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一項新研究發現,心臟激素對於慢性腎病患者的診斷、監測治療和預後評估具有重要價值。這些激素如何在心血管疾病和腎臟功能減退的背景下發揮作用,對於醫生們在日常管理患者時具有重大意義。該研究探討了心臟激素在調節對腎功能損失的反應中的角色,並闡明了在重度腎功能衰竭患者中對這些激素進行臨床評估的主要因素。
利用利尿肽在慢性腎病中的臨床價值
Clinical value of natriuretic peptides in chronic kidney disease
Santos-Araújo C, Leite-Moreira A, Pestana M. Clinical value of natriuretic peptides in chronic kidney disease. Nefrologia. 2015;35(3):227-233. doi:10.1016/j.nefro.2015.03.002
https://pubmed.ncbi.nlm.nih.gov/26299165/#:~:text=According%20to%20several%20lines%20of,blood%20pressure%20and%20vascular%20function.
ABSTRACT
According to several lines of evidence, natriuretic peptides (NP) are the main components of a cardiac-renal axis that operate in clinical conditions of decreased cardiac hemodynamic tolerance to regulate sodium homeostasis, blood pressure and vascular function. Even though it is reasonable to assume that NP may exert a relevant role in the adaptive response to renal mass ablation, evidence gathered so far suggest that this contribution is probably complex and dependent on the type and degree of the functional mass loss.
In the last years NP have been increasingly used to diagnose, monitor treatment and define the prognosis of several cardiovascular (CV) diseases. However, in many clinical settings, like chronic kidney disease (CKD), the predictive value of these biomarkers has been questioned. In fact, it is now well established that renal function significantly affects the plasmatic levels of NP and that renal failure is the clinical condition associated with the highest plasmatic levels of these peptides. The complexity of the relation between NP plasmatic levels and CV and renal functions has obvious consequences, as it may limit the predictive value of NP in CV assessment of CKD patients and be a demanding exercise for clinicians involved in the daily management of these patients.
This review describes the role of NP in the regulatory response to renal function loss and addresses the main factors involved in the clinical valorization of the peptides in the context of significant renal failure.
摘要
根據多條證據線索,利尿肽(NP)是心腎軸的主要組成部分,在心臟血液動力學耐受性下降的臨床條件下運作,以調節鈉的恆定、血壓和血管功能。儘管合理假設NP可能在對腎臟質量切除的適應性反應中發揮重要作用,但迄今收集的證據表明,這一貢獻可能相當複雜,並取決於功能質量損失的類型和程度。
近年來,NP在診斷、監測治療以及界定多種心血管(CV)疾病的預後中的應用越來越廣泛。然而,在許多臨床環境中,如慢性腎病(CKD),這些生物標誌物的預測價值受到質疑。事實上,目前已經確立腎功能顯著影響NP的血漿水平,腎衰竭是與這些肽最高血漿水平相關的臨床條件。NP血漿水平與CV和腎功能之間關係的複雜性有明顯的後果,因為它可能限制NP在CKD患者CV評估中的預測價值,並對涉及這些患者日常管理的臨床醫生構成挑戰。
本評論描述了NP在對腎功能損失的調節反應中的角色,並著重論述了在顯著腎衰竭背景下評估這些肽的臨床價值所涉及的主要因素。
導言
利尿肽(NP)是一類激素,具有相似的化學結構和生物功能,在心血管(CV)生理和病理學中發揮著重要作用。NP的經典生理作用包括促進腎臟排鈉和水,有助於血壓(BP)調節。此外,NP還在循環系統內發揮自分泌和旁分泌作用,具體包括通過放鬆血管肌細胞實現血管擴張、抗纖維化和抗增生效應,以及調節腎素、孕酮、內皮素和血管加壓素的分泌。
在急性或慢性容量負荷過多的情況下,NP可能作為一種重要的反調節激素,以抵消交感神經系統和腎素-血管緊張素-醛固酮系統釋放的血管收縮-促增生-保鈉激素的效果,有助於維持循環系統的恆定。此外,NP先前被認為是對腎臟功能質量損失綜合反應的可能介質,具有特定的貢獻作用,這取決於腎衰竭的程度和腎功能下降開始後經過的時間。
與NP最高循環水平相關的疾病狀態是腎衰竭。在這種情況下,增加的NP循環水平不能線性地被解釋為NP系統激活的表達,如在心力衰竭(HF)或容量負荷過多與左心室(LV)壁壓力相關的情境中所觀察到的那樣。實際上,先前來自多項研究的證據表明,NP的血漿水平可能既受到NP合成/心臟釋放率的調節,也受到從循環系統中移除肽的速率的調節。因此,患有顯著腎功能衰竭的患者的NP循環水平必須根據腎功能障礙的嚴重程度來解釋,並且隨著慢性腎病(CKD)階段的進展,預期會有更高的切點。
本文的目的是回顧NP系統在對腎功能損失的適應性反應中的作用,並探討在有嚴重腎功能障礙的患者的心血管管理中NP循環水平的臨床應用。
利尿肽系統
利尿肽在維持鈉和體液容積恆定以及調節增殖和纖維化反應中發揮重要作用。到目前為止,已描述了NP家族的四個成員,所有這些成員都共有一個共同的17個氨基酸環結構。心房NP(ANP)在心房中產生,並在心房壁張力增加時分泌。B型利尿肽(BNP)作為一種氨基酸前體蛋白(pro-BNP)合成,並在心室壁壓力增加時從心室釋放。分泌時,pro-BNP激素以1:1的等摩爾比被切割成一個32個氨基酸的C末端片段(BNP),這是生物活性的,和一個76個氨基酸的N末端片段(N末端前體B型利尿肽 – NT-pro-BNP),這是生物無活性的。與BNP相比,NT-pro-BNP具有更長的血漿半衰期和更低的生物變異性的優勢。C型利尿肽(CNP)有兩種類型:一種是22個氨基酸的形式,更有力,主要在中樞神經系統和內皮組織中應對剪切應力而分泌;另一種是52個氨基酸的形式。所有這些類型的NP都可以在人類血漿中檢測到。D型利尿肽(DNP)存在於綠曼巴蛇的毒液中,主要刺激和主要功能在人類中目前仍然未知。
B型利尿肽
B型利尿肽最初於1988年從豬腦提取物中分離出來,但很快就被認識到主要在心室應對左心室(LV)壁壓力增加時合成和釋放。BNP通過激活跨膜鸟苷酸环化酶、利尿肽受體A(NPR-A)發揮大部分的細胞效應。另一種利尿肽受體,利尿肽受體C(NPR-C),不具有鸟苷酸环化酶活性,負責NP的內吞作用和降解。然而,NPR-C可能不僅僅作為一個清除受體,還可能通過抑制腺苷酸环化酶信號轉導系統,干擾涉及細胞生長調節的細胞機制,從而發揮生理功能。
在幾種疾病狀態下,可以觀察到BNP的循環水平增加,這通常被解釋為NP系統激活的表現。然而,BNP的血漿濃度同時受到NP的合成和釋放率以及從循環中移除肽的速率的調節。BNP的清除涉及兩條途徑:中性內肽酶的酶促降解和經NPR-C的受體介導的內吞作用後通過溶酶體降解。儘管這兩種機制在從循環中移除NP的相對重要性仍然存在爭議,但在NPR-C敲除小鼠中已經證明,缺乏這種清除機制與外源BNP的血漿半衰期顯著延長相關。此外,靶器官受體表達的調節可能是決定NP局部生物可用性的關鍵因素,通過該機制,在NP系統活動的區域控制中發揮重要作用。因此,NP的局部作用可能受到NPR-C腎表達增加和/或NPRA下調的限制。根據這一點,幾條證據線索表明,由於NPR-A在腎臟表達的變化而導致的對NP的抵抗,可能部分解釋了在水腫形成條件下,特別是在充血性HF中,體積擴張(VE)的維持。
在正常人群中,NT-pro-BNP從心臟持續釋放,可以在血漿中測量,與BNP的濃度相當。然而,在左心室功能障礙的患者中,通過尚未明確的機制,NT-pro-BNP的濃度系統性地高於BNP。基於此,一些作者主張,NT-proBNP的血漿水平可能是心力衰竭進展的更好標記。
BNP與適應性腎質量損失
單側腎切除
單側腎切除後立即刺激殘餘腎質量的生長和功能。這種急性補償反應在單側腎切除(Unx)後的頭幾天內被認識到,其特徵是電解質排泄增加,心輸出量輕度下降和血壓(BP)短暫上升。幾週後,觀察到收縮壓和舒張壓同時增加,以及對體積擴張(VE)的利尿反應持續減弱,表明利尿系統在鈉平衡控制中的相對作用可能隨時間變化而不同。
心房利尿肽先前被認為是對側腎切除急性腎反應的可能介質。實際上,先前的研究已記錄了在一種通過右心房附屬切除獲得的ANP釋放減少的大鼠模型中,對Unx的利尿反應受抑制。利尿肽系統在對單側腎切除反應中鈉平衡調節中的重要性也通過在Unx動物模型中觀察到的在循環ANP被單克隆抗體阻斷後受損的腎鈉排泄反應得到加強。BNP的作用,對選擇性腎調節的效應(NPR-A)和清除(NPR-C)NPR的作用,以及更重要的是,這些變化在Unx後的時間進程最近在單側腎切除的大鼠模型中被描述。在這項研究中,NPR-A的腎上調節與NPR-C的下調節表明,腎NP系統可能是Unx後長期鹽和水平衡、體外液體容量和BP調節的重要介質,部分抵消了在其他神經-激素利尿系統中記錄到的活性減弱。此外,建議Unx大鼠腎髓質中NPR-C表達的局部變化,導致這種受體表達減少,可能作為單側腎切除後觀察到的補償性生長的促進因素,支持NP在Unx後觀察到的補償反應中的重要作用。儘管如此,NP系統在調節對單側腎質量切除的適應性反應中的確切功能仍待完全澄清。
慢性腎病
在慢性腎病(CKD)中,觀察到NP循環水平的增加,並與腎小球過濾率(GFR)的補償性增加以及在正常和高鹽狀態下鈉重吸收的減少有關。雖然CKD經常與心血管(CV)血液動力學的紊亂相關聯,但在這種情況下NP循環水平增加的機制仍有待闡明。實際上,先前在沒有心臟功能障礙的正常老年人群中描述了BNP循環水平的提高,這被歸因於NP的腎清除率下降。此外,腎衰竭本身也已顯示影響BNP的血漿水平,這一狀態未被腎替代治療顯著改變,尤其是腹膜透析(PD)。
尚未完全闡明CKD中NP血漿水平提高是否反映了系統的激活並實際上導致了靶器官的刺激。鑑於CKD患者中血漿NP的大幅增加與正常對照或腎功能良好保存的腎炎患者相比,導致的利鈉反應較為溫和,這一點非常重要。此外,NP對腎小球血液動力學的影響被建議是獨立於與腎小管鈉重吸收減少有關的影響,這意味著靶器官受體表達在控制系統活動中發揮著突出作用。
在一項通過¾腎切除(¾nx)誘導的腎功能不全的大鼠實驗模型中,加強了調節靶器官受體表達可能對CKD中NP的局部生物可用性至關重要並通過該機制在NP系統活動的區域控制中發揮重要作用的證據。在這項研究中,¾nx大鼠的BP升高和對VE的利鈉反應受損與循環BNP水平的早期和時間依賴性增加相關,且沒有心臟功能障礙。這些變化伴隨著腎髓質中NPR-A的早期、選擇性和持續性表達受損以及腎皮質中NPR-C的上調,暗示了殘餘腎臟中NPRs的不同調節可能定義了CKD中NP抗性的可能機制。這有助於解釋在NP融入對抗毒素誘導的腎衰竭的腎保護中以及在失代償性HF患者的腎功能保護中觀察到的一些令人失望的結果,並限制了NP在心腎功能障礙治療中的臨床使用。
慢性腎病中BNP和NT-pro-BNP的臨床應用
多項研究顯示,在心力衰竭(HF)患者中,隨著功能障礙的程度增加,心室肌細胞分泌的BNP增加,證實了這些肽在診斷、篩查、預後和監測心血管(CV)狀況患者治療中的應用。實際上,旨在減少HF臨床表現的治療似乎主要通過與NP水平變化相關的機制起作用,使臨床醫生能夠指導治療並調整治療,以實現這些藥物的血漿水平低於關鍵值。然而,在腎衰竭中,NP作為血液動力學生物標記的作用並不直接。
NP血漿水平和腎功能
腎功能影響BNP和NT-pro-BNP的血漿水平。在慢性腎病(CKD)中NP水平升高的責任因素尚未完全明了,但這些肽的腎清除減少可能不是主要的作用機制。其他解釋包括由於功能性腎質量減少而導致的腎反應性降低、第二信使產生減少和由於腎組織中清除受體減少而導致NP移除減少的可能性。一些支持這些機制的證據已在本文中提及。儘管如此,迄今收集的證據表明,嚴重腎功能障礙中觀察到的NP升高主要可能與來自心臟對腎的反調節反應有關,支持將這些藥物作為慢性腎病患者左心室重塑的潛在標記的使用。
腎衰竭中NP循環水平與心臟功能障礙
最近的證據表明,循環BNP水平強烈反映了收縮性和舒張性心力衰竭患者的左心室舒張末期壁壓,即使在存在顯著腎衰竭的情況下,這種相關性仍然維持。實際上,對血液透析(HD)和腹膜透析(PD)患者進行的研究表明,BNP循環水平在檢測左心室肥大並排除這一人群的收縮功能障礙方面保持顯著的潛在價值。儘管如此,腎功能系統地被識別為解釋BNP和NT-pro-BNP升高的主要混淆因素,並且是NP在慢性腎病(CKD)人群中當前應用的潛在限制。事實上,之前有報導在沒有心臟功能障礙的情況下,腎素肌酐清除率降低的患者中BNP血漿水平上升到大約200pg/ml,而在這一人群中推薦NT-pro-BNP參考值為1200pg/ml。因此,隨著CKD階段的進展,這些NP的更高切點被暗示。NT-pro-BNP血漿水平似乎與GFR的關聯更強,並且比循環BNP水平更受正常與年齡相關的腎功能下降的影響。因此,一些作者主張,在GFR低於60ml/min/1.73m2和老年人中,應謹慎使用NT-pro-BNP血漿水平。
末期腎病透析患者的NP血漿水平
血液透析對BNP和NT-pro-BNP血漿水平的影響並未完全澄清,一些研究報告了相互矛盾的結果。多項研究記錄了末期腎病患者在透析前BNP和NT-pro-BNP的預期升高,以及一次HD治療後BNP血漿水平約20-40%的顯著下降。這種BNP和NT-pro-BNP水平在透析治療後的降低可能由於透析清除增加或由於改善的容量控制導致左心室壁壓降低和這些肽從心室心肌的分泌減少來解釋。在腹膜透析患者中反復記錄到BNP和NT-pro-BNP的水平升高,但與HD觀察到的情況不同,PD似乎不顯著改變這些肽的血漿水平。
透析患者中NP血漿水平的預後價值
在HD和PD患者中,心臟NP都是可靠的死亡預測因子,與透析模式對液體體積控制的影響以及其他被認為是所有原因和心血管死亡風險因素的臨床和生化標誌物無關。然而,并非所有NP家族成員具有相同的預測價值。實際上,一些直接比較BNP和NT-pro-BNP血漿水平的研究表明,NT-pro-BNP在預測死亡方面可能略優于BNP,這一發現歸因於NT-pro-BNP的半衰期較長以及此肽對左心室肥大的更準確指標。因此,一些作者建議,BNP,尤其是NT-pro-BNP,可能同時在指導風險分層和針對CKD人群的治療干預方面具有價值。
移植腎中的NP
在選定的臨床設置中,已經討論了NP的臨床價值,如腎移植接受者(RTR)。實際上,已經顯示提高的NP水平能夠預測穩定RTR中的過度容量和移植物功能障礙,這可能對這些患者的細胞外體積狀態的客觀測量很有價值。此外,如果將GFR視為一個混淆因素,NP對於檢測RTR中的左心室舒張功能障礙也可能是有用的。NP的血漿水平還與高血壓RTR中的左心室肥大呈正相關,並且在這種臨床情況下,被提議用於篩查存在左心室肥大風險的移植患者。在活體腎移植中,有關NP臨床價值的信息很少,對於評估NP水平的意義和效用的研究幾乎不存在。
主要概念
BNP和NT-pro-BNP是心臟生物標記,在正常腎功能患者中與心血管發病率和死亡率相關,對患有心力衰竭的患者具有診斷、治療和預后價值。
• 在腎臟質量切除後,NP在鈉平衡中的作用似乎受到腎臟NP系統的局部調節的顯著影響,並且可能根據功能性腎臟質量損失的程度而有所不同。
• 腎功能影響BNP和NT-pro-BNP的血漿水平,可能限制它們作為血液動力學生物標記物在腎功能衰竭中的實用性。
• 在血液透析和腹膜透析患者中,NP的血漿水平已與左心室結構和功能相關,但這種關聯可能受到在嚴重腎功能惡化中作用的其他因素的顯著影響。
• 關於在透析患者中使用NP診斷體積狀態的效用仍然存在廣泛爭議,部分取決於不同透析技術對肽的清除程度。
• 儘管如此,在透析患者中,心臟NP是可靠的死亡預測因子,獨立於透析模式和液體體積控制程度,可能有助於早期識別高死亡風險的患者亞群。
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