Cardiorenal Nexus: Kev Ntsuam Xyuas Nrog Kev tsom mus rau kev sib xyaw ua ke mob plawv thiab lub raum tsis ua haujlwm, thiab kev nkag siab los ntawm kev sim tshuaj tsis ntev los no

PATHOPHYSIOLOGY

Cov kab mob cardiorenal tshwm sim nyob rau hauv ib qho kev sib txuas ntawm pathophysiological trajectory (Daim duab).1–3Nyob rau hauv hom 2 syndrome, lub xub ntiag ntawm lub sij hawm ntevplawv tsis ua haujlwmthiab covcuam ​​tshuam nrog kev hloov pauv ntevrautxo lub plawv tso zisthiabtus nqi ntwsthiab tsavenous siabua rau mob raum hypoperfusion. Hauv kev teb, muaj kev ua haujlwm ntev ntev ntawm ob qho tib si renin-angiotensin-aldosterone system (RAAS) thiab lub paj hlwb sympathetic. Angiotensin txhawb nqa vasoconstriction thiab nce ntshav ntim los ntawm aldosterone-triggered sodium thiab dej tuav. Tshaj aldosterone tuaj yeem ua rau muaj kev cuam tshuam tsis zoo ntawm interstitial fibrosis thiab pab txhawb kev loj hlob thiab kev loj hlob ntawm CVD thiab CKD.35Qhov sib txawv ntawm kev rov qab los tom qab mob hnyav rau cov neeg mob uas muaj HF ntev yuav tshwm sim vim qhov xwm txheej ntawm lub raum parenchyma thiab tag nrho kev ua haujlwm ntawm cov seem tsis zoo lossis hyperfiltering nephrons - muaj qhov sib txawv ntawm qhov ntsuas GFR tam sim no lossis kev kwv yees thiab GFR ua tau zoo ( tseem hu ua lub raum ua haujlwm cia), uas tsis niaj hnub ntsuas hauv cov neeg mob.36Cov kab mob plawv ntev ntev hauv cov neeg uas muaj HF nrog kev khaws cia ejection feem cuam tshuam nrog cov kab mob ntawm cov kab mob hauv lub cev, nce siab hauv nruab nrab venous, thiab endothelial, diastolic, thiab txoj cai ventricular tsis ua haujlwm.37

Nyem qhov no kom tau txais NATURAL CISTANCHE EXTRACT rau CKDTSIS TXAUS SIAB

Kev txo qis hauv cov ntshav hauv lub raum, yog tias hnyav txaus, yuav ua rau GFR txo qis. Lub raum kev ua haujlwm poob qis ua rau lub plawv ua haujlwm poob qis uas tau tsav los ntawm kev mob plawv sodium thiab dej ntau dhau, calcium thiab potassium txawv txav, thiab CKD ntsig txog ntshav qab zib. Kev loj hlob ntawm kev mob ntev tuaj yeem tshwm sim hauv qhov chaw uasmob raum raug mob, induced los ntawm mob HF, accelerates cardiovascular pathophysiology ntawm inflammatory pathway activation. Hauv kev tshawb fawb lub raum ultrasound hauv cov neeg mob uas mob HF (n=68), cov tib neeg uas muaj lub raum Doppler pulsatile index saum nruab nrab muaj qhov hnyav ntawm CKD theem tom qab 6 lub hlis piv rau cov neeg uas muaj pulsatile index.38 Pulsatile. Performance index - qhov taw qhia ntawm downstream lub raum hlab ntsha tsis kam thiab txhav - yog ib qho kev ywj pheej kwv yees ntawm kev hloov pauv hauv eGFR.38 Cov txiaj ntsig tau qhia tias lub raum pulse siab nce siab nyob rau hauv HF ntev vim tias muaj zog ntawm cov hlab ntsha, ua rau muaj kev nce hauv lub raum vascular tsis kam thiab txo qis. nyob rau hauv lub raum ntshav khiav thiab GFR.38

Nyob rau hauv hom 4 syndrome, CKD-txog ntshav qab zib, electrolyte imbalances, nce nyob rau hauv uremic co toxins, mob o, thiab oxidative kev nyuaj siab ua rau mob plawv thiab vascular dysfunction.1-3 Nrog kev nce qib.txo lub raum ua haujlwm, phosphate retention nce, thiab phosphate homeostasis raug cuam tshuam txawm tias nce qib ntawm FGF23 (fibroblast loj hlob yam 23) thiab parathyroid hormone.39 Qhov nce ntawm FGF23 qib thiab hyperphosphatemia ua rau txoj hauv kev uastxhawb kev kub siab, sab laug ventricular hypertrophy, thiab vascular calcification, ua rau CVD kev loj hlob.39 Kev loj hlob ntawm CKD feem ntau yog vim muaj ntshav qab zib hauv qab thiab / lossis kub siab. Lub raum tsis ua haujlwm ntev yog cuam tshuam nrog kev cuam tshuam ntawm erythropoietin signaling thiab cov ntshav liab hloov pauv, ua rau cov ntshav tsis txaus, uas yog ib qho tseem ceeb ntawm CKD thiab HF.40 Cachexia yog tshwm sim rau cov tib neeg uas muaj cov kab mob cardiorenal mob ntev thiab tuaj yeem ua rau muaj kev cuam tshuam ntawm pathophysiological ntawm lub raum tsis ua haujlwm.lub plawv thiab lub raumntawm kev tiv thaiv kab mob, neuroendocrine, thiab proinflammatory pathways.41

Txoj cai HF thiab hemodynamic dysfunction los ntawm pulmonary hypertension kuj tseem tuaj yeem ua rau kev txhim kho ntawm cov mob plawv mob ntev nrog rau kev ua haujlwm ntawm CKD.42,43 Hauv cov neeg mob uas muaj theem kawg CKD ntawm hemodialysis, arteriovenous fistula xav tau rau kev nkag tau tuaj yeem ua rau ntau dhau. pulmonary ntshav khiav, ua rau preload nce ntawm lub plawv sab xis thiab pulmonary hypertension.43,44

Hom 2 mob ntshav qab zib mellitus yog qhov tshwm sim ntawm qhov tshwm sim hauv HF thiabCKD. Ntxiv rau nws qhov txuas nrog endothelial dysfunction thiab atherosclerotic vascular kab mob, hom 2 mob ntshav qab zib kuj tseem cuam tshuam nrog glomerular hyperfiltration thiab ntim expansion, thiab tubuloglomerular tawm tswv yim cuam tshuam.45 Txoj kev xav vascular ntawm hom 2 mob ntshav qab zib piav qhia dysregulation ntawm vasoactive yam thiab inactivation ntawm tubuloglomerular tawm tswv yim. Hom 2 mob ntshav qab zib mellitus, uas ua rau kom lub raum afferent arteriole thiab constriction ntawm efferent arterioles, yog li ua rau glomerular hypertension thiab hyperfiltration.46

PATIENT CARE

Kev sib txuas ntawm pathophysiology ntawm lub plawv thiab ob lub raum nyob rau hauv lub cardiorenal syndromes yuav tsum muaj ib tug holistic, tag nrho mus kom ze rau kev tswj. Yuav tsum muaj kev tiv thaiv thawj zaug thiab theem nrab ntawm qhov tshwm sim tsis zoo hauv cov neeg mob CVD, CKD, hom 2 mob ntshav qab zib, thiab HF. CKD thiab HF mob ntev zuj zus zuj zus thiab yuav tsum tau tswj xyuas kom zoo. Tsis tas li ntawd, kev pheej hmoo ntawm evolution ntawm ib qho mob hnyav mus ntev yuav tsum tau txheeb xyuas cov neeg mob uas muaj kev pheej hmoo thiab kev siv cov kev tiv thaiv. Nws yog ib qho tseem ceeb uas ua rau muaj kev pheej hmoo xws li ntshav siab thiab ntshav qab zib, thiab cov teeb meem tseem ceeb xws li ntshav ntshav, tswj hwm. Kev sib txuas lus ntawm tus neeg mob-tus kws kho mob yog ib feem tseem ceeb ntawm kev saib xyuas. Kev npaj saib xyuas suav nrog kev tswj xyuas kev txiav txim siab nyob ib puag ncig cov tsos mob hnyav, uas suav nrog kev qaug zog, mob ntev, thiab kev nyuaj siab.3

Daim duab 1. Flow daim duab qhia txog kev sib cuam tshuam ntawm cov hlab plawv thiab lub raum hauv cov kab mob raum ntev thiab kab mob plawv. RAAS qhia renin-angiotensin-aldosterone

Kev tswj kom zoo ua ntej yuav tsum tau kuaj xyuas thiab paub txog kab mob thaum ntxov. Cov neeg mob uas muaj HF, nrog rau cov neeg uas muaj cov qauv ua ntej ntawm CKD uas muaj proteinuria tab sis khaws cia GFR, yuav tsum raug txheeb xyuas hauv kev kho mob niaj hnub. Txawm li cas los xij, tus nqi ntawm kev tshuaj xyuas cov neeg muaj kev pheej hmoo los ntawm kev sim niaj hnub (xws li, los ntawm kev ntsuam xyuas UACR txhua xyoo) yog qis (35%-57%) hauv kev saib xyuas thawj, 42,47 qhia txog qhov xav tau kom muaj kev paub ntau ntxiv ntawm cardiorenal nexus hauv kev kho mob. Kev kho mob thawj zaug. Tam sim no UACR tau muab tso ua ib qho tseem ceeb ua rau txo qis systolic ntshav siab lub hom phiaj ntawm 120 mm Hg lossis qis dua raws li 2021 Kab Mob Raum Txhim Kho Ntiaj Teb Cov Txheej Txheem Txheej Txheem.48 Ib zaug pom, qhov nyuaj ntawm kev mob plawv mob ntev yuav tsum muaj kev sib koom tes rau kev tswj hwm, suav nrog. pab neeg ua haujlwm ntau yam uas suav nrog tus kws kho mob thawj zaug, kws kho plawv, kws kho mob nephrologist, thiab endocrinologist. Kev taw qhia los ntawm tus kws kho mob tuaj yeem pab cov neeg mob ua raws li lub plawv- thiab lub raum-kev noj qab haus huv. Kev saib xyuas txuas ntxiv ntawm tsev kho mob thiab kev saib xyuas sab nraud yuav tsum tau ua kom ntseeg tau. Kev hloov pauv ntawm kev saib xyuas thiab ua raws li cov tshuaj noj yog cov tswv yim tseem ceeb hauv kev tiv thaiv kab mob thiab txo qis ntawm kev loj hlob ntawm tus kab mob.

Keeb kwm, kev kho mob los txo cov tsos mob HF tshwj xeeb yog txwv los ntawm kev ntshai ntawm kev cuam tshuam rau lub raum tsis ua haujlwm. Ntshai ntawm cov xwm txheej tsis zoo xws li hyperkalemia tuaj yeem ua rau muaj kev cuam tshuam rau kev kho nrog aldosterone antagonists vim tias ntau tus neeg mob uas muaj CKD siab heev-tshwj xeeb yog cov uas tau txais angiotensin-hloov enzyme inhibitors lossis angiotensin receptor blocker therapy - twb muaj kev pheej hmoo ntawm hyperkalemia.49

Tam sim no muaj cov lus qhia txog kev kho mob, los ntawm RAAS inhibitors mus rau, tsis ntev los no, sodium-glucose cotransporter-2 (SGLT2) inhibitors-ob qho tib si muaj cov ntaub ntawv tau txais txiaj ntsig zoo hauv kev sim HF thiab CKD-thiab glucagon-zoo li peptide -1 receptor antagonists, uas muaj cov ntaub ntawv zoo hauv hom 2 mob ntshav qab zib mellitus.6,50 Thaum ntxov, kev xav-tsim cov txiaj ntsig los ntawm cov txiaj ntsig ntawm cov hlab plawv nrog cov glucagon-zoo li peptide-1 receptor antagonists tau sau tseg qee qhov kev tiv thaiv lub raum nrog cov no Cov neeg sawv cev, ntxiv rau lawv lub peev xwm los txo cov txiaj ntsig CVD hauv cov neeg mob uas muaj ntshav qab zib hom 2.51 Kev soj ntsuam ntawm cov txiaj ntsig ntawm glucagon-zoo li peptide-1 receptor antagonist ntawm lub raum tshwm sim hauv cov neeg mob ntshav qab zib hom 2 tseem txuas ntxiv (NCT03819153) . Cov txiaj ntsig tsis ntev los no nrog aldosterone antagonism, los ntawm FIDELIO DKD thiab FIGARO-DKD, qhia txog kev txo qis CKD thiab CVD cov xwm txheej hauv cov neeg mob CKD thiab hom 2 mob ntshav qab zib.28,29 Cov chav kawm SGLT2 inhibitor muaj cov kev xaiv tshiab uas tuaj yeem muaj txiaj ntsig zoo ntawm cardiorenal nexus: SGLT2 inhibition txo qis CKD kev nce qib thiab CVD cov xwm txheej hauv cov neeg mob CKD hauv DAPA-CKD23 thiab txo cov txiaj ntsig tsis zoo CVD cuam tshuam nrog rau HF zuj zus hauv DAPA-HF, 24 EMPEROR-Txo, 25 thiab EMPEROR-Preserved, 30 tsis hais txog qhov muaj lossis tsis muaj. mob ntshav qab zib hom 2.

SGLT2 inhibitors muaj ntau lub luag haujlwm hauv kev ua kom zoo rau kev thuam ntawm cardiorenal syndromes. Ntxiv rau kev txhim kho glycemic tswj, SGLT2 inhibitors tuaj yeem ua rau cov ntshav liab loj thiab hematocrit los ntawm lub raum erythropoietin ntau lawm thiab muaj peev xwm muaj lub luag haujlwm hauv kev txo qis oxidative kev nyuaj siab thiab mob los ntawm inhibiting proinflammatory pathways, inducing autophagy, thiab activating nonclassic RAAS pathways.52,53 SGLT2. inhibition nrog canagliflozin txo qhov kev pheej hmoo ntawm hyperkalemia hauv cov neeg mob kho nrog RAAS inhibitors (angiotensin-hloov enzyme inhibitors lossis angiotensin receptor blockers) hauv CREDENCE, uas tuaj yeem ua rau cov txiaj ntsig cardiorenal.54 Txawm li cas los xij, kev soj ntsuam thib ob ntawm DAPACKD pom tsis muaj qhov sib txawv tseem ceeb hauv kev lag luam. hyperkalemia ntawm dapagliflozin thiab placebo caj npab (tsis hais txog kev siv cov mineralocorticoid receptor antagonist). Kev hloov kho hemodynamic ntawm glomerular ntshav txaus thiab qib ntawm hyperfiltration hauv cov nephrons tsis zoo. Hyperfiltration induces activation ntawm profibrotic txoj kev thiab yog li kev hloov kho ntawm hyperfiltration, thiab tubular kev ua si yuav muaj kev cuam tshuam rau kev ua haujlwm ntev nephron.

TSEEM CEEB

Nrog rau qhov muaj txiaj ntsig zoo ntawm cov tshuaj tshiab los ua kom pom tseeb dua ntawm cardiorenal nexus. Lub hauv paus pathophysiology ntawm cardiorenal nexus tseem yuav tsum tau piav qhia ntxiv. Kev ntes cov kab mob hauv qab no yuav ua rau cov kws kho mob xaiv cov kev kho mob tsim nyog ua ntej. Kev lees paub dav dav ntawm cardiorenal nexus yuav hais txog qhov yuav tsum tau ntsuas thiab tswj CKD hauv cov neeg mob uas feem ntau raug kho rau CVD teeb meem thiab rov ua dua. Ua tib zoo saib xyuas cov kab mob plawv hauv qab yuav ua rau cov kws kho mob thawj zaug thiab kws kho mob endocrinologist coj txoj hauv kev zoo rau kev saib xyuas lawv cov neeg mob ntshav siab, ntshav qab zib hom 2, thiab rog rog. Kev txhim kho ntawm cov phiaj xwm sib xyaw ua ke uas pom pom muaj kev pheej hmoo ntawm cardiorenal syndrome hauv cov ntaub ntawv kho mob hluav taws xob raws li CVD thiab CKD qhov hnyav, thiab qhov kev pheej hmoo no cuam tshuam li cas los ntawm hom 2 mob ntshav qab zib, yuav pab txheeb xyuas ua ntej thiab kho cov neeg mob uas muaj kev pheej hmoo siab. Kev tshawb fawb ntxiv rau hauv cov txheej txheem ntawm kev ua ntawm cov tshuaj uas muaj peev xwm hloov kho cov tshuaj, thiab lub luag haujlwm uas cov tshuaj no yuav muaj thaum siv ua ke, yuav txhim kho kev kho algorithms. Kev tshawb fawb ntxiv txog kev lag luam kev noj qab haus huv thiab cov txiaj ntsig yuav ua rau muaj kev txhim kho hauv kev saib xyuas mus ntev.

REFERENCES

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10. Lub Chaw Tiv Thaiv thiab Tiv Thaiv Kab Mob. Mob raum mobkev soj ntsuam system - United States. Muaj nyob ntawm:https://nccd.cdc.gov/ckd ua. Tau txais Lub Plaub Hlis 7, 2021.

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