guān)數(shù)據(jù)，總?cè)巳褐懈哜浹Y的患病率約為2%~3%[6]，住院患者的患病率約為1%~10%[7]。在中國，一項高鉀血癥流行病學(xué)研究顯示，我國門診患者的高鉀血癥患病率約為3.86%，其中CKD患者的高鉀血癥患病率則高達22.89%[8]。當(dāng)腎小球濾過率（GFR）>60 ml·min-1·(1.73 m2)-1時，高鉀血癥并不常見，但隨著GFR下降，高鉀血癥的患病率將升高。日本真實世界研究數(shù)據(jù)顯示，CKD G3a、G3b、G4、G5期的高鉀血癥患病率分別為13.22%、24.56%、43.65%、51.19%[7]；此外，使用腎素-血管緊張素-醛固酮系統(tǒng)（RAAS）抑制劑會進一步加重高鉀風(fēng)險，G4、G5期使用RAAS抑制劑患者高鉀血癥患病率分別升高至51.00%、62.79%[7]。

高鉀血癥的治療包括急性治療和長期管理兩部分。急性治療的目標是盡可能將血鉀降低到安全范圍內(nèi)，以防止危及生命的心律失常發(fā)生。急性治療方法包括：①通過靜脈注射鈣劑穩(wěn)定膜電位，以拮抗高鉀血癥引起的心臟毒性；②通過使用胰島素+葡萄糖、β腎上腺素能激動劑等促進鉀從細胞外移至細胞內(nèi)，從而降低血鉀；③使用利尿劑、陽離子樹脂或透析從體內(nèi)清除鉀離子[9]。

目前臨床實踐中，高鉀血癥的治療往往止于急性處理。近年來研究發(fā)現(xiàn)，高鉀血癥是一種容易反復(fù)發(fā)作的疾病，復(fù)發(fā)率高，復(fù)發(fā)間隔時間逐漸縮短[10-11]，55.6%的患者在1年內(nèi)復(fù)發(fā)輕度以上的高鉀血癥（血鉀>5.0 mmol/L），19.9%的患者在1年內(nèi)復(fù)發(fā)中重度高鉀血癥（血鉀>5.5 mmol/L）[7]，而高鉀血癥的反復(fù)發(fā)作則與患者不良心血管事件發(fā)生率及死亡率增加相關(guān)。這意味著，在高鉀血癥急性治療后，仍然需要采取措施保持血鉀長期穩(wěn)態(tài)，預(yù)防高血鉀癥的反復(fù)發(fā)作。本文將就CKD高血鉀癥長期管理的研究進展作一綜述。

一、低鉀飲食

低鉀飲食是目前高鉀血癥長期管理的手段之一，得到了多項指南的推薦。但是，鉀存在于多種食物中，患者往往難以憑借簡單方法予以區(qū)分，因此患者對低鉀飲食的依從性差異較大。更值得關(guān)注的是，許多高鉀食物，如終止高血壓膳食（dietary approaches to stop hypertension，DASH），被認為對心臟健康有益，但低鉀飲食可能會加重CKD患者的心血管疾病負擔(dān)[12]。此外，低鉀飲食缺乏膳食纖維，患者更容易出現(xiàn)便秘[13]等癥狀，進而影響患者的社會活動[3]。因此，低鉀飲食不是管理高鉀血癥最主要的措施。

二、停用或減量使用誘發(fā)高鉀血癥的藥物

腎功能受損和低醛固酮血癥患者容易出現(xiàn)藥物誘發(fā)的高鉀血癥，其中在老年人中尤為常見。容易誘發(fā)高鉀血癥的藥物包括RAAS抑制劑[14]、保鉀利尿劑、非甾體類抗炎藥（non-steroidal anti-inflammatory drugs，NSAIDs）及中藥制劑等，對于高鉀血癥高危人群，應(yīng)盡量避免使用這些藥物。但是，RAAS抑制劑作為有確切心腎保護獲益的治療藥物，獲得了多項指南推薦，停用或減量使用將影響患者預(yù)后[15-16]。因此，對于使用RAAS抑制劑而出現(xiàn)高鉀血癥的患者，應(yīng)使用其他方法積極控制高鉀血癥，盡量避免RAAS抑制劑的停用或減量使用。

三、糾正代謝性酸中毒

代謝性酸中毒是CKD患者的常見并發(fā)癥，特別是在腎功能嚴重受損情況下，多數(shù)患者代謝性酸中毒長期存在。在代謝性酸中毒情況下，機體處于缺氧狀態(tài)，細胞鈉鉀泵供能不足，鉀離子向細胞內(nèi)的轉(zhuǎn)運減少；同時，腎小管鈉氫交換代償性增多，導(dǎo)致鈉鉀交換較少，腎臟排鉀減少，導(dǎo)致高鉀血癥發(fā)生[17-18]。目前，對于合并代謝性酸中毒的CKD患者，使用碳酸氫鈉可緩解酸中毒，促進鉀離子轉(zhuǎn)移至細胞內(nèi)，使血鉀降低。但碳酸氫鈉不宜長期使用，以免鈉在體內(nèi)潴留。

四、促進腎臟排鉀

髓袢/噻嗪類利尿劑是增加尿鉀排出的常用藥物，通過阻斷腎單位中的鈉鉀氯離子交換泵來增加腎臟對離子的排泄，但其療效取決于殘余腎功能[19]，且無法預(yù)測利鈉和利鉀效果[20]，臨床上需謹慎使用。應(yīng)排除低血容量情況或在有液體超負荷的患者中使用排鉀利尿劑，同時需要密切監(jiān)測尿量，以避免因醫(yī)源性血容量不足引起的腎臟損害。此外，還需要密切監(jiān)測其潛在不良反應(yīng)，如引起高尿酸血癥等風(fēng)險。

五、促進腸道排鉀

（一）陽離子交換樹脂

陽離子交換樹脂是具有負電荷結(jié)構(gòu)單元的交聯(lián)聚合物，經(jīng)口服或經(jīng)直腸給藥進入人體，在鉀離子濃度最高的結(jié)腸遠端基于競爭性結(jié)合，將樹脂本身的鈉離子或鈣離子交換為包括鉀離子在內(nèi)的其他陽離子。

1. 聚磺苯乙烯鈉（sodium polystyrene sulfonate，SPS）：1958年，美國食品和藥物管理局（Food and Drug Administration，F(xiàn)DA）批準SPS用于急、慢性腎功能不全的高鉀血癥[21]。SPS的作用機制是在胃腸道中（主要是結(jié)腸）通過離子交換作用，以鈉離子置換鉀離子，增加糞便中鉀離子的排泄[22]。

2015年，Lepage等[21]首次報道了SPS在CKD高鉀血癥中療效的隨機對照臨床試驗。該研究納入33例非透析腎病門診患者[eGFR<40 ml·min-1·(1.73 m2)-1，血鉀為5.0~5.9 mmol/L]，按照1∶1的比例隨機分配患者進入SPS組（n=16）或安慰劑組（n=17）（30 g口服，每日1次），治療時間為期7 d。研究結(jié)果顯示，治療7 d后，SPS組血鉀平均降幅達1.25 mmol/L，安慰劑組降幅為0.21 mmol/L，降幅差異達到1.04 mmol/L（95%CI 0.71~1.37，P<0.001）[21]。因該研究的樣本量較小，無法得出SPS的安全性結(jié)論，安全性評估顯示SPS組惡心、嘔吐、便秘比例更高，安慰劑組腹瀉比例更高，但差異無統(tǒng)計學(xué)意義，未見結(jié)腸壞死；電解質(zhì)紊亂較輕微，SPS組觀察到的最嚴重低鉀血癥的血鉀水平為3.0 mmol/L[21]。

對于SPS的長期用藥療效及安全性，目前尚無超過7 d的前瞻性研究證據(jù)，多為回顧性研究報道。2009年9月，F(xiàn)DA對SPS發(fā)布了黑框警告，要求警惕SPS與山梨醇合并用藥帶來的腸壞死風(fēng)險。既往認為SPS出現(xiàn)胃腸道不良反應(yīng)是由于SPS制劑中添加了山梨醇，增加了腸道苯乙烯的含量[23???-27]。但近年來研究發(fā)現(xiàn)SPS本身可能存在一定的不良反應(yīng)。2013年Harel等[27]對58例（41例使用含山梨醇的SPS和17例使用不含山梨醇的SPS）不良事件進行鑒定，結(jié)果顯示，結(jié)腸是SPS最常見的損傷部位（n=44；76%），而透壁壞死（n=36；62%）是最常見的組織病理學(xué)變化。此外，無論是否合并使用山梨醇，使用SPS均可導(dǎo)致胃腸道損傷[27]。

2. 聚苯乙烯磺酸鈣（calcium polystyrene sulfonate，CPS）：CPS是新一代口服陽離子交換樹脂，與SPS不同之處在于，其通過鈣離子置換鉀離子，增加糞便中鉀離子的排泄。2010年CPS在我國獲批用于治療急、慢性腎功能不全患者的高鉀血癥。

CPS的1項單臂、開放、多中心Ⅳ期研究納入診斷為CKD且血鉀為5.50~6.50 mmol/L的非透析患者98例，接受為期7 d的CPS治療（5 g/次，每天3次）[28]。研究結(jié)果顯示，CPS治療1 d后，98例患者血鉀由（5.85±0.26）mmol/L降至（5.16±0.51）mmol/L（P<0.01），治療1周后血鉀降至（4.67±0.57）mmol/L（P<0.01），停藥1周后血鉀水平為（4.96±0.66）mmol/L（P<0.01），與基線值相比，差異均有統(tǒng)計學(xué)意義（均P<0.01）[28]。安全性方面，10.2%的患者出現(xiàn)與CPS相關(guān)的胃腸道不良事件，其中，便秘是最常見的藥物不良反應(yīng)（9.2%），未發(fā)現(xiàn)治療相關(guān)的嚴重不良事件[28]。

對于CPS的長期用藥療效及安全性，文獻報道顯示，CPS可引起消化系統(tǒng)不良事件，例如惡心、嘔吐、便秘、腸梗阻[29-30]、腸炎[31]、結(jié)腸壞死[32-33]等。2015年，Kao等[34]報道CPS嚴重并發(fā)癥1例，一例59歲女性腹膜透析相關(guān)性腹膜炎患者在服用大劑量CPS后，出現(xiàn)回腸和結(jié)腸穿孔，最終感染休克死亡，術(shù)后腸組織病理顯示透壁壞死和穿孔伴嗜堿性的角狀晶體。

（二）新型口服降鉀藥物

1. Patiromer：2015年FDA批準Patiromer用于治療高鉀血癥，目前該藥尚未在中國上市。與傳統(tǒng)降鉀樹脂不同，Patiromer是一種不可吸收的人工合成聚合物，在胃腸道（主要在結(jié)腸）通過置換鈣離子結(jié)合鉀離子，從而降低血鉀濃度，而結(jié)合的鉀離子隨著糞便排出體外[35]。臨床試驗顯示，對于接受RAAS抑制劑治療的CKD合并高鉀血癥患者，Patiromer可降低血鉀濃度，同時可以降低高鉀血癥的復(fù)發(fā)率[36]。

多項體外藥物相互作用研究顯示（28種口服藥），Patiromer會使其中14種藥物（包括纈沙坦和羅格列酮）的生物利用度降低超過30%[37]。為避免藥物間相互作用，F(xiàn)DA建議將初始劑量控制在8.4 g/d（限單次服用），并與其他口服藥前后間隔3 h使用。需要注意的是，Patiromer除了與鉀離子結(jié)合外，還可與NH4+、Mg2+結(jié)合，因此Patiromer可導(dǎo)致輕度低鎂血癥[37]。此外，Patiromer常見的不良反應(yīng)還包括便秘、腹瀉、惡心、腹部不適和胃腸脹氣等胃腸道不良事件[38]。

2. 環(huán)硅酸鋯鈉：環(huán)硅酸鋯鈉是一種穩(wěn)定的無機晶體，其獨特的立方晶體結(jié)構(gòu)包含3個鋯原子和4個硅原子，組成七元環(huán)結(jié)構(gòu)，可根據(jù)離子直徑選擇性結(jié)合陽離子，以達到最佳能量平衡狀態(tài)。該七元環(huán)孔隙與陽離子的結(jié)合部分直徑為3?，與鉀離子直徑2.98?完全匹配，所以環(huán)硅酸鋯鈉可高度特異地結(jié)合鉀離子，每克環(huán)硅酸鋯鈉最多可置換出2.7 mmol的鉀，其與鉀離子的結(jié)合力是鈣離子/鎂離子的25倍[39]。環(huán)硅酸鋯鈉可在全消化道通過置換鈉離子/氫離子以結(jié)合鉀離子，最終通過糞便將鉀離子排出體外。

目前，基于2項雙盲、安慰劑對照臨床試驗及1項開放標簽長達1年的臨床試驗數(shù)據(jù)，2019年12月30日環(huán)硅酸鋯鈉獲批在中國用于治療成人高鉀血癥[40??-43]。報道顯示，環(huán)硅酸鋯鈉首次用藥10 g后1 h即可起效，恢復(fù)正常血鉀水平的中位時間為2.2 h[43]；此外，在長達12個月的高鉀血癥長期管理中，約90%患者血鉀水平<5.1 mmol/L[41]。在安全性方面，環(huán)硅酸鋯鈉不被人體吸收、不溶于水且遇水不膨脹，消化道耐受性良好；同時，其不會影響其他離子代謝，長期治療對血鎂、血鈣濃度無顯著影響；但大劑量（15 g，每天1次）組患者可出現(xiàn)水腫及低鉀血癥[41]?？傮w而言，環(huán)硅酸鋯鈉可迅速降低血清鉀水平，并可長期維持血鉀在正常水平，長期（12個月）治療安全有效，總體耐受性良好，目前已經(jīng)獲得了多項國際指南推薦用于高鉀血癥治療[44]。可喜的是，該藥2019年已被納入《臨床急需境外新藥名單》，給腎內(nèi)科醫(yī)師降低CKD高鉀血癥提供了一種新的選擇。

六、總結(jié)

對于CKD及心力衰竭等持續(xù)存在高鉀血癥誘因的患者，長期監(jiān)控和持續(xù)管理患者血鉀水平將有助于降低因高鉀血癥急性發(fā)作導(dǎo)致的嚴重心律失常和猝死的風(fēng)險；同時，也可減少因單純高鉀血癥而進入慢性透析的患者比例。除定期監(jiān)測血鉀外，目前高鉀血癥的長期管理主要包括合理控制飲食、避免使用誘發(fā)高鉀血癥藥物以及適當(dāng)使用相關(guān)藥物促進腎臟或腸道排鉀，但不同治療手段各有優(yōu)勢及局限性，臨床醫(yī)生應(yīng)酌情制定個體化治療方案。

口服鉀離子結(jié)合劑因用藥便捷，對高鉀血癥的長期管理具有重要意義；但SPS、CPS缺乏長期用藥的療效及安全性證據(jù)，且存在一定胃腸道不良反應(yīng)風(fēng)險，可能不適宜用于高鉀血癥的長期管理。隨著環(huán)硅酸鋯鈉、Patiromer等新型口服降鉀藥物的出現(xiàn)，患者將有更多更好的選擇，讓高鉀血癥的長期管理成為可能。

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Ainsworth C

, et al. Canadian cardiovascular society/canadian cardiovascular critical care society/canadian association of interventional cardiology position statement on the optimal care of the postarrest patient[J]. Can J Cardiol, 2017, 33(1): 1-16. DOI: 10.1016/j.cjca.2016.10.021.

Out of hospital cardiac arrest (OHCA) is associated with a low rate of survival to hospital discharge and high rates of neurological morbidity among survivors. Programmatic efforts to institute and integrate OHCA best care practices from the bystander response through to the in-hospital phase have been associated with improved patient outcomes. This Canadian Cardiovascular Society position statement was developed to provide comprehensive yet practical recommendations to guide the in-hospital care of OHCA patients. Using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system recommendations have been generated. Recommendations on initial care delivery on the basis of presenting rhythm, appropriate use of targeted temperature management, postarrest angiography, and revascularization in the initial phase of care of the OHCA patient are detailed within this statement. In addition, further description of best practices on sedation, use of neuromuscular blockade, oxygenation targets, hemodynamic monitoring, and blood product transfusion triggers in the critical care environment are contained in this document. Last, discussion of optimal care systems for the OHCA patient is provided. These guidelines aim to serve as a practical guide to optimize the in-hospital care of survivors of cardiac arrest and encourage the adoption of "best practice" protocols and treatment pathways. Emphasis is placed on integrating these aspects of in-hospital care as part of a postarrest "care bundle." It is hoped that this position statement can assist all medical professionals who treat survivors of cardiac arrest.Copyright ? 2016 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.

{{custom_citation.pmid}9}https://doi.org/{{custom_citation.pmid}5}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}1}{{custom_citation.pmid}7}本文引用 [{{custom_citation.url}8}]摘要{{custom_citation.url}6}[2]Bianchi S

Aucella F

De Nicola L

, et al. Management of hyperkalemia in patients with kidney disease: a position paper endorsed by the Italian Society of Nephrology[J]. J Nephrol, 2019, 32(4): 499-516. DOI: 10.1007/s40620-019-00617-y.

Hyperkalemia (HK) is the most common electrolyte disturbance observed in patients with kidney disease, particularly in those in whom diabetes and heart failure are present or are on treatment with renin-angiotensin-aldosterone system inhibitors (RAASIs). HK is recognised as a major risk of potentially life threatening cardiac arrhythmic complications. When an acute reduction of renal function manifests, both in patients with chronic kidney disease (CKD) and in those with previously normal renal function, HK is the main indication for the execution of urgent medical treatment and the recourse to extracorporeal replacement therapies. In patients with end-stage renal disease, the presence of HK not responsive to medical therapy is an indication at the beginning of chronic renal replacement therapy. HK can also be associated indirectly with the progression of CKD, because the finding of high potassium values leads to withdrawal of treatment with RAASIs, which constitute the first choice nephro-protective treatment. It is therefore essential to identify patients at risk of developing HK, and to implement therapeutic interventions aimed at preventing and treating this dangerous complication of kidney disease. Current strategies aimed at the prevention and treatment of HK are still unsatisfactory, as evidenced by the relatively high prevalence of HK also in patients under stable nephrology care, and even in the ideal setting of randomized clinical trials where optimal treatment and monitoring are mandatory. This position paper will review the main therapeutic interventions to be implemented for the prevention, detection and treatment of HK in patients with CKD on conservative care, in those on dialysis, in patients in whom renal disease is associated with diabetes, heart failure, resistant hypertension and who are on treatment with RAASIs, and finally in those presenting with severe acute HK.

{{custom_citation.url}4}https://doi.org/{{custom_citation.url}0}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.url}6}{{custom_citation.url}2}本文引用 [{{custom_citation.url}3}]摘要{{custom_citationIndex}1}[3]Clase CM

Carrero JJ

Ellison DH

, et al. Potassium homeostasis and management of dyskalemia in kidney diseases: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference[J]. Kidney Int, 2020, 97(1): 42-61. DOI: 10.1016/j.kint.2019.09.018.

Potassium disorders are common in patients with kidney disease, particularly in patients with tubular disorders and low glomerular filtration rate. A multidisciplinary group of researchers and clinicians met in October 2018 to identify evidence and address controversies in potassium management. The issues discussed encompassed our latest understanding of the regulation of tubular potassium excretion in health and disease; the relationship of potassium intake to cardiovascular and kidney outcomes, with increasing evidence showing beneficial associations with plant-based diet and data to suggest a paradigm shift from the idea of dietary restriction toward fostering patterns of eating that are associated with better outcomes; the paucity of data on the effect of dietary modification in restoring abnormal serum potassium to the normal range; a novel diagnostic algorithm for hypokalemia that takes into account the ascendency of the clinical context in determining cause, aligning the educational strategy with a practical approach to diagnosis; and therapeutic approaches in managing hyperkalemia when chronic and in the emergency or hospital ward. In sum, we provide here our conference deliberations on potassium homeostasis in health and disease, guidance for evaluation and management of dyskalemias in the context of kidney diseases, and research priorities in each of the above areas.Copyright ? 2019 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.

{{custom_ref.citationList}9}https://doi.org/{{custom_ref.citationList}5}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_ref.citationList}1}{{custom_citation.annotation}7}本文引用 [{{custom_citation.annotation}8}]摘要0}9}!=''" class="glyphicon glyphicon-triangle-bottom biaotijiantoush biaotijiantoush1" onclick="ckwx_show_hide(this)">0}8} && {{custom_ref.citedCount>0}7}!=''" class="mag_main_zhengwen_left_div_ckwx_table_ckwx_xiangqing">{{custom_ref.citedCount>0}6}[4]Kovesdy CP

Matsushita K

Sang Y

, et al. Serum potassium and adverse outcomes across the range of kidney function: a CKD prognosis consortium meta-analysis[J]. Eur Heart J, 2018, 39(17): 1535-1542. DOI: 10.1093/eurheartj/ehy100.

Both hypo- and hyperkalaemia can have immediate deleterious physiological effects, and less is known about long-term risks. The objective was to determine the risks of all-cause mortality, cardiovascular mortality, and end-stage renal disease associated with potassium levels across the range of kidney function and evaluate for consistency across cohorts in a global consortium.We performed an individual-level data meta-analysis of 27 international cohorts [10 general population, 7 high cardiovascular risk, and 10 chronic kidney disease (CKD)] in the CKD Prognosis Consortium. We used Cox regression followed by random-effects meta-analysis to assess the relationship between baseline potassium and adverse outcomes, adjusted for demographic and clinical characteristics, overall and across strata of estimated glomerular filtration rate (eGFR) and albuminuria. We included 1 217 986 participants followed up for a mean of 6.9?years. The average age was 55?±?16?years, average eGFR was 83?±?23?mL/min/1.73?m2, and 17% had moderate- to-severe increased albuminuria levels. The mean baseline potassium was 4.2?±?0.4?mmol/L. The risk of serum potassium of >5.5?mmol/L was related to lower eGFR and higher albuminuria. The risk relationship between potassium levels and adverse outcomes was U-shaped, with the lowest risk at serum potassium of 4-4.5?mmol/L. Compared with a reference of 4.2?mmol/L, the adjusted hazard ratio for all-cause mortality was 1.22 [95% confidence interval (CI) 1.15-1.29] at 5.5?mmol/L and 1.49 (95% CI 1.26-1.76) at 3.0?mmol/L. Risks were similar by eGFR, albuminuria, renin-angiotensin-aldosterone system inhibitor use, and across cohorts.Outpatient potassium levels both above and below the normal range are consistently associated with adverse outcomes, with similar risk relationships across eGFR and albuminuria.

0}5}" m-for-val="custom_citation" m-for-index="custom_citationIndex">{{custom_ref.citedCount>0}4}0}3} && {{custom_ref.citedCount>0}2}!=''" class="new_full_rich_cankaowenxian_zuozhe new_full_rich_cankaowenxian_lianjie">https://doi.org/{{custom_ref.citedCount>0}0}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citationIndex}6}{{custom_citationIndex}2}本文引用 [{{custom_ref.citationList}3}]摘要{{custom_ref.id}1}[5]De Nicola L

Di Lullo L

Paoletti E

, et al. Chronic hyperkalemia in non-dialysis CKD: controversial issues in nephrology practice[J]. J Nephrol, 2018, 31(5): 653-664. DOI: 10.1007/s40620-018-0502-6.

Chronic hyperkalemia is a major complication of chronic kidney disease (CKD) that occurs frequently, heralds poor prognosis, and necessitates careful management by the nephrologist. Current strategies aimed at prevention and treatment of hyperkalemia are still suboptimal, as evidenced by the relatively high prevalence of hyperkalemia in patients under stable nephrology care, and even in the ideal setting of randomized trials where best treatment and monitoring are mandatory. The aim of this review was to identify and discuss a range of unresolved issues related to the management of chronic hyperkalemia in non-dialysis CKD. The following topics of clinical interest were addressed: diagnosis, relationship with main comorbidities of CKD, therapy with inhibitors of the renin-angiotensin-aldosterone system, efficacy of current dietary and pharmacological treatment, and the potential role of the new generation of potassium binders. Opinion-based answers are provided for each of these controversial issues.

{{custom_ref.citedCount}9}https://doi.org/{{custom_ref.citedCount}5}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_ref.citedCount}1}{{custom_citationIndex}7}本文引用 [{{custom_ref.citationList}8}]摘要{{custom_ref.bodyP_ids}6}[6]Kovesdy CP

. Management of hyperkalaemia in chronic kidney disease[J]. Nat Rev Nephrol, 2014, 10(11): 653-662. DOI: 10.1038/nrneph.2014.168.

Hyperkalaemia is common in patients with chronic kidney disease (CKD), in part because of the effects of kidney dysfunction on potassium homeostasis and in part because of the cluster of comorbidities (and their associated treatments) that occur in patients with CKD. Owing to its electrophysiological effects, severe hyperkalaemia represents a medical emergency that usually requires prompt intervention, whereas the prevention of hazardous hyperkalaemic episodes in at-risk patients requires measures aimed at the long-term normalization of potassium homeostasis. The options for effective and safe medical interventions to restore chronic potassium balance are few, and long-term management of hyperkalaemia is primarily limited to the correction of modifiable exacerbating factors. This situation can result in a difficult trade-off in patients with CKD, because drugs that are beneficial to these patients (for example, renin-angiotensin-aldosterone-system antagonists) are often the most prominent cause of their hyperkalaemia. Maintaining the use of these beneficial medications while implementing various strategies to control potassium balance is desirable; however, discontinuation rates remain high. The emergence of new medications that specifically target hyperkalaemia could lead to a therapeutic paradigm shift, emphasizing preventive management over ad hoc treatment of incidentally discovered elevations in serum potassium levels.

{{custom_ref.bodyP_ids}4}https://doi.org/{{custom_ref.bodyP_ids}0}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_ref.id}6}{{custom_ref.id}2}本文引用 [{{custom_bodyP_id}3}]摘要{{custom_citation.annotation}1}[7]Kashihara N

Kohsaka S

Kanda E

, et al. Hyperkalemia in real-world patients under continuous medical care in Japan[J]. Kidney Int Rep, 2019, 4(9): 1248-1260. DOI: 10.1016/j.ekir.2019.05.018.

An abnormal serum potassium (S-K) level is an important electrolyte disturbance. However, its relation to clinical outcomes in real-world patients, particularly hyperkalemia burden, is not extensively studied.An observational retrospective cohort study using a Japanese hospital claims database was done (April 2008-September 2017; = 1,022,087). Associations between index S-K level and 3-year survival were modeled using cubic spline regression. Cox regression model was applied to estimate the time to death according to different S-K levels. Prevalence, patient characteristics, treatment patterns, and management of patients with hyperkalemia from first episode were assessed.Hyperkalemia prevalence was 67.9 (95% confidence interval [CI]: 67.1-68.8) per 1000 and increased in patients with chronic kidney disease (CKD) (227.9; 95% CI: 224.3-231.5), heart failure (134.0; 95% CI: 131.2-136.8), and renin-angiotensin-aldosterone system inhibitor (RAASi) use (142.2; 95% CI: 139.6-144.7). U-shaped associations between S-K level and 3-year survival were observed with nadir 4.0 mEq/l. The risk of death was increased at S-K 5.1-5.4 mEq with hazard ratio of 7.6 (95% CI: 7.2-8.0). The 3-year mortality rate in patients with CKD stages 3a, 3b, 4, and 5 with normokalemia were 1.51%, 3.93%, 10.86%, and 12.09%, whereas that in patients with CKD stage 3a at S-K 5.1-5.4, 5.5-5.9, and ≥6.0 mEq/l increased to 10.31%, 11.43%, and 22.64%, respectively. Despite treatment with loop diuretics (18.5%) and potassium binders (5.8%), >30% of patients had persistently high S-K (≥5.1 mEq/l).This study provides real-world insight on hyperkalemia based on a large number of patients with various medical backgrounds.

{{custom_citation.annotation}9}https://doi.org/{{custom_citation.annotation}5}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.annotation}1}{{custom_citation.annotation}7}本文引用 [{{custom_citation.annotation}8}]摘要{{custom_citation.annotation}6}[8]{{custom_citation.annotation}4}https://doi.org/{{custom_citation.annotation}0}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.annotation}6}{{custom_citation.annotation}2}本文引用 [{{custom_citation.annotation}3}]摘要{{referenceList}1}[9]Rossignol P

Legrand M

Kosiborod M

, et al. Emergency management of severe hyperkalemia: guideline for best practice and opportunities for the future[J]. Pharmacol Res, 2016, 113(Pt A): 585-591. DOI: 10.1016/j.phrs.2016.09.039.

Hyperkalemia is a common electrolyte disorder, especially in chronic kidney disease, diabetes mellitus, or heart failure. Hyperkalemia can lead to potentially fatal cardiac dysrhythmias, and it is associated with increased mortality. Determining whether emergency therapy is warranted is largely based on subjective clinical judgment. The Investigator Network Initiative Cardiovascular and Renal Clinical Trialists (INI-CRCT) aimed to evaluate the current knowledge pertaining to the emergency treatment of hyperkalemia. The INI-CRCT developed a treatment algorithm reflecting expert opinion of best practices in the context of current evidence, identified gaps in knowledge, and set priorities for future research. We searched PubMed (to August 4, 2015) for consensus guidelines, reviews, randomized clinical trials, and observational studies, limited to English language but not by publication date. Treatment approaches are based on small studies, anecdotal experience, and traditional practice patterns. The safety and real-world effectiveness of standard therapies remain unproven. Prospective research is needed and should include studies to better characterize the population, define the serum potassium thresholds where life-threatening arrhythmias are imminent, assess the potassium and electrocardiogram response to standard interventions. Randomized, controlled trials are needed to test the safety and efficacy of new potassium binders for the emergency treatment of severe hyperkalemia in hemodynamically stable patients. Existing emergency treatments for severe hyperkalemia are not supported by a compelling body of evidence, and they are used inconsistently across institutions, with potentially significant associated side effects. Further research is needed to fill knowledge gaps, and definitive clinical trials are needed to better define optimal management strategies, and ultimately to improve outcomes in these patients.Copyright ? 2016 Elsevier Ltd. All rights reserved.

{{custom_ref.id}9}https://doi.org/{{custom_ref.id}5}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_ref.id}1}{{custom_index}7}本文引用 [{{custom_ref.nian}8}]摘要{{custom_ref.citedCount}6}[10]Aoki K

Akaba K

. Characteristics of nonoliguric hyperkalemia in preterm infants: a case-control study in a single center[J]. Pediatr Int, 2020, 62(5): 576-580. DOI: 10.1111/ped.14115.

Preterm infants often present with hyperkalemia during the first days after birth without showing oliguria. This is known as nonoliguric hyperkalemia (NOHK). As its clinical features have not been completely understood to date, we aimed to elucidate the characteristics of NOHK, including its risk factors, in preterm infants.For this case-control study, we reviewed the files of all infants born before 32 weeks of gestational age in our neonatal intensive care unit between 2011 and 2018. We distinguished the NOHK and non-NOHK groups and compared their characteristics and blood potassium levels. Nonoliguric hyperkalemia was defined as peak blood potassium concentration of ≥6.0 mmol/L during the first 72 h of life with a urine output of ≥1 mL/kg/h.Of the 99 infants enrolled, 21 (21%) demonstrated NOHK. Infants with NOHK were more likely to have been exposed to antenatal magnesium sulfate (MgSO ) (P = 0.019) than those in the non-NOHK group. Acute morbidities and mortality were not statistically different. Multivariate analysis indicated that administration of maternal MgSO for longer than 24 h at any point before delivery was a risk factor for NOHK. Its adjusted odds ratio and 95% confidence interval were 4.0 and 1.4-12.3, respectively (P = 0.012).In this study, maternal MgSO administration for longer than 24 h proved to be a risk factor for NOHK in infants born before 32 weeks of gestational age. Infants born to mothers who have received MgSO should be regularly monitored for their electrolytes.? 2019 Japan Pediatric Society.

{{custom_ref.citedCount}4}https://doi.org/{{custom_ref.citedCount}0}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_ref.label}6}{{custom_ref.label}2}本文引用 [{{custom_ref.citationList}3}]摘要{{custom_citation.content}1}[11]Sarwar CM

Papadimitriou L

Pitt B

, et al. Hyperkalemia in heart failure[J]. J Am Coll Cardiol, 2016, 68(14): 1575-1589. DOI: 10.1016/j.jacc.2016.06.060.

Disorders of potassium homeostasis can potentiate the already elevated risk of arrhythmia in heart failure. Heart failure patients have a high prevalence of chronic kidney disease, which further heightens the risk of hyperkalemia, especially when renin-angiotensin-aldosterone system inhibitors are used. Acute treatment for hyperkalemia may not be tolerated in the long term. Recent data for patiromer and sodium zirconium cyclosilicate, used to treat and prevent high serum potassium levels on a more chronic basis, have sparked interest in the treatment of hyperkalemia, as well as the potential use of renin-angiotensin-aldosterone system inhibitors in patients who were previously unable to take these drugs or tolerated only low doses. This review discusses the epidemiology, pathophysiology, and outcomes of hyperkalemia in heart failure; provides an overview of traditional and novel ways to approach management of hyperkalemia; and discusses the need for further research to optimally treat heart failure.Copyright ? 2016 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

{{custom_citation.doi}9}https://doi.org/{{custom_citation.doi}5}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.doi}1}{{custom_citation.doi}7}本文引用 [{{custom_citation.doi}8}]摘要{{custom_citation.doi}6}[12]Kalantar-Zadeh K

Tortorici AR

Chen JL

, et al. Dietary restrictions in dialysis patients: is there anything left to eat?[J]. Semin Dial, 2015, 28(2): 159-168. DOI: 10.1111/sdi.12348.

A significant number of dietary restrictions are imposed traditionally and uniformly on maintenance dialysis patients, whereas there is very little data to support their benefits. Recent studies indicate that dietary restrictions of phosphorus may lead to worse survival and poorer nutritional status. Restricting dietary potassium may deprive dialysis patients of heart‐healthy diets and lead to intake of more atherogenic diets. There is little data about the survival benefits of dietary sodium restriction, and limiting fluid intake may inherently lead to lower protein and calorie consumption, when in fact dialysis patients often need higher protein intake to prevent and correct protein‐energy wasting. Restricting dietary carbohydrates in diabetic dialysis patients may not be beneficial in those with burnt‐out diabetes. Dietary fat including omega‐3 fatty acids may be important caloric sources and should not be restricted. Data to justify other dietary restrictions related to calcium, vitamins, and trace elements are scarce and often contradictory. The restriction of eating during hemodialysis treatment is likely another incorrect practice that may worsen hemodialysis induced hypoglycemia and nutritional derangements. We suggest careful relaxation of most dietary restrictions and adoption of a more balanced and individualized approach, thereby easing some of these overzealous restrictions that have not been proven to offer major advantages to patients and their outcomes and which may in fact worsen patients' quality of life and satisfaction. This manuscript critically reviews the current paradigms and practices of recommended dietary regimens in dialysis patients including those related to dietary protein, carbohydrate, fat, phosphorus, potassium, sodium, and calcium, and discusses the feasibility and implications of adherence to ardent dietary restrictions and future research.

{{custom_citation.doi}4}https://doi.org/{{custom_citation.doi}0}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}6}{{custom_citation.pmid}2}本文引用 [{{custom_citation.pmid}3}]摘要{{custom_citation.pmid}1}[13]Kelly JT

Rossi M

Johnson DW

, et al. Beyond sodium, phosphate and potassium: potential dietary interventions in kidney disease[J]. Semin Dial, 2017, 30(3): 197-202. DOI: 10.1111/sdi.12580.

People with kidney disease are advised to restrict individual nutrients, such as sodium, potassium, and phosphate, in line with current best practice guidelines. However, there is limited evidence to support the efficacy of single nutrient strategies, and compliance remains a challenge for clinicians to overcome. Many factors contribute to poor compliance with dietary prescriptions, including conflicting priorities for single nutrient restriction, the arduous self‐monitoring required, and the health‐related knock‐on effects resulting from targeting these nutrients in isolation. This paper reviews the evidence base for the overall pattern of eating as a potential tool to deliver a diet intervention in which all the nutrients and foods work cumulatively and synergistically to improve clinical outcomes. These interventions may assist in kidney disease management and overcome these innate challenges that single nutrient interventions possess. Healthy dietary patterns are typically plant‐based and lower in sodium and animal proteins. These patterns may have numerous mechanistic benefits for cardiovascular health in kidney disease, most notably through the increase in fruit, vegetables, and plant‐based protein, as well as improved gut health through the increase in dietary fiber. The evidence to date on optimal dietary patterns points toward use of a predominantly plant‐based diet, and suggests its adoption may improve clinical outcomes in dialysis patients. However, clinical trials are needed to determine whether these diet interventions are feasible, safe, and effective in this patient population.

{{custom_citation.pmid}9}https://doi.org/{{custom_citation.pmid}5}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}1}{{custom_citation.url}7}本文引用 [{{custom_citation.url}8}]摘要{{custom_citation.url}6}[14]Weir MR

Rolfe M

. Potassium homeostasis and renin-angiotensin-aldosterone system inhibitors[J]. Clin J Am Soc Nephrol, 2010, 5(3): 531-548. DOI: 10.2215/CJN.07821109.

Shah M

Foote E

. Potassium-lowering agents for the treatment of nonemergent hyperkalemia: pharmacology, dosing and comparative efficacy[J]. Nephrol Dial Transplant, 2019, 34 Suppl 3: iii45-iii50. DOI: 10.1093/ndt/gfz223.

{{custom_citation.annotation}9}https://doi.org/{{custom_citation.annotation}5}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.annotation}1}{{custom_citation.annotation}7}本文引用 [{{custom_ref.citedCount>0}8}]0}7}=={{custom_ref.citedCount>0}6}.length-1" m-for-val="custom_bodyP_id" m-for-array="{{custom_ref.citedCount>0}5}">0}4}" value="{{custom_ref.citedCount>0}3}">0}2} && {{custom_ref.citedCount>0}1}!=''" style="color: #666;">摘要0}0} && {{custom_citationIndex}9}!=''" class="glyphicon glyphicon-triangle-bottom biaotijiantoush biaotijiantoush1" onclick="ckwx_show_hide(this)">{{custom_citationIndex}6}[16]Wetmore JB

Yan H

Horne L

, et al. Risk of hyperkalemia from renin-angiotensin-aldosterone system inhibitors and factors associated with treatment discontinuities in a real-world population[J]. Nephrol Dial Transplant, 2019: gfz263. DOI: 10.1093/ndt/gfz263.

{{custom_citationIndex}4}https://doi.org/{{custom_citationIndex}0}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_ref.citationList}6}{{custom_ref.citationList}2}本文引用 [{{custom_ref.id}3}]摘要{{custom_ref.citedCount}1}[17]Harris AN

Grimm PR

Lee HW

, et al. Mechanism of hyperkalemia-induced metabolic acidosis[J]. J Am Soc Nephrol, 2018, 29(5): 1411-1425. DOI: 10.1681/ASN.2017111163.

Hyperkalemia in association with metabolic acidosis that are out of proportion to changes in glomerular filtration rate defines type 4 renal tubular acidosis (RTA), the most common RTA observed, but the molecular mechanisms underlying the associated metabolic acidosis are incompletely understood. We sought to determine whether hyperkalemia directly causes metabolic acidosis and, if so, the mechanisms through which this occurs. We studied a genetic model of hyperkalemia that results from early distal convoluted tubule (DCT)-specific overexpression of constitutively active Ste20/SPS1-related proline-alanine-rich kinase (DCT-CA-SPAK). DCT-CA-SPAK mice developed hyperkalemia in association with metabolic acidosis and suppressed ammonia excretion; however, titratable acid excretion and urine pH were unchanged compared with those in wild-type mice. Abnormal ammonia excretion in DCT-CA-SPAK mice associated with decreased proximal tubule expression of the ammonia-generating enzymes phosphate-dependent glutaminase and phosphoenolpyruvate carboxykinase and overexpression of the ammonia-recycling enzyme glutamine synthetase. These mice also had decreased expression of the ammonia transporter family member Rhcg and decreased apical polarization of H-ATPase in the inner stripe of the outer medullary collecting duct. Correcting the hyperkalemia by treatment with hydrochlorothiazide corrected the metabolic acidosis, increased ammonia excretion, and normalized ammoniagenic enzyme and Rhcg expression in DCT-CA-SPAK mice. In wild-type mice, induction of hyperkalemia by administration of the epithelial sodium channel blocker benzamil caused hyperkalemia and suppressed ammonia excretion. Hyperkalemia decreases proximal tubule ammonia generation and collecting duct ammonia transport, leading to impaired ammonia excretion that causes metabolic acidosis.Copyright ? 2018 by the American Society of Nephrology.

{{custom_citationIndex}9}https://doi.org/{{custom_citationIndex}5}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citationIndex}1}{{custom_ref.citationList}7}本文引用 [{{custom_ref.bodyP_ids}8}]摘要{{custom_ref.id}6}[18]Pfob CH

Eiber M

Luppa P

, et al. Hyperkalemia in patients treated with endoradiotherapy combined with amino acid infusion is associated with severe metabolic acidosis[J]. EJNMMI Res, 2018, 8(1): 17. DOI: 10.1186/s13550-018-0370-z.

Background: Amino acid co-infusion for renal protection in endoradiotherapy (ERT) applied as prostate-specific membrane antigen (PSMA)-targeted radioligand therapy (RLT) or peptide receptor radionuclide therapy (PRRT) has been shown to cause severe hyperkalemia. The pathophysiology behind the rapid development of hyperkalemia is not well understood. We hypothesized that the hyperkalemia should be associated with metabolic acidosis.Results: Twenty- two patients underwent ERT. Prior to the first cycle, excretory kidney function was assessed by mercapto-acetyltriglycine (MAG-3) renal scintigraphy, serum biochemistry, and calculated glomerular filtration rate (eGFR). All patients received co-infusion of the cationic amino acids L-arginine and L-lysine for nephroprotection. Clinical symptoms, electrolytes, and acid-base status were evaluated at baseline and after 4 h. No patient developed any clinically relevant side effects. At baseline, acid base status and electrolytes were normal in all patients. Excretory kidney function was normal or only mildly impaired in all except two patients with stage 3 renal insufficiency. All patients developed hyperkalemia. Base excess and HCO3 were significantly lower after 4 h. In parallel, mean pH dropped from 7.36 to 7.29. There was a weak association between calculated (r = -0.21) as well as MAG-3-derived GFR (r = -0.32) and the rise in potassium after 4 h.Conclusion: Amino acid co-infusion during ERT leads to severe metabolic acidosis which induces hyperkalemia by potassium hydrogen exchange. This novel finding implies that commercially available bicarbonate solutions might be an easy therapeutic option to correct metabolic acidosis rapidly.

{{custom_ref.id}4}https://doi.org/{{custom_ref.id}0}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_bodyP_id}6}{{custom_bodyP_id}2}本文引用 [{{custom_citation.annotation}3}]摘要{{custom_citation.annotation}1}[19]Dunn JD

Benton WW

Orozco-Torrentera E

, et al. The burden of hyperkalemia in patients with cardiovascular and renal disease[J]. Am J Manag Care, 2015, 21(15 Suppl): s307-s315.

Hyperkalemia is a potentially serious condition that can result in life-threatening cardiac arrhythmias and is associated with an increased mortality risk. Patients older than 65 years who have an advanced stage of chronic kidney disease (stage 3 or higher), diabetes, and/or chronic heart failure are at higher risk for hyperkalemia. To reduce disease progression and improve outcomes in these groups of patients, modulation of the renin-angiotensin-aldosterone system (RAAS) is recommended by guidelines. One limiting factor of RAAS inhibitors at proven doses is the increased risk for hyperkalemia associated with their use. Although there are effective therapeutic options for the short-term, acute management of hyperkalemia, the available strategies for chronic control of high potassium levels have limited effectiveness. The management of high potassium in the long term often requires withdrawing or reducing the doses of drugs proven to reduce cardiovascular and renal outcomes (eg, RAAS inhibitors) or implementing excessive and often intolerable dietary restrictions. Furthermore, withholding RAAS inhibitors may lead to incremental healthcare costs associated with poor outcomes, such as end-stage renal disease, hospitalizations due to cardiovascular causes, and cardiovascular mortality. As such, there is an important unmet need for novel therapeutic options for the chronic management of patients at risk for hyperkalemia. Potential therapies in development may change the treatment landscape in the near future.

Peacock WF

Liu KD

, et al. Management of hyperkalemia in the acutely ill patient[J]. Ann Intensive Care, 2019, 9(1): 32. DOI: 10.1186/s13613-019-0509-8.

To review the mechanisms of action, expected efficacy and side effects of strategies to control hyperkalemia in acutely ill patients.We searched MEDLINE and EMBASE for relevant papers published in English between Jan 1, 1938, and July 1, 2018, in accordance with the PRISMA Statement using the following terms: "hyperkalemia," "intensive care," "acute kidney injury," "acute kidney failure," "hyperkalemia treatment," "renal replacement therapy," "dialysis," "sodium bicarbonate," "emergency," "acute." Reports from within the past 10 years were selected preferentially, together with highly relevant older publications.Hyperkalemia is a potentially life-threatening electrolyte abnormality and may cause cardiac electrophysiological disturbances in the acutely ill patient. Frequently used therapies for hyperkalemia may, however, also be associated with morbidity. Therapeutics may include the simultaneous administration of insulin and glucose (associated with frequent dysglycemic complications), β-2 agonists (associated with potential cardiac ischemia and arrhythmias), hypertonic sodium bicarbonate infusion in the acidotic patient (representing a large hypertonic sodium load) and renal replacement therapy (effective but invasive). Potassium-lowering drugs can cause rapid decrease in serum potassium level leading to cardiac hyperexcitability and rhythm disorders.Treatment of hyperkalemia should not only focus on the ability of specific therapies to lower serum potassium level but also on their potential side effects. Tailoring treatment to the patient condition and situation may limit the risks.

{{custom_citation.annotation}4}https://doi.org/{{custom_citation.annotation}0}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.annotation}6}{{custom_citation.annotation}2}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[21]Lepage L

Dufour AC

Doiron J

, et al. Randomized clinical trial of sodium polystyrene sulfonate for the treatment of mild hyperkalemia in CKD[J]. Clin J Am Soc Nephrol, 2015, 10(12): 2136-2142. DOI: 10.2215/CJN.03640415.

Ng J

Valdez K

, et al. The use of sodium polystyrene sulfonate in the inpatient management of hyperkalemia[J]. J Hosp Med, 2011, 6(3): 136-140. DOI: 10.1002/jhm.834.

Limited data exist on the precise dose of sodium polystyrene sulfonate (SPS) needed for specific potassium concentrations in the management of mild to moderate hyperkalemia in an inpatient hospital setting.A retrospective cohort study involving a review of electronic medical records of inpatients receiving SPS for the treatment of hyperkalemia was conducted at the Jesse Brown Veteran Affairs Medical Center, between January 1, 2006 and December 31, 2006. Hyperkalemia was defined as a serum potassium concentration >5.1 mmol/L. The primary endpoint was the mean change in potassium concentration associated with specific SPS dosage administration.A total of 122 patients were selected for inclusion in the analysis. The mean potassium concentrations before SPS administration were 5.40 ± 0.18 mmol/L, 5.51 ± 0.30, 5.83 ± 0.46, and 5.92 ± 0.30 in the 15, 30, 45, and 60 gm groups, respectively. The mean potassium concentration decreased by 0.82 ± 0.48 mmol/L in the 15 gm group, 0.95 ± 0.47 in the 30 gm group, 1.11 ± 0.58 in the 45 gm group, and 1.40 ± 0.42 in the 60 gm group. After a single dose of SPS, the mean potassium concentration was within normal range in 115 patients (94%).A possible direct dose response relationship between SPS and the reduction in serum potassium concentration was found and should be evaluated prospectively.2011 Society of Hospital Medicine.

Moffett BS

. Treatment of pediatric hyperkalemia with sodium polystyrene sulfonate[J]. Pediatr Nephrol, 2016, 31(11): 2113-2117. DOI: 10.1007/s00467-016-3414-5.

To describe the safety and efficacy of sodium polystyrene sulfonate (SPS) in pediatric patients with acute hyperkalemia.A retrospective chart review of all patients less than 18 years of age administered SPS for acute hyperkalemia at Texas Children's Hospital between 2011 and 2014.Our cohort consisted of 156 patients (mean age 6.8?±?6.1 years). The peak mean potassium concentration observed was 6.5?±?0.77 mmol/l prior to administration of SPS. The mean SPS dose was 0.64?±?0.32 g/kg. The majority (91 %) of the SPS doses were given orally. The nadir mean potassium concentration in the 48 h post-SPS was 4.7?±?1.2 mEq/l, which occurred at 16.7?±?14.7 h post-dose. In the 48 h following SPS administration, 68 (43 %) patients required at least one additional intervention after SPS dose. Patients who required an additional intervention after initial SPS dose differed significantly in weight, baseline serum potassium, and were more likely to have received SPS treatment via the rectal route. A gastrointestinal adverse event was documented in 24 (15 %) patients.SPS was used effectively and safely in the majority of patients in this report. However, it may not be appropriate as a first single-line agent in patients with severe acute hyperkalemia who require a greater than 25 % reduction in serum potassium levels or those at a high risk for cardiac arrhythmias.

Sable RA

Friedman K

. Colonic ulceration in a patient with renal disease and hyperkalemia[J]. JAAPA, 2012, 25(10): 34, 37-38. DOI: 10.1097/01720610-201210000-00008.

Lewis JT

Bruining DH

. Kayexalate-induced esophageal ulcer in a patient with gastroparesis[J]. Clin Gastroenterol Hepatol, 2012, 10(5): A28. DOI: 10.1016/j.cgh.2011.12.026.

Bae WK

Kim NH

, et al. Colonic mucosal necrosis following administration of calcium polystryrene sulfonate (Kalimate) in a uremic patient[J]. J Korean Med Sci, 2009, 24(6): 1207-1211. DOI: 10.3346/jkms.2009.24.6.1207.

Colonic necrosis is known as a rare complication following the administration of Kayexalate (sodium polystryrene sulfonate) in sorbitol. We report a rare case of colonic mucosal necrosis following Kalimate (calcium polystryrene sulfonate), an analogue of Kayexalate without sorbitol in a 34-yr-old man. He had a history of hypertension and uremia. During the management of intracranial hemorrhage, hyperkalemia developed. Kalimate was administered orally and as an enema suspended in 20% dextrose water to treat hyperkalemia. Two days after administration of Kalimate enema, he had profuse hematochezia, and a sigmoidoscopy showed diffuse colonic mucosal necrosis in the rectum and sigmoid colon. Microscopic examination of random colonic biopsies by two consecutive sigmoidoscopies revealed angulated crystals with a characteristic crystalline mosaic pattern on the ulcerated mucosa, which were consistent with Kayexalate crystals. Hematochezia subsided with conservative treatment after a discontinuance of Kalimate administration.

Harel S

Shah PS

, et al. Gastrointestinal adverse events with sodium polystyrene sulfonate (Kayexalate) use: a systematic review[J]. Am J Med, 2013, 126(3): 264.e9-e24. DOI: 10.1016/j.amjmed.2012.08.016.

目的    觀察聚苯乙烯磺酸鈣治療慢性腎臟病高鉀血癥患者的臨床療效和安全性。方法    采用多中心、單臂、開放的方法開展為期2周的Ⅳ期臨床試驗。起止時間2011年9 月5 日至2012 年6 月21 日，11 個中心共納入慢性腎臟病非透析患者98 例，年齡18～65 歲、血鉀5.50～6.50 mmol/L。治療方案為聚苯乙烯磺酸鈣口服，5 g/次，3 次/d，為期1 周。分別于試驗第0、2、4、8和14天檢測血鉀。結(jié)果    聚苯乙烯磺酸鈣治療1 d后，98例患者平均血鉀由（5.85±0.26）mmol/L 降至（5.16±0.51）mmol/L（P＜0.01）；治療3 d后血鉀降至（4.88±0.58）mmol/L（P＜0.01）；治療1 周后血鉀降至（4.67±0.57）mmol/L（P＜0.01）；停藥1 周后，血鉀水平為（4.96±0.66）mmol/L（P＜0.01），與基線值相比，差異均有統(tǒng)計學(xué)意義（均P＜0.01）。與基線值比較，觀察期間血鈉、血磷、血鈣的改變差異無統(tǒng)計學(xué)意義。便秘為最常見藥物不良反應(yīng)（9.2%），未發(fā)現(xiàn)與治療有關(guān)的嚴重不良事件。結(jié)論    聚苯乙烯磺酸鈣治療慢性腎臟病高鉀血癥是有效、安全的，且對血鈉、磷、鈣無不良影響。

Ono Y

Takagi T

, et al. [Case report; a case of ileus due to ileal stenosis caused by oral intake of calcium polystyrene sulfonate][J]. Nihon Naika Gakkai Zasshi, 2013, 102(1): 150-152. DOI: 10.2169/naika.102.150.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[30]{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[31]Kubo T

Yamashita K

Yokoyama Y

, et al. Hepatic portal venous gas due to polystyrene sulfonate-induced enteritis[J]. Clin J Gastroenterol, 2018, 11(3): 220-223. DOI: 10.1007/s12328-018-0818-8.

A 78-year-old man with acute right lower abdominal pain and nausea was referred to our hospital. Computed tomography (CT) demonstrated hepatic portal venous gas and a thickened wall of the terminal ileum, and colonoscopy demonstrated ulcers and erosions of the ileocecal region. Histological examination of biopsy samples revealed basophilic crystals consistent with the component of calcium polystyrene sulfonate (CPS). This patient started taking CPS 2 months prior for chronic hyperkalemia. The symptoms resolved soon after ceasing CPS, and subsequent imaging studies confirmed the disappearance of the portal venous gas and ileocolitis.

Pereira E

Banhudo A

. Colonic necrosis induced by calcium polystyrene sulfonate[J]. GE Port J Gastroenterol, 2018, 25(4): 205-207. DOI: 10.1159/000481288.

Trombotto V

Lucchetta RC

, et al. Efficacy and safety of the pharmacotherapy used in the management of hyperkalemia: a systematic review[J]. Pharm Pract (Granada), 2019, 17(1): 1361. DOI: 10.18549/PharmPract.2019.1.1361.

Tsai YC

Chiang WC

, et al. Ileum and colon perforation following peritoneal dialysis-related peritonitis and high-dose calcium polystyrene sulfonate[J]. J Formos Med Assoc, 2015, 114(10): 1008-1010. DOI: 10.1016/j.jfma.2013.02.006.

Anker SD

Bushinsky DA

, et al. Evaluation of the efficacy and safety of RLY5016, a polymeric potassium binder, in a double-blind, placebo-controlled study in patients with chronic heart failure (the PEARL-HF) trial[J]. Eur Heart J, 2011, 32(7): 820-828. DOI: 10.1093/eurheartj/ehq502.

To evaluate efficacy and safety of RLY5016 (a non-absorbed, orally administered, potassium [K+]-binding polymer) on serum K+ levels in patients with chronic heart failure (HF) receiving standard therapy and spironolactone.One hundred and five patients with HF and a history of hyperkalaemia resulting in discontinuation of a renin-angiotensin-aldosterone system inhibitor/blocker and/or beta-adrenergic blocking agent or chronic kidney disease (CKD) with an estimated glomerular filtration rate of <60 mL/min were randomized to double-blind treatment with 30 g/day RLY5016 or placebo for 4 weeks. Spironolactone, initiated at 25 mg/day, was increased to 50 mg/day on Day 15 if K+ was ≤5.1 mEq/L. Endpoints included the change from baseline in serum K+ at the end of treatment (primary); the proportion of patients with hyperkalaemia (K+ >5.5 mEq/L); and the proportion titrated to spironolactone 50 mg/day. Safety assessments included adverse events (AEs) and clinical laboratory tests. RLY5016 (n= 55) and placebo (n= 49) patients had similar baseline characteristics. At the end of treatment, compared with placebo, RLY5016 had significantly lowered serum K+ levels with a difference between groups of -0.45 mEq/L (P < 0.001); a lower incidence of hyperkalaemia (7.3% RLY5016 vs. 24.5% placebo, P= 0.015); and a higher proportion of patients on spironolactone 50 mg/day (91% RLY5016 vs. 74% placebo, P= 0.019). In patients with CKD (n= 66), the difference in K+ between groups was -0.52 mEq/L (P= 0.031), and the incidence of hyperkalaemia was 6.7% RLY5016 vs. 38.5% placebo (P= 0.041). Adverse events were mainly gastrointestinal, and mild or moderate in severity. Adverse events resulting in study withdrawal were similar (7% RLY5016, 6% placebo). There were no drug-related serious AEs. Hypokalaemia (K+ <3.5 mEq/L) occurred in 6% of RLY5016 patients vs. 0% of placebo patients (P= 0.094).RLY5016 prevented hyperkalaemia and was relatively well tolerated in patients with HF receiving standard therapy and spironolactone (25-50 mg/day).

Bakris GL

Bushinsky DA

, et al. Patiromer in patients with kidney disease and hyperkalemia receiving RAAS inhibitors[J]. N Engl J Med, 2015, 372(3): 211-221. DOI: 10.1056/NEJMoa1410853.

De Castro AM

Shottland D

, et al. Patiromer: the first potassium binder approved in over 50 years[J]. Cardiol Rev, 2016, 24(6): 316-323. DOI: 10.1097/CRD.0000000000000123.

For over 50 years, there have been limited options for the management of hyperkalemia, especially among patients with chronic kidney disease (CKD), diabetic nephropathy, hypertension, and heart failure, who were receiving concomitant renin-angiotensin-aldosterone system (RAAS) inhibitor therapy. Hyperkalemia is a potential, life-threatening electrolyte abnormality that frequently challenges clinicians from maximizing the mortality benefit and organ-protective properties of RAAS inhibitors especially in CKD and heart failure populations. Patiromer is a novel nonabsorbed, cation-exchange polymer that binds and exchanges potassium for calcium, predominantly in the gastrointestinal tract. It has demonstrated potassium-lowering effects in normo- or hyperkalemic patients on concomitant RAAS inhibitors with heart failure, diabetic nephropathy, and CKD, in the PEARL-HF, AMETHYST-DN, and OPAL-HK studies, respectively. Across all studies, it appears to be generally effective and well tolerated, with adverse events predominantly gastrointestinal in nature. Additional investigational studies are needed to explore its use for an extended duration of treatment and in larger patient populations, as well as exploring drug-drug interactions. Overall, patiromer demonstrates a promising role in the chronic management of hyperkalemia that will allow optimization of RAAS inhibitor therapy, thus delaying progression of CKD and improving the mortality benefit in heart failure patients.

Pitt B

Weir MR

, et al. Effect of patiromer on serum potassium level in patients with hyperkalemia and diabetic kidney disease: the AMETHYST-DN randomized clinical trial[J]. JAMA, 2015, 314(2): 151-161. DOI: 10.1001/jama.2015.7446.

Hyperkalemia is a potentially life-threatening condition predominantly seen in patients treated with renin-angiotensin-aldosterone system (RAAS) inhibitors with stage 3 or greater chronic kidney disease (CKD) who may also have diabetes, heart failure, or both.To select starting doses for a phase 3 study and to evaluate the long-term safety and efficacy of a potassium-binding polymer, patiromer, in outpatients with hyperkalemia.Phase 2, multicenter, open-label, dose-ranging, randomized clinical trial (AMETHYST-DN), conducted at 48 sites in Europe from June 2011 to June 2013 evaluating patiromer in 306 outpatients with type 2 diabetes (estimated glomerular filtration rate, 15 to <60 mL/min/1.73 m2 and serum potassium level >5.0 mEq/L). All patients received RAAS inhibitors prior to and during study treatment.Patients were stratified by baseline serum potassium level into mild or moderate hyperkalemia groups and received 1 of 3 randomized starting doses of patiromer (4.2 g [n?=?74], 8.4 g [n?=?74], or 12.6 g [n?=?74] twice daily [mild hyperkalemia] or 8.4 g [n?=?26], 12.6 g [n?=?28], or 16.8 g [n?=?30] twice daily [moderate hyperkalemia]). Patiromer was titrated to achieve and maintain serum potassium level 5.0 mEq/L or lower.The primary efficacy end point was mean change in serum potassium level from baseline to week 4 or prior to initiation of dose titration. The primary safety end point was adverse events through 52 weeks. Secondary efficacy end points included mean change in serum potassium level through 52 weeks.A total of 306 patients were randomized. The least squares mean reduction from baseline in serum potassium level at week 4 or time of first dose titration in patients with mild hyperkalemia was 0.35 (95% CI, 0.22-0.48) mEq/L for the 4.2 g twice daily starting-dose group, 0.51 (95% CI, 0.38-0.64) mEq/L for the 8.4 g twice daily starting-dose group, and 0.55 (95% CI, 0.42-0.68) mEq/L for the 12.6 g twice daily starting-dose group. In those with moderate hyperkalemia, the reduction was 0.87 (95% CI, 0.60-1.14) mEq/L for the 8.4 g twice daily starting-dose group, 0.97 (95% CI, 0.70-1.23) mEq/L for the 12.6 g twice daily starting-dose group, and 0.92 (95% CI, 0.67-1.17) mEq/L for the 16.8 g twice daily starting-dose group (P?<?.001 for all changes vs baseline by hyperkalemia starting-dose groups within strata). From week 4 through week 52, statistically significant mean decreases in serum potassium levels were observed at each monthly point in patients with mild and moderate hyperkalemia. Over the 52 weeks, hypomagnesemia (7.2%) was the most common treatment-related adverse event, mild to moderate constipation (6.3%) was the most common gastrointestinal adverse event, and hypokalemia (<3.5 mEq/L) occurred in 5.6% of patients.Among patients with hyperkalemia and diabetic kidney disease, patiromer starting doses of 4.2 to 16.8 g twice daily resulted in statistically significant decreases in serum potassium level after 4 weeks of treatment, lasting through 52 weeks.clinicaltrials.gov Identifier:NCT01371747.

Yang A

Leon A

, et al. Characterization of structure and function of ZS-9, a K+ selective ion trap[J]. PLoS One, 2014, 9(12): e114686. DOI: 10.1371/journal.pone.0114686.

Spinowitz BS

Lerma EV

, et al. Efficacy and safety of sodium zirconium cyclosilicate for treatment of hyperkalemia: an 11-month open-label extension of HARMONIZE[J]. Am J Nephrol, 2019, 50(6): 473-480. DOI: 10.1159/000504078.

Sodium zirconium cyclosilicate (SZC; formerly ZS-9) is a selective potassium (K+) binder for treatment of hyperkalemia. An open-label extension (OLE) of the -HARMONIZE study evaluated efficacy and safety of SZC for ≤11 months.Patients from HARMONIZE with point-of-care device i-STAT K+ 3.5-6.2 mmol/L received once-daily SZC 5-10 g for ≤337 days. End points included achievement of mean serum K+ ≤5.1 mmol/L (primary) or ≤5.5 mmol/L (secondary).Of 123 patients who entered the extension (mean serum K+ 4.8 mmol/L), 79 (64.2%) completed the study. The median daily dose of SZC was 10 g (range 2.5-15 g). The primary end point was achieved by 88.3% of patients, and 100% achieved the secondary end point. SZC was well tolerated with no new safety concerns.In the HARMONIZE OLE, most patients maintained mean serum K+ within the normokalemic range for ≤11 months during ongoing SZC treatment.The Author(s). Published by S. Karger AG, Basel.

Fishbane S

Pergola PE

, et al. Sodium zirconium cyclosilicate among individuals with hyperkalemia: a 12-month phase 3 study[J]. Clin J Am Soc Nephrol, 2019, 14(6): 798-809. DOI: 10.2215/CJN.12651018.

Oral sodium zirconium cyclosilicate (formerly ZS-9) binds and removes potassium via the gastrointestinal tract. Sodium zirconium cyclosilicate–associated restoration and maintenance of normokalemia and adverse events were evaluated in a two-part, open label, phase 3 trial.

Rasmussen HS

Lavin PT

, et al. Sodium zirconium cyclosilicate in hyperkalemia[J]. N Engl J Med, 2015, 372(3): 222-231. DOI: 10.1056/NEJMoa1411487.

Rasmussen HS

Lavin P

, et al. Effect of sodium zirconium cyclosilicate on potassium lowering for 28 days among outpatients with hyperkalemia the HARMONIZE randomized clinical trial[J]. JAMA, 2014, 312(21): 2223-2233. DOI: 10.1001/jama.2014.15688.

Hyperkalemia is a common electrolyte abnormality that may be difficult to manage because of a lack of effective therapies. Sodium zirconium cyclosilicate is a nonabsorbed cation exchanger that selectively binds potassium in the intestine.To evaluate the efficacy and safety of zirconium cyclosilicate for 28 days in patients with hyperkalemia.HARMONIZE was a phase 3, multicenter, randomized, double-blind, placebo-controlled trial evaluating zirconium cyclosilicate in outpatients with hyperkalemia (serum potassium ≥5.1 mEq/L) recruited from 44 sites in the United States, Australia, and South Africa (March-August 2014).Patients (n?=?258) received 10 g of zirconium cyclosilicate 3 times daily in the initial 48-hour open-label phase. Patients (n?=?237) achieving normokalemia (3.5-5.0 mEq/L) were then randomized to receive zirconium cyclosilicate, 5 g (n?=?45 patients), 10 g (n?=?51), or 15 g (n?=?56), or placebo (n?=?85) daily for 28 days.The primary end point was mean serum potassium level in each zirconium cyclosilicate group vs placebo during days 8-29 of the randomized phase.In the open-label phase, serum potassium levels declined from 5.6 mEq/L at baseline to 4.5 mEq/L at 48 hours. Median time to normalization was 2.2 hours, with 84% of patients (95% CI, 79%-88%) achieving normokalemia by 24 hours and 98% (95% CI, 96%-99%) by 48 hours. In the randomized phase, serum potassium was significantly lower during days 8-29 with all 3 zirconium cyclosilicate doses vs placebo (4.8 mEq/L [95% CI, 4.6-4.9], 4.5 mEq/L [95% CI, 4.4-4.6], and 4.4 mEq/L [95% CI, 4.3-4.5] for 5 g, 10 g, and 15 g; 5.1 mEq/L [95% CI, 5.0-5.2] for placebo; P?<?.001 for all comparisons). The proportion of patients with mean potassium <5.1 mEq/L during days 8-29 was significantly higher in all zirconium cyclosilicate groups vs placebo (36/45 [80%], 45/50 [90%], and 51/54 [94%] for the 5-g, 10-g, and 15-g groups, vs 38/82 [46%] with placebo; P?<?.001 for each dose vs placebo). Adverse events were comparable between zirconium cyclosilicate and placebo, although edema was more common in the 15-g group (edema incidence: 2/85 [2%], 1/45 [2%], 3/51 [6%], and 8/56 [14%] patients in the placebo, 5-g, 10-g, and 15-g groups). Hypokalemia developed in 5/51 (10%) and 6/56 patients (11%) in the 10-g and 15-g zirconium cyclosilicate groups, vs none in the 5-g or placebo groups.Among outpatients with hyperkalemia, open-label sodium zirconium cyclosilicate reduced serum potassium to normal levels within 48 hours; compared with placebo, all 3 doses of zirconium cyclosilicate resulted in lower potassium levels and a higher proportion of patients with normal potassium levels for up to 28 days. Further studies are needed to evaluate the efficacy and safety of zirconium cyclosilicate beyond 4 weeks and to assess long-term clinical outcomes.clinicaltrials.gov Identifier: NCT02088073.

Ponikowski P

Anker SD

, et al. Clinical practice update on heart failure 2019: pharmacotherapy, procedures, devices and patient management. An expert consensus meeting report of the Heart Failure Association of the European Society of Cardiology[J]. Eur J Heart Fail, 2019, 21(10): 1169-1186. DOI: 10.1002/ejhf.1531.

The European Society of Cardiology (ESC) has published a series of guidelines on heart failure (HF) over the last 25?years, most recently in 2016. Given the amount of new information that has become available since then, the Heart Failure Association (HFA) of the ESC recognized the need to review and summarise recent developments in a consensus document. Here we report from the HFA workshop that was held in January 2019 in Frankfurt, Germany. This expert consensus report is neither a guideline update nor a position statement, but rather a summary and consensus view in the form of consensus recommendations. The report describes how these guidance statements are supported by evidence, it makes some practical comments, and it highlights new research areas and how progress might change the clinical management of HF. We have avoided re-interpretation of information already considered in the 2016 ESC/HFA guidelines. Specific new recommendations have been made based on the evidence from major trials published since 2016, including sodium-glucose co-transporter 2 inhibitors in type 2 diabetes mellitus, MitraClip for functional mitral regurgitation, atrial fibrillation ablation in HF, tafamidis in cardiac transthyretin amyloidosis, rivaroxaban in HF, implantable cardioverter-defibrillators in non-ischaemic HF, and telemedicine for HF. In addition, new trial evidence from smaller trials and updated meta-analyses have given us the chance to provide refined recommendations in selected other areas. Further, new trial evidence is due in many of these areas and others over the next 2?years, in time for the planned 2021 ESC guidelines on the diagnosis and treatment of acute and chronic heart failure.? 2019 The Authors. European Journal of Heart Failure ? 2019 European Society of Cardiology.

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網(wǎng)址: Long http://m.u1s5d6.cn/newsview436573.html

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Long

一、低鉀飲食

二、停用或減量使用誘發(fā)高鉀血癥的藥物

三、糾正代謝性酸中毒

四、促進腎臟排鉀

五、促進腸道排鉀

六、總結(jié)

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一、低鉀飲食

二、停用或減量使用誘發(fā)高鉀血癥的藥物

三、糾正代謝性酸中毒

四、促進腎臟排鉀

五、促進腸道排鉀

六、總結(jié)

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二、停用或減量使用誘發(fā)高鉀血癥的藥物

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四、促進腎臟排鉀

五、促進腸道排鉀

六、總結(jié)

從出汗看健康出汗透露你的健康信號

早上怎么喝水最健康？