Yuav Ua Li Cas Thiab Tswj Cov Ntshav Qab Zib Tom Qab Hloov Raum
Feb 24, 2022
Ekamol Tantisattamo1,2,3 *, Miklos Z. Molnar 4,5,6, Bing T. Ho7, Uttam G. Reddy1,2ua al
Ntshav siabyog ib qho ntawm feem ntau cov hlab plawv co-morbidities tom qab ua tiavraumhloov pauv. Nws feem ntau tshwm sim hauv cov neeg mob uas muaj lwm yam kab mob metabolic, xws li ntshav qab zib mellitus, hyperlipidemia, thiab rog rog. Lub pathogenesis ntawm post-transplant hypertension yog complex thiab yog ib tug tshwm sim ntawm interplay ntawm immunological thiab non-immunological yam. Post-transplant hypertension tuaj yeem muab faib ua tam sim, ntxov, thiab lig tom qab hloov lub sijhawm. Qhov kev faib tawm no tuaj yeem pab cov kws kho mob txiav txim siab txog etiology thiab muab kev tswj hwm tsim nyog rau cov neeg mob nyuaj. Volume overload los ntawm intravenous uid tswj yog tshwm sim thaum lub sij hawm tam sim tom qab hloov lub sij hawm thiab feem ntau ua rau kub siab pom thaum ntxov tom qab hloov. Cov tshuaj tiv thaiv kab mob thiab cov neeg pub lub raum muaj feem cuam tshuam nrog kev hloov pauv tom qabntshav siabtshwm sim nyob rau txhua lub sij hawm taw tes tom qab transplantation. Transplant renal artery stenosis (TRAS) thiab obstructive pw tsaug zog apnea (OSA) tau lees paub tab sis feem ntau thiab kho tau ua rau mob ntshav siab tom qab hloov pauv. Thaum lub sij hawm lig post-transplant lub sij hawm, ntevlub raumallograft dysfunction ua ib qho ntxiv ua rau kub siab. Raws li cov neeg mob no txhim kho ntau yammob ntevraumkab mobcuam tshuam rau lawv cov allografts, fibroblast kev loj hlob zoo tshaj plaws 23 (FGF23) nce thiab cuam tshuam nrog kev nce siab ntawm cov hlab plawv thiab tag nrho cov neeg tuag hauv lub raum hloov pauv. Qhov tseeb kev sib raug zoo ntawm kev nce FGF23 thiab post-transplant hypertension tseem tsis to taub. Ntshav siab (BP) lub hom phiaj thiab kev tswj hwm koom nrog kev kho mob tsis yog tshuaj thiab kws tshuaj thiab yuav tsum yog tus kheej. Kom txog rau thaum muaj pov thawj muaj zog nyob rau hauv lubraumhloov pauvpejxeem muaj, ib tug BP ntawm<130 0="" mmhg="" is="" a="" reasonable="" target.="" similar="" to="" complete="" renal="" denervation="" in="" non-transplant="" patients,="" bilateral="" native="" nephrectomy="" is="" another="" treatment="" option="" for="" resistant="" post-transplant="" hypertension.="" native="" renal="" denervation="" offers="" promising="" outcomes="" for="" controlling="" resistant="" hypertension="" with="" no="" significant="" procedure-related="" complications.="" this="" review="" addresses="" the="" epidemiology,="" pathogenesis,="" and="" specific="" etiologies="" of="" post-transplant="" hypertension="" including="" tras,="" calcineurin="" inhibitor="" effects,="" osa,="" and="" failed="" native="" kidney.="" the="" cardiovascular="" and="" survival="" outcomes="" related="" to="" post-transplant="" hypertension="" and="" the="" utility="" of="" 24-h="" blood="" pressure="" monitoring="" will="" be="" briefly="" discussed.="" antihypertensive="" medications="" and="" their="" mechanism="" of="" action="" relevant="" to="" kidney="" transplantation="" will="" be="" highlighted.="" a="" summary="" of="" guidelines="" from="" different="" professional="" societies="" for="" bp="" targets="" and="" antihypertensive="" medications="" as="" well="" as="" non-pharmacological="" interventions,="" including="" bilateral="" native="" nephrectomy="" and="" native="" renal="" denervation,="" will="" be="">
Ntsiab lus:tshuaj antihypertensive, ob tog neeg nephrectomy, ntshav siab lub hom phiaj, kab mob plawv,raumhloov pauv, ncej-raumhloov pauvntshav siab, haiv neeg lub raum sympathetic denervation, 24-h ntshav siab xyuas
Hu rau:joanna.jia@wecistanche.com/ WhatsApp: 008618081934791
Cistanche tubulosa tiv thaiv kab mob raum, nyem qhov no kom tau txais cov qauv
Taw qhia
Kev tiv thaiv contraindications,raumhloov pauvyog kev kho mob ntawm kev xaiv rau qib siabmob ntevraumkab mob(CKD) thiab kab mob raum kawg (ESRD) (1). Cov txiaj ntsig muaj sia nyob thiab kev ua neej zoo tau zoo dua qub tom qab hloov lub raum zoo nrog rau lub raum allograft muaj nuj nqi. Txij li thaum pib ntawm calcineurin inhibitors (CNI) nyob rau xyoo 1980s, lub raum luv luv allograft muaj sia nyob tau zoo heev, tab sis tsis muaj qhov cuam tshuam loj rau lub raum mus ntev allograft ciaj sia (2, 3). Ntau qhov kev tiv thaiv kab mob thiab tsis muaj kab mob ua rau muaj kev cuam tshuam rau lub raum mus sij hawm ntev thiab cov neeg mob muaj sia nyob. Zoo ib yam li cov neeg mob tsis hloov pauv, cov kab mob plawv (CVD) tseem yog qhov ua rau muaj mob hnyav thiab tuag rau cov neeg tau txais kev hloov hauv lub raum (4). Hypertension (HTN) yog ib qho kev tshawb pom ib txwm muaj nyob rau hauv cov pej xeem no thiab ib qho ntawm feem ntau muaj feem cuam tshuam rau CVD (5). Tsab ntawv xov xwm no yuav tshuaj xyuas cov kab mob tom qab hloov HTN, suav nrog kev hloov pauv hauv lub raum hlab ntsha stenosis (TRAS) thiab kev tswj hwm kev sib txawv raws li etiology ntawm kub siab nyob rau hauv ntau qhov chaw kho mob hloov pauv tau txais cov xwm txheej. Kev txiav txim siab thaum tsis yog tshuaj kho mob, suav nrog kev hloov pauv lub raum hlab ntsha angioplasty thiab / lossis stenting, ob tog neeg nephrectomy, thiab cov neeg lub raum denervation (RDN), kuj tseem yuav tau tham txog.
EPIDEMILOGY OF POST-TRANSPLANT HYPERTENSION
Raws li cov ntsiab lus thiab cov txheej txheem ntawm kev ntsuas ntshav siab (BP) siv, qhov ntau ntawm HTN tom qab hloov pauv tau nthuav dav, thiab feem ntau nws tau nce ntau dhau sijhawm. Qhov tshwm sim ntau dua ntawm kev hloov ntshav siab tom qab hloov pauv tuaj yeem cuam tshuam nrog kev qhia txog cyclosporine (CsA) (6-8). Ib txoj kev tshawb fawb hauv Spain tau saib cov neeg mob hloov pauv hauv peb lub xyoo sib txawv (1990 vs. 1994 vs. 1998) thiab tau sau tseg tias muaj kev nce ntxiv ntawm qhov tshwm sim tom qab hloov HTN nrog rau xyoo tom ntej rau tag nrho peb lub sijhawm. Tus naj npawb ntawm cov tshuaj antihypertensive xav tau hauv kev hloov pauv tsis ntev los no kuj tau nce ntxiv piv rau cov neeg mob uas tau hloov pauv ua ntej (9). Tag nrho qhov kev nthuav dav ntawm kev hloov pauv tom qab HTN tau nyob ntawm 24 txog 90 feem pua (5, 8-19).
TXOJ CAI NTAWM POST-TRANSPLANT HYPERTENSION
Tom qab hloov lub raum HTN tuaj yeem txhais tau tias yog qhov nce siab BP tsis tu ncua lossis tsis muaj zog nrog kev siv cov tshuaj tiv thaiv kab mob siab tom qab hloov lub raum zoo. Txawm li cas los xij, cov lus nug tseem ceeb uas tseem tshuav yog dab tsi yog qib BP ib txwm? Cov kev tshawb fawb sib txawv tau txiav txim siab tom qab hloov HTN nrog cov qib sib txawv rau cov ntshav siab systolic thiab diastolic (SBP thiab DBP) thiab cov kev cai sib txawv rau kev siv cov tshuaj tiv thaiv. Table 1 qhia cov ntsiab lus ntawm cov kev tshawb fawb no (8, 9, 16–18).
Ntxiv rau qhov txhais cov qib BP ib txwm muaj, qhov muaj lossis tsis muaj HTN thaum lub sijhawm hloov pauv hauv lub raum ua ntej tuaj yeem faib cov neeg raum hloov pauv mus rau plaub pawg: HTN tsis tu ncua, rov qab HTN, tsis tu ncua, thiab tom qab hloov HTN. Persisent HTN tshwm sim hauv cov neeg mob uas muaj HTN ob qho tib si hauv lub sijhawm ua ntej thiab tom qab hloov pauv, thaum cov neeg mob rov zoo HTN muaj HTN nkaus xwb thaum lub sijhawm ua ntej tab sis tsis yog lub sijhawm hloov pauv tom qab. Cov neeg mob normotensive tsis tu ncua tsis muaj keeb kwm ntawm HTN ua ntej hloov pauv thiab nyob twj ywm tom qab hloov pauv. Tom qab hloov HTN yuav tsum tau tsim de novo HTN tom qab hloov lub raum (Daim duab 1). Malek-Hosseini et al. (17) qhia txog qhov tshwm sim ntawm HTN tsis tu ncua, rov qab HTN, tsis tu ncua tsis tu ncua, thiab tom qab hloov HTN li 40, 28, 13, thiab 19 feem pua, raws li. Hauv qhov kev tshuaj xyuas no, tom qab hloov lub raum HTN hais txog kev pheej hmoo thiab tom qab hloov pauv (de novo) HTN tshwj tsis yog tau teev tseg.
Cov ntawv cais ntawm HTN ob qho tib si systolic thiab diastolic tseem tshwm sim tom qab hloov lub raum. Cov European Society of Hypertension thiab European Society of Cardiology cov lus qhia tau txiav txim siab cais cov systolic HTN hauv cov pej xeem raws li SBP Ntau dua lossis sib npaug rau 140 thiab DBP<90 mmhg="" (20).="" this="" is="" the="" most="" common="" phenotype="" of="" htn="" in="" elderly="" patients="" (21).="" the="" linear="" increase="" in="" systolic="" and="" diastolic="" bp="" occurs="" with="" age="" until="" the="" fifth="" or="" the="" sixth="" decades="" of="" life="" when="" sbp="" continues="" increasing,="" but="" dbp="" tends="" to="" decrease="" (22).="" pathogenesis="" of="" isolated="" systolic="" htn="" involves="" both="" intrinsic="" alterations="" resulting="" from="" the="" normal="" aging="" process="" accompanied="" by="" the="" development="" of="" modifiable="" risk="" factors="" leading="" to="" increased="" arterial="" stiffness="">
Xwb, diastolic HTN txhais tau tias yog DBP ntawm Ntau dua lossis sib npaug rau 90 mmHg, nrog SBP<140 mmhg,="" and="" is="" more="" common="" in="" younger,="" sedentary="" individuals="" with="" a="" higher="" body="" mass="" index="" (bmi)="">
A recent large randomized controlled clinical trial of blood pressure management in non-diabetic patients (SPRINT) demonstrated cardiovascular (CV) benefits of tighter BP control (25) leading to new BP guidelines and re-defined HTN for the general population as systolic blood pressure (SBP) >130 or DBP >80 mmHg (26, 27). Txawm hais tias tau muaj kev hloov pauv hauv lub ntsiab lus ntawm HTN hauv cov neeg tsis hloov pauv, lub ntsiab lus ntawm HTN hauv cov neeg tau txais kev hloov lub raum tseem muaj teeb meem, thiab cov txiaj ntsig nyuaj cuam tshuam txog BP qib tseem txwv. Tsis ntev los no 2017 American College of Cardiology/American Heart Association (ACC/AHA) cov lus qhia pom zoo rau lub hom phiaj BP ntawm<130 0="" mmhg="" (26,="" 27).="" until="" there="" figure="" 1="" |="" post-kidney="" transplant="" hypertension="" stratified="" by="" presence="" and="" absence="" of="" pre-transplant="" hypertension.="" htn,="" hypertension;="" ktx,="" a="" kidney="" transplant.="" is="" stronger="" evidence="" of="" an="" association="" between="" bp="" level="" and="" outcomes="" in="" kidney="" transplant="" recipients,="" a="" bp="" ≥130/80="" mmhg="" may="" be="" a="" reasonable="" definition="" for="" htn="" in="" this="">
PATHOGENESIS OF POST-TRANSPLANTHYPERTENSION
Qhov kev hloov pauv ntawm qhov tshwm sim tom qab hloov HTN thoob plaws lub sijhawm tom qab hloov pauv hloov pauv tuaj yeem rov kho qhov tsis zoo ntawm cov kab mob tom qab hloov HTN dhau sijhawm (Daim duab 2). Kev txheeb xyuas thaum tom qab hloov HTN thawj zaug tshwm sim tuaj yeem nqaim qhov kev kuaj mob rau qhov etiology ntawm kev hloov HTN tom qab thiab ua rau kev kho kom haum.
Tam sim ntawd tom qab hloov lub sij hawm
Thaum lub sijhawm no, tom qab hloov HTN feem ntau yog tshwm sim los ntawm lwm yam xws li kev hloov pauv, IV uids, thiab koob tshuaj steroids siab.
Peri-transplant Hypervolemia IV kev pab muab thaum lub sijhawm phais thiab hauv lub sijhawm tom qab ua haujlwm tam sim tuaj yeem ua rau hypervolemia, tshwj xeeb tshaj yog rau cov neeg mob uas muaj kev ua haujlwm qeeb qeeb (DGF). Ib txoj kev tshawb nrhiav ib qho chaw hla ntu qhia tau hais tias qhov tshwm sim ntawm hypervolemia ntsuas los ntawm kev ntsuas ntau zaus bioimpedance rau extracellular uid hauv cov neeg tau txais kev hloov hauv lub raum ruaj khov yog 30 feem pua, thiab txog li 5 feem pua tau mob hnyav hypervolemia. Txoj kev tshawb no tau pom tias hypervolemia tseem ceeb cuam tshuam nrog nce systolic, diastolic, thiab txhais tau tias cov hlab ntsha siab (28). Txawm hais tias txoj kev tshawb no tau tso npe rau 123 tus neeg tau txais kev hloov pauv lub raum nrog lub sijhawm nruab nrab ntawm kev tso npe ntawm 5 xyoos tom qab hloov pauv, hypervolemia feem ntau tshwm sim thaum lub sijhawm hloov pauv tam sim ntawd, thiab qhov hnyav nce siab tshaj qhov kev hloov pauv ua ntej kwv yees qhov hnyav qhuav yog txuam nrog HTN.
Ntau qhov ntsuas tuaj yeem siv los kwv yees qhov xwm txheej ntim. Cov no suav nrog cov kev ntsuas ib txwm muaj xws li BP, lub plawv dhia, tso zis tso zis, lub hauv siab venous siab, thiab pulmonary artery siab nrog rau cov kev ntsuas tsis zoo xws li intraoperative transesophageal echocardiography thiab non-invasive dynamic cardiac output technology, eg, pulse contour analysis, pulse. yoj lub sij hawm thauj mus los, thoracic hluav taws xob bioimpedance / bioreactance, thiab carbon dioxide rebreathing technologies (29, 30). Txawm hais tias ntau qhov kev ntsuas uas tsis yog ib txwm muaj txiaj ntsig zoo rau kev ntsuas ntim, lawv tsis tuaj yeem muaj nyob rau lub sijhawm hloov pauv thiab cov kev ntsuas pa tseem yog tus qauv hauv kev kho mob.
High-Dose Steroids
High-dose steroids feem ntau yog siv cov tshuaj tiv thaiv kab mob hauv lub sijhawm hloov pauv. Qhov xwm txheej ntawm steroid-induced HTN thaum lub sijhawm hloov pauv tam sim ntawd tsis paub. Cov txheej txheem ntawm steroid-induced HTN tsis meej, tab sis nws yuav tshwm sim los ntawm kev hloov pauv hauv cov lus teb hauv lub cev ua rau cov hlab ntsha tsis kam (31). Txij li thaum koob tshuaj steroid ntau tshaj 20mg ntawm prednisone ib hnub twg yog qhov pib muaj HTN (32), cov koob tshuaj IV steroids siab tuaj yeem ua rau HTN thaum lub sijhawm hloov pauv tam sim ntawd.
Rebound Hypertension
Cov neeg mob ESRD feem ntau muaj kev tswj tsis tau HTN thiab xav tau ntau yam tshuaj los tswj lawv cov BP. Thaum lub sijhawm hloov pauv tam sim ntawd, nws yog ib qho kev coj ua kom tuav qee yam yog tias tsis yog tag nrho cov tshuaj BP ua ntej hloov pauv hauv eort kom tsis txhob muaj ntshav siab thaum ntxov. Txawm li cas los xij, qhov kev txiav tawm sai sai ntawm kev kho cov tshuaj tiv thaiv kab mob tuaj yeem ua rau rov ua kom ntshav siab, nce BP siab dua qib pretreatment, vim yog kev ua siab ntev. Beta-adrenergic agonists, clonidine (ob lub qhov ncauj thiab cov ntaub ntawv transdermal) (33), thiab beta-blockers feem ntau cuam tshuam nrog qhov tshwm sim no, tshwj xeeb tshaj yog thaum nres sai. Geys et al. pom tau hais tias yuav luag txhua tus neeg mob uas tau noj clonidine 900 mcg ib hnub rau ntau tshaj 1 lub hlis tau mob ntshav siab tom qab noj tshuaj tsis tau. Sympathetic overactivity yam tsis muaj renin-angiotensin qhov kev sib kho kom haum xeeb plays lub luag haujlwm tseem ceeb hauv cov txheej txheem ntawm rebound HTN los ntawm clonidine (34).
Zoo ib yam li clonidine, rebound HTN los ntawm beta-blockers ua rau siab BP thiab lub plawv dhia. Nws kuj tseem ua rau cov xwm txheej hauv plawv xws li angina, myocardial infarction, lossis tuag sai sai hauv cov neeg mob uas muaj kab mob hauv cov hlab ntsha (CAD) (35-39). Ua kom muaj kev sib raug zoo nrog rau kev tswj hwm adrenergic receptors hauv cov tib neeg noj beta-blockers yog xav tias yog lub tswv yim ntawm beta-blockers rebound HTN (36, 38, 40). Muab kev pheej hmoo plawv nrog peri-operative beta-blocker tshem tawm (41, 42), 2014 ACC / AHA cov lus qhia muab cov lus pom zoo hauv chav kawm nrog B qib pov thawj rau kev txuas ntxiv ntawm beta-blockers thaum lub sijhawm ua haujlwm hauv cov neeg mob uas mob ntev. siv lawv (43).
Kev Tswj Kev Kho Mob tsis tsim nyog
Kev mob hnyav yog txuam nrog nce BP los ntawm kev ua siab ntev ntawm lub paj hlwb, ua rau muaj kev nce ntxiv hauv peripheral vascular tsis kam, lub plawv dhia, thiab mob stroke. Ntxiv rau qhov kev txhawb nqa ntawm cov neuroendocrine system ntawm hypothalamic-pituitary- adrenal axis ua rau mob HTN (44). Tsis txaus peri-
Kev tswj xyuas qhov mob yog ib qho ntawm feem ntau ua rau HTN tam sim tom qab hloov pauv. Opioid analgesic feem ntau yog siv los tswj qhov mob thaum lub sijhawm hloov pauv tam sim ntawd. Cov tshuaj uas tsis yog-steroidal anti-inmmatory (NSAID) tuaj yeem muab kev kho mob eective, tab sis yuav tsum tau zam rau lub sijhawm tom qab hloov pauv vim lawv lub raum tsis zoo, suav nrog txo lub raum ntshav ow tshwj xeeb tshaj yog cov neeg mob tsis tau tsim lub raum allograft muaj nuj nqi lossis cov uas muaj DGF.
Thaum Ntxov Lub Sijhawm Hloov Hloov
Tsis tau muaj ib lub sij hawm tom qab hloov lub raum uas tau raug suav hais tias yog lub sijhawm hloov pauv thaum ntxov. Txawm li cas los xij, peb pom tias systolic HTN (140 mmHg) tshwm sim nyob rau lub sijhawm nruab nrab ntawm 26-50 lub lis piam tom qab hloov lub raum (45), thaum lub raum ua haujlwm ntawm lub raum allograft thiab cov koob tshuaj ruaj khov ntawm kev saib xyuas cov tshuaj tiv thaiv kab mob feem ntau mus txog li 3-6 lub hlis tom qab. - hloov pauv. Yog li ntawd, peb txiav txim siab lub sijhawm hloov pauv thaum ntxov rau qhov kev tshuaj xyuas no yog lub sijhawm ntawm 24 thiab 52 lub lis piam tom qab hloov pauv. Lub sijhawm ntawd ntau yam ua rau HTN.
Qhov hnyav nce
Nruab nrab ntawm 6- thiab 12- hli tom qab hloov pauv, qhov hnyav nce feem ntau tshwm sim (46, 47). Qhov nruab nrab qhov hnyav nce thiab nce hauv BMI ntawm 1 xyoos tom qab hloov pauv yog 6.2 10.7kg thiab 2.1 3.8 kg/m2, raws li (47). Kev rog dhau (BMI 30 kg / m2) tom qab hloov lub raum yog qhov cuam tshuam nrog kev hloov pauv tom qab HTN (48). Qhov txiaj ntsig zoo ntawm uid tau txais los ntawm kev sib koom ua ke thiab tom qab kev ua haujlwm IV uid yog ib qho ua rau qhov hnyav nce thaum lub sijhawm hloov pauv thaum ntxov (49). Tus nqi ntawm sodium hauv IV uid tuaj yeem ua rau HTN. Txawm li cas los xij, tom qab tau txais lub raum allograft muaj nuj nqi, tso zis tso tawm ntawm qhov nce hauv cov zis tuaj yeem txhawb nqa sodium thiab dej. Qhov no tuaj yeem pab tswj tau BP.
Calcineurin Inhibitors
Feem ntau ntawm HTN nyob rau hauv cov neeg tau txais kev hloov hauv lub raum yog nyob nruab nrab ntawm 70 thiab 90 feem pua (50,51), uas yog ntau dua li qhov tshwm sim nyob rau hauv pre-CNI era ntawm 40–50 feem pua (52,53). Muaj ob lub ntsiab mechanism ntawm CNI-induced post-transplant HTN uas tshwm sim los ntawm kev cuam tshuam vascular tone thiab lub raum sodium thauj tuav.
Hloov vascular tone
Ob leeg nce vasoconstriction thiab impaired vasodilation pab rau CNI-induced post-transplant HTN; txawm li cas los xij, tom kawg yog xav tias yog lub ntsiab mechanism (54).
Lub raum vasoconstriction.
Lub raum vasoconstriction yog kho los ntawm endothelin, vasoconstrictor, ntau dua li angiotensin II, vim captopril tsis tiv thaiv CsA-induced raum vasoconstriction (55). Txawm li cas los xij, vasoconstrictive eect ntawm lub raum lossis lub cev vasculature tseem tsis meej (56). Muaj cov lus ceeb toom tsis sib haum txog qhov cuam tshuam ntawm angiotensin II ntawm cov hlab ntsha. CsA ua rau hauv zos eect ntawm cov leeg nqaij leeg los ntawm kev nce tus naj npawb ntawm angiotensin II receptors uas ua rau vasoconstriction (57).
Lub raum vasodilation. Kev tsis pom kev vasodilation yog tshwm sim los ntawm CNI-induced txo ntawm nitric oxide, vasodilator. CNIs inhibits inducible nitric oxide synthase hauv vascular du leeg hlwb (58).
Ua kom lub raum sodium thauj tuav Sympathetic paj hlwb ua kom. CSA ua rau muaj kev mob siab rau thiab tom qab sodium retention (59). Muaj kev sib txuas ntawm CNI-induced HTN thiab phospho-protein synapsin pom ntawm microvesicles hauv lub raum kev hnov qab paj hlwb (60).
Nrog-No-K(Lys)—STE20/SPS1-txog proline/alanine-nplua nuj kinase—Sodium Chloride Cotransporter (WNK-SPAK- NCC) txoj kev. CNI induces ntsev-rhiab heev HTN los ntawm kev ua kom lub WNK- SPAK-NCC txoj kev zoo ib yam li ib tug tsawg genetic daim ntawv ntawm HTN, hu ua familial hyperkalemic hypertension (FHHt, kuj hu ua Gordon syndrome los yog pseudohypoaldosteronism hom 2) (61). FHHt tshwm sim los ntawm kev poob-ntawm-kev hloov pauv ntawm WNK kinases uas ua rau NCC (62) thiab tshwm sim raws li kev kub siab hyperkalemic nrog rau qhov tsis muaj anion gap metabolic acidosis thiab hypercalciuria (61). Hauv qhov xwm txheej ib txwm muaj, calcineurin, phosphatase, inhibits qee cov kinases, suav nrog kinases WNK3, WNK4, thiab SPAK hauv qhov distal convoluted tubule (DCT), uas cuam tshuam rau phosphorylate thiab qhib NCC (54, 63). CNI inhibits calcineurin thiab ua rau phosphorylation thiab ua kom WNK thiab SPAK kinases thiab NCC. Yog li, sodium thiab chloride reabsorption hauv DCT yog nce thiab ntsev-rhiab HTN tshwm sim. Tsawg fractional excretion ntawm chloride txhawb nqa kev ua haujlwm NCC (64), thiab txo qis plasma aldosterone qib zoo ib yam nrog ntim nthuav dav (54). Los ntawm kev pom zoo, thiazide diuretics yuav tsum tau siv rau CNI-induced HTN (54,65).
Cov tshuaj steroids
Txij li thaum cov tshuaj steroids tuaj yeem ua rau HTN, steroid zam lossis tshem tawm (SAW) cov tshuaj tiv thaiv kab mob tiv thaiv kab mob tuaj yeem raug txiav txim siab. Txawm li cas los xij, eect ntawm SAW ntawm kev hloov pauv tom qab HTN tau muab cov ntaub ntawv sib txawv. Curtis et al. (10) qhia tau tias qhov ntau ntawm HTN txo qis hauv cov neeg mob noj cov tshuaj steroid alternate-hnub. Kev tshuaj xyuas thiab kev tshuaj ntsuam xyuas meta tau qhia tias kev zam steroid los yog tshem tawm tseem ceeb txo qis CV cov txiaj ntsig suav nrog HTN tab sis ua rau muaj kev pheej hmoo ntawm kev tsis lees paub (66). Nws yog qhov tshwm sim rau cov tshuaj steroids yuav tsum tau rov qhia dua tom qab kuaj pom qhov tsis lees paub hauv cov neeg tau txais kev tswj hwm thawj zaug nrog SAW kev tswj hwm. Ib qho kev sim randomized, txawm li cas los xij, pom tias tsis muaj kev hloov pauv hauv ntshav siab ntawm lwm hnub thiab niaj hnub prednisone (67). SAW cov txheej txheem yuav tsum raug txiav txim siab hauv cov neeg mob xaiv, tshwj xeeb yog cov neeg uas yuav muaj kev pheej hmoo ntau dua rau cov txiaj ntsig CV tab sis muaj kev tiv thaiv kab mob qis dua ntawm kev tsis lees paub.
Hypertensive Donor raum
Kev noj ntsev tuaj yeem ua rau cov dej tuav thiab HTN, tshwj xeeb tshaj yog rau cov neeg muaj ntsev (68). Tsis tas li ntawd, ntau qhov kev tshawb fawb tsiaj tau pom tias lub raum lub luag haujlwm hauv kev loj hlob ntawm HTN (69-73). Kev hloov pauv hauv lub raum los ntawm idiopathic hypertensive nas pub rau cov neeg tau txais cov noob caj noob ces coj mus rau tom qab hloov HTN uas tshwm sim los ntawm kev txo qis raum ntsev tawm. Ntawm qhov tod tes, kev hloov pauv los ntawm cov noob caj noob ces normotensive nas pub rau cov nas muaj zog nrog kev hloov ua ntej ob tog neeg nephrectomy ua rau normotension tom qab hloov pauv (74).
Ib txoj kev tshawb fawb hauv cov neeg tau txais kev hloov hauv lub raum uas tau txais kev kho mob nephrectomy ua ntej hloov lub raum los ntawm cov neeg pub dawb pom tau tias txhua tus neeg tau txais kev hloov pauv tsis zoo tom qab hloov pauv yam tsis xav tau kev kho mob ntshav siab (75). Lwm txoj kev tshawb fawb hauv cov neeg tau txais kev hloov lub raum los ntawm cov tsev neeg tsis muaj zog pom tau tias muaj kev nce ntxiv hauv cov tshuaj tiv thaiv hypertensive tom qab hloov lub raum thaum lub raum los ntawm cov neeg pub nyiaj nrog cov tsev neeg mob ntshav siab piv rau cov neeg tau txais lub raum los ntawm cov neeg pub dawb nrog cov tsev neeg tsis muaj zog. Txawm li cas los xij, hauv cov neeg tau txais kev pab nrog tsev neeg HTN, hloov lub raum los ntawm txhua hom lub raum tsis ua rau muaj qhov tshwm sim tom qab hloov HTN (76). Tsis tas li ntawd, ntawm cov neeg tau txais kev hloov hauv lub raum uas tsis muaj tsev neeg keeb kwm ntawm HTN, cov neeg mob tau txais lub raum los ntawm cov neeg pub dawb nrog tsev neeg keeb kwm ntawm HTN xav tau 10 npaug ntau dua cov tshuaj tiv thaiv kab mob siab dua piv rau cov neeg tau txais lub raum los ntawm cov neeg pub dawb yam tsis muaj tsev neeg keeb kwm ntawm HTN (77). Qhov no txhua yam qhia txog lub luag haujlwm rau lub raum thiab caj ces kab mob hauv lub raum hauv kev tsim HTN.
Transplant Renal Artery Stenosis (TRAS)
Cov teeb meem vascular yog ib qho ntawm cov laj thawj tseem ceeb ntawm kev hloov pauv tsis zoo. TRAS yog ib qho kev lees paub zoo thiab muaj teeb meem vascular, uas ua rau lub raum ua haujlwm tsis zoo thiab CV teeb meem nrog rau tom qab hloov HTN. Nws yog ib qho tseem ceeb kom paub txog qhov no thaum ntxov vim tias kev kho mob ua rau rov qab cov txiaj ntsig tsis zoo. Kwv yees li ntawm 1-5 feem pua ntawm kev hloov HTN tom qab hloov pauv mus rau TRAS (78, 79). Txawm li cas los xij, vim hais tias ntawm diering denitions siv nyob rau hauv cov kev tshawb fawb, qhov tshwm sim ntawm TRAS tau tshaj tawm los ntawm 1 mus rau 23 feem pua (80). Wong et al. (81) tau tshaj tawm tias qhov kev nthuav dav ntawm TRAS tau nce los ntawm 2.4 mus rau 12.4 feem pua tom qab qhia cov xim Doppler ultrasonography (CDU) hauv xyoo 1985, yuav muaj feem cuam tshuam txog kev txhim kho kev kuaj pom nrog kev kuaj tsis pom. TRAS tuaj yeem tshwm sim txhua lub sijhawm tom qab hloov lub raum tab sis feem ntau kuaj pom ntawm 3 thiab 24 lub hlis tom qab hloov pauv (82-84). Tsis zoo li lub raum artery stenosis (RAS) nyob rau hauv cov neeg mob uas tsis yog-transplantation, lub pathogenesis ntawm TRAS yog complex thiab koom nrog non-immunological thiab immunological yam (81,85). Cov yam tsis muaj kev tiv thaiv kab mob muaj xws li vascular puas tsuaj thaum lub sijhawm phais anastomosis ntawm tus neeg mob lub raum cov hlab ntsha thiab cov hlab ntsha uas tau txais nrog rau qhov muaj cov kab mob vascular hauv ob leeg pub dawb thiab cov neeg txais cov hlab ntsha (86). Vim tias tus neeg tau txais cov hlab ntsha iliac, tsis yog lub plab aorta, yog lub hom phiaj vascular tshaj plaws rau tus neeg mob lub raum hlab ntsha anastomosis, qhov kev sib txuas ntawm cov hlab ntsha me me no yuav ua rau kev nqaim thiab kev loj hlob ntxiv ntawm TRAS physiology (87). Fibromuscular dysplasia tsis yog ib qho ua rau RAS hauv cov neeg mob hloov pauv. Immunological yam ua rau vascular endothelial tsis ua haujlwm tuaj yeem ua rau TRAS. Lwm yam kev pheej hmoo ntawm kev hloov pauv tau raug tshaj tawm suav nrog cytomegalovirus (CMV) kab mob (88). Zoo ib yam li cov neeg mob tsis hloov pauv, kab mob atherosclerotic tuaj yeem ua rau TRAS, tab sis cov kab mob ntawm atherosclerotic TRAS tuaj yeem ua rau tuag taus. Atherosclerotic TRAS tsis zoo li tshwm sim nyob rau lub sijhawm pib hloov pauv tshwj tsis yog tias muaj cov neeg pub dawb thiab / lossis tus neeg tau txais cov kab mob atherosclerotic (89). Ntxiv nrog rau cov xwm txheej pheej hmoo rau kab mob atherosclerotic, qee qhov kev tiv thaiv kab mob kuj tseem tuaj yeem ua si hauv atherosclerotic TRAS. Piv txwv li, diuse stenosis yuav qhia txog kev tiv thaiv kab mob vascular endothelial raug mob (90). Ntxiv mus, zoo ib yam li histological ndings ntawm vascular rejection thiab stenotic hloov lub raum cov hlab ntsha (82, 91) nrog rau kev koom tes ntawm post anastomotic TRAS thiab de novo class II pub-specic antibodies (92) nce qhov muaj peev xwm ntawm immunologic contribution rau atherosclerotic TRAS.
Cov tsos mob thiab cov cim qhia ntawm TRAS tsis yog tshwj xeeb; Txawm li cas los xij, cov ntaub ntawv kho mob uas yuav tsum tau ua rau kev ua haujlwm rau TRAS yog qhov tsis tau piav qhia ua rau lub raum allograft ua haujlwm lossis tsis tswj HTN (79). Txij li thaum lub raum hypoperfusion ua rau muaj zog renin, angiotensin, thiab aldosterone, ntsev tuav tuaj yeem ua rau peripheral edema, congestive plawv tsis ua hauj lwm, thiab tshauv pulmonary edema. Tshwj xeeb, paradoxical normotension lossis hypotension tuaj yeem pom nrog kev siv cov tshuaj diuretics siab thiab / lossis angiotensin-hloov enzyme inhibitors (ACEI) lossis angiotensin II receptor blockers (ARB) (93). Bruits tshaj kev hloov lub raum allografts site muaj ntau tab sis tsis yog tshwj xeeb. Bruits tuaj yeem cuam tshuam rau lwm yam ua rau xws li arteriovenous stula (AVF) hauv lub raum tom qab kuaj ntshav (94).
Ntau cov kev tshawb fawb pom tau siv los kuaj xyuas TRAS. CDU feem ntau yog qhov kev tshawb fawb thawj zaug siv vim nws tsis muaj kev cuam tshuam, muaj dav, thiab pheej yig. Txawm li cas los xij, cov duab zoo thiab kev txhais lus yog nyob ntawm tus txheej txheem ultrasonographer thiab kev paub dhau los. Peak systolic tshaj tawm (PSV) ntawm lub raum cov hlab ntsha loj thiab post stenotic intrarenal arterial resistive index (RI) yog siv los txiav txim siab thiab qib qhov hnyav ntawm TRAS (79). Txawm li cas los xij, txij li tus nqi kuaj mob ntawm CDU yog tus neeg teb xov tooj-nyob ntawm tus neeg teb xov tooj, lwm yam kev kuaj pom yuav raug siv los txheeb xyuas qhov kev kuaj mob. Lub raum hlab ntsha suav tomography (CT) lossis magnetic resonance angiography (MRA) yuav tsum tau siv los piav qhia ntxiv lossis paub meej qhov kev kuaj mob. Txawm li cas los xij, qhov kev pheej hmoo ntawm qhov sib txawv-induced nephropathy (CIN) thiab nephrogenic systemic fibrosis yuav tsum tau txiav txim siab thiab yuav txwv tsis pub siv cov kev tshawb fawb no. Lub raum hlab ntsha angiography tseem yog tus qauv ntsuas kub ntsuas rau TRAS, tab sis nws tuaj yeem cuam tshuam thiab tuaj yeem ua rau CIN. Cov pa roj carbon dioxide (CO2) angiography tuaj yeem txo qee qhov kev pheej hmoo ntawm CIN, tab sis, feem ntau, me me ntawm IV qhov sib piv tseem yuav tsum tau kom muaj cov duab ntxaws ntxaws.
Peb txoj kev kho mob rau TRAS yog kev kho tshuaj ib leeg lossis kev kho tshuaj kho mob ntxiv rau lub raum hlab ntsha angioplasty nrog stenting lossis phais revascularization (90).
Rau kev kho tshuaj pharmacological, pathophysiology ntawm TRAS zoo ib yam li ob sab RAS hauv cov neeg tsis hloov pauv. Kev txo qis hauv lub raum ntshav vim yog hloov pauv lub raum allograft ua rau muaj zog RAAS ua rau ua rau ntsev thiab dej tuav thiab HTN tom qab. ACEI lossis ARB ntxiv rau cov tshuaj diuretics yog ib txoj hauv kev zoo rau kev tswj BP. Txawm li cas los xij, qhov kev kho tshuaj no yog txwv los ntawm kev txo qis rau lub raum ua haujlwm los ntawm kev txo qis hauv cov kab mob BP ua rau txo qis raum perfusion thiab intraglomerular siab hauv qab qhov txwv ntawm autoregulation. Qhov no ua rau muaj kev cuam tshuam ntawm arteriolar tsis kam kho los ntawm angiotensin II. Los ntawm thaiv qhov kev txiav txim ntawm angiotensin II, autoregulation yog blunted, thiab GFR txo (95). Kev txo qis ntawm cov tshuaj diuretics kuj tseem tuaj yeem ua rau nce ntshav creatinine hauv cov xwm txheej no. Vim li no, nws tsis yog ib txwm siv RAAS thiab / lossis diuretics thaum lub sijhawm hloov pauv thaum ntxov. Thaum lub hauv paus ua haujlwm rau lub raum allograft tau tsim, txawm li cas los xij, thiab tsis muaj kev txwv rau RAAS thiab / lossis cov tshuaj diuretics, xws li nce ntshav creatinine, hyperkalemia, lossis ntim depletion, kev kho mob yuav raug siv los tswj ntshav siab (79). Statins thiab acetylsalicylic acid kuj tseem yog ib feem ntawm kev kho tshuaj kho mob txawm hais tias tsis muaj pov thawj tseeb rau cov kev siv no tshwj xeeb hauv TRAS (79).
Cov neeg mob uas muaj cov ntshav creatinine hnyav zuj zus thiab / lossis tsis tswj HTN tshwm sim rau TRAS yuav tsum tau mus rau lub raum hlab ntsha angioplasty nrog stenting. Tsis muaj randomized tswj kev sim tshuaj ntsuam xyuas (RCT) piv cov ecacy ntawm angioplasty stenting vs. phais revascularization vs. pharmacological therapy ib leeg nyob rau hauv lub raum hloov neeg pej xeem. Cov ntaub ntawv los ntawm cov neeg mob uas tsis hloov pauv los ntawm 4 RCT (96–99) tsis tau qhia qhov benet ntawm angioplasty ntawm BP tswj, thiab 4 RCT (97, 99– 101) tsis tau pom cov txiaj ntsig zoo rau lub raum. Txawm li cas los xij, ntau qhov kev soj ntsuam kev tshawb fawb pom tau tias muaj kev vam meej heev ntawm kev ua haujlwm thiab kev kho mob (88-100 thiab 65-94 feem pua) nrog cov txheej txheem sib txawv ntawm cov teeb meem (0-25.5 feem pua) hauv cov neeg tau txais kev hloov raum (102-105). Lub raum ntev allograft thiab cov neeg mob muaj sia nyob nrog mus txog 21 xyoo ntawm kev soj ntsuam tsis muaj kev cuam tshuam ntawm tus neeg mob nrog TRAS tab tom ua rau percutaneous angioplasty lossis stent tso thiab cov neeg mob uas tsis muaj TRAS (105). Ib txoj kev tshawb fawb pom tau hais tias ob qho tib si tam sim ntawd thiab mus sij hawm ntev qhov kev vam meej tau qis dua hauv angioplasty piv rau kev phais revascularization; Txawm li cas los xij, qhov qub tseem yog ib txoj kev nyiam thaum TRAS tsis ntev los no, linear, thiab distal. Txawm li cas los xij, kev phais revascularization feem ntau ua rau cov tib neeg uas muaj kinking thiab proximal TRAS (106). Muaj ntau yam kev phais, suav nrog kev phais thiab kho dua ntawm anastomosis, saphenous leeg bypass graft ntawm ntu stenotic, localized endarterectomy, thiab kev txiav tawm / rov ua dua ntawm lub raum hlab ntsha (90, 107). Feem ntau, kev phais revascularization yog tshwj tseg rau cov xwm txheej ntawm angioplasty tsis ua tiav. Lub raum mus ntev allograft muaj nuj nqi thiab ciaj sia nrog lub ntsiab lus rov qab ntawm 9.
Late Post-transplant Period
Sib nrug los ntawm cov kev sib tham saum toj no uas ua rau HTN nyob rau lub sijhawm hloov pauv thaum ntxov, qee yam tuaj yeem ua rau HTN nyob rau lub sijhawm hloov pauv tom qab lig.
Chronic Renal Allograft Dysfunction
Kev sib raug zoo ntawm lub raum tsis ua haujlwm ntawm lub raum tsis ua haujlwm thiab HTN tsis tau raug pov thawj tab sis ua raws los ntawm kev tshuaj xyuas qhov tseeb ntawm pathophysiology. Lub raum allograft raug mob - ob qho tib si mob thiab mob ntev - yog txuam nrog HTN. Feem ntau ua rau mob raum allograft muaj xws li mob allograft rejection-ob leeg mob antibody-mediated-thiab mob cellular rejection. Kev raug mob rau lub raum tsis zoo tshwm sim los ntawm kev tsis lees txais cov tshuaj tiv thaiv kab mob sib kis tsis tu ncua, interstitial fibrosis / tubular atrophy, thrombotic microangiopathy, thiab cov kab mob glomerular rov tshwm sim hauv lub raum allograft (19). Kev tshawb fawb tsiaj hauv nas pom tau tias HTN ib leeg ua rau mob allograft nephropathy (CAN). Txoj kev tshawb no tau siv cov nas uas muaj deoxycorticosterone acetate thiab ntsev vim ntshav siab thiab muab piv rau cov nas uas tsis muaj zog. Cov nas muaj zog muaj proteinuria ntau dua, cov leeg nqaij leeg-loj hlob zoo, platelet-derived growth factor (PDGF), tubular cell qhia ntawm proliferating cell nuclear antigen, extracellular matrix deposition, thiab muaj chav kawm I thiab II loj histocompatibility complex (MHC). Qhov no qhia tau hais tias HTN thiab immunologic yam cuam tshuam rau kev qhia txog kev loj hlob ntawm lub raum allografts thiab tej zaum yuav ua rau mob raum allograft dysfunction (109).
Fibroblast Growth Factor (FGF) 23
Tom qab hloov lub raum, FGF23 qib txo qis. Tus nqi ntawm FGF23 qib normalize tom qab hloov pauv yog nyob ntawm kev lim ntshav luv vintage ua ntej hloov lub raum thiab lub sijhawm rau normalization ntawm lub raum allograft muaj nuj nqi suav nrog cov ntxhia hauv cov metabolism (110,111). FGF 23 yog qhov paub tias muaj kev pheej hmoo txaus ntshai ntawm lub raum allograft poob, hlab plawv thiab tag nrho cov neeg tuag hauv cov neeg tau txais kev hloov pauv raum (112, 113). Kev sib raug zoo ntawm FGF 23 qib hauv lub sijhawm ua ntej thiab tom qab lub raum hloov mus rau qib BP lossis kev loj hlob ntawm HTN tom qab hloov lub raum tsis paub. Txawm li cas los xij, vim tias qib siab dua ntawm FGF23 cuam tshuam nrog nce SBP thiab DBP nrog rau qhov xwm txheej HTN hauv 1,758 cov tub ntxhais hluas uas tsis muaj ntshav siab tsis muaj CKD lossis CVD (114), lub koom haum no yuav muaj tseeb rau cov neeg hloov pauv. Txawm li cas los xij, kev tshawb fawb ntxiv yog tsim nyog.
Obstructive pw tsaug zog Apnea
Feem ntau ntawm obstructive pw tsaug zog apnea (OSA) nyob rau hauv cov neeg mob raum hloov pauv hloov nrog qhov hnyav ntawm OSA. Qhov tshwm sim ntawm qhov mob me, nruab nrab, thiab hnyav OSA hauv cov neeg tau txais kev hloov pauv raum uas koom nrog Kev Pw Tsaug Zog Kev Ntsuam Xyuas Hauv Cov Neeg Mob Tom Qab Lub Raum Hloov (SLEPT) Txoj Kev Kawm uas muaj qhov nruab nrab eGFR ntawm 52 19 ml / min / 1.73 m2 yog 18, 11, thiab 14 feem pua, feem. Hauv txoj kev tshawb no, cov neeg mob hloov lub raum nrog OSA xav tau ntau dua ntawm cov tshuaj tiv thaiv kab mob siab thiab nyiam muaj SBP ntau dua piv rau cov neeg mob uas tsis yog OSA (115).
Zoo ib yam li cov neeg tsis hloov pauv, cov teeb meem muaj feem cuam tshuam rau OSA hauv cov neeg tau txais kev hloov hauv lub raum yog txiv neej los ntawm poj niam txiv neej, rog rog, kev siv tshuaj hypnotic, muaj kev mob hnyav (xws li, kab mob plawv, kab mob cerebrovascular, kab mob peripheral vascular, ntshav qab zib mellitus), thiab tsis zoo. lub raum ua haujlwm (116). Muaj kev sib raug zoo ntawm HTN, CKD, thiab OSA, thiab lawv muaj cov xwm txheej txaus ntshai thiab kab mob pathophysiology, suav nrog kev ua siab ntev, kev ua haujlwm tsis zoo ntawm endothelial, nce inflammatory markers, hyperaldosteronism, thiab ntev ntim overload. Tsis tas li ntawd, peb cov xwm txheej no cuam tshuam nrog CV kev pheej hmoo, kev mob nkeeg, thiab kev tuag (117). Yog tias ib qho ntawm peb cov kab mob no tswj tsis tau lossis nce ntxiv, ob qho xwm txheej yuav ua rau mob hnyav dua lossis nyuaj rau tswj. Yog li ntawd, kev tswj kom tsim nyog ntawm OSA yog ib qho tseem ceeb ntawm cov khoom
cov kev kho mob antihypertensive nyob rau hauv cov neeg tau txais kev hloov hauv lub raum uas tom qab tsim lub raum allograft dysfunction tshwj xeeb tshaj yog nrog HTN resistant. Ntxiv mus, cov neeg tau txais kev hloov lub raum uas muaj feem cuam tshuam rau OSA yuav tsum tau kuaj xyuas ntxov (115, 118) thiab kho kom raug.
Hauv cov ntsiab lus, qhov pathogenesis ntawm kev hloov HTN tom qab hloov pauv tuaj yeem raug cais los ntawm lub sijhawm thaum lub sijhawm kub siab tshwm sim tom qab hloov lub raum. Lwm txoj hauv kev los sib txawv ntawm etiologies ntawm kev hloov pauv tom qab HTN yog los ntawm kev faib cov ua rau hauv kev tiv thaiv kab mob thiab tsis muaj kab mob. Cov yam ntxwv ntawm kev tiv thaiv kab mob, raws li tau hais tseg, feem ntau suav nrog rau lub raum allograft dysfunction thiab cov tshuaj tiv thaiv kab mob; thaum uas tsis yog-immunological yam cuam tshuam nrog tus pub, tus neeg tau txais kev pab, thiab lwm yam kev phais (Daim duab 3).
TXOJ CAI NTAWM HYPERTENSION tom qab
KIDNEY TRANSPLANTATION
Kev hloov pauv ua ntej BP cuam tshuam nrog rau lub raum allograft thiab cov txiaj ntsig ntawm cov neeg mob ciaj sia tom qab hloov lub raum. Tsawg heev ua ntej hloov SBP (<110 mmhg)="" and="" dbp=""><50 mmhg)="" are="" associated="" with="" a="" decrease="" in="" renal="" allograft="" loss.="" specifically="" during="" dialysis="" lower="" pre-="" and="" post-dialysis="" dbp="" are="" associated="" with="" better="" patient="" survival="" post-transplantation="">
During the post-transplant period, elevated BP is associated with poorer renal allograft and patient outcomes. However, as discussed above, various forms of renal allograft injury are also associated with post-transplant HTN. Several studies have demonstrated an association between post-transplant HTN and renal allograft failure (120–122). Opelz et al. (120) conducted a retrospective study of 29,751 kidney transplant recipients followed for over 7 years. Increased post-transplant SBP and DBP were associated with progressively decreased renal allograft function and death-censored chronic graft failure. Another study from the same cohort database examined the association between changes in BP levels at 1- and 3-years post-transplantation and long-term graft outcomes up to 10 years following transplantation. They found that patients with an SBP >140 mmHg at 1 year who were controlled to an SBP 140 mmHg at 3 years post-transplantation had improved renal allograft outcomes and reduced CV death compared to those with persistent SBP of >140 mmHg ob qho tib si ntawm 1 thiab 3 xyoos tom qab hloov pauv (123).
Muaj cov ntaub ntawv tsis txaus txog CV thiab cov txiaj ntsig kev tuag muaj feem cuam tshuam nrog kev sib cais diastolic HTN hauv cov neeg tau txais kev hloov hauv lub raum, thiab ntau cov kev tshawb fawb yuav tsum tau txiav txim siab txog kev tswj hwm lub hom phiaj tsim nyog rau cais diastolic HTN hauv cov neeg no.
Cardiovascular Outcomes-Raws li kev hloov pauv tom qabNtshav siab
HTN yog ib qho tseem ceeb tshaj plaws ntawm kev pheej hmoo rau lub plawv tsis ua hauj lwm, tshwj xeeb tshaj yog lub plawv tsis ua hauj lwm nrog kev khaws cia ejection feem (HFpEF) (124). Cov neeg tau txais kev hloov pauv hauv lub raum nrog sab laug ventricular hypertrophy (LVH) lossis HFpEF tau nce kev mob thiab kev tuag thiab muaj kev pheej hmoo siab rau cov xwm txheej mob plawv. Ob lub siab thiab ntim ntau dhau ua rau LVH, uas yog ntxiv rau lub hnub nyoog, caj ces yam, vascular hemodialysis nkag, dialysis vintage, ntshav qab zib, thiab ntshav siab (125).
Lub raum tsis txaus yog koom nrog hauv pathogenesis ntawm HFpEF (126) thiab ua rau ntsev-sensitive HTN (126, 127). Qhov tseem ceeb, lub voj voog tsis zoo ntawm lub raum tsis ua haujlwm tuaj yeem tshwm sim los ntawm ntsev thiab ntim ntau dhau (126). Yog li ntawd, BP tswj, lub raum allograft muaj nuj nqi, thiab lub plawv muaj nuj nqi yog ze ze. Kev tswj tsis tau HTN tom qab hloov lub raum ua rau muaj kev puas tsuaj rau ob lub raum allograft thiab lub plawv thaum kawg ua rau lub raum thiab lub plawv tsis ua haujlwm.
Ntshav siab ntsuas
BP yog ib qho ntawm cov cim tseem ceeb tshaj plaws uas tau txais hauv txhua qhov chaw kho mob; Txawm li cas los xij, nws feem ntau yuav tsis ntseeg tau vim qhov hloov pauv ntawm lub cev lus teb rau sab hauv thiab sab nraud stimuli nrog rau cov txheej txheem ntsuas BP tsis tsim nyog. Kev ntsuas BP ntseeg tau yuav tsum yog qhov yuav tsum tau ua hauv kev kho mob thiab tuaj yeem ua tus qauv nrog cov lus qhia hauv qab no: qhov nruab nrab ntawm peb qhov kev ntsuas BP tsis yog raug xa mus rau ib qho ntshav siab (OBP); Kev kaw tsawg kawg ob zaug ntawm qhov nruab nrab txhua hnub ntawm ob lub tsev ntshav siab nyeem ntawv tsawg kawg 4 hnub yog hu ua kev soj ntsuam ntshav siab hauv tsev (HBPM), thiab 24- h ambulatory ntshav ntsuas ntshav siab (24-h ABPM ), uas yuav tsum tau hnav lub tshuab ntsuas ntshav hauv hluav taws xob los sau thiab nruab nrab ntau qhov kev nyeem ntawv hauv 24 teev (128). Lub hom phiaj, cov ntsiab lus kho mob, thiab kev ua tau zoo yuav tsum tau muab coj los txiav txim siab thaum xaiv txoj kev ntsuas BP tsim nyog. Cov txheej txheem ntsuas BP Dierent muab cov ntaub ntawv muaj txiaj ntsig, uas tuaj yeem muaj txiaj ntsig zoo rau kev txheeb xyuas cov kab mob pathophysiology tom qab hloov HTN. Nws yog ib qho tseem ceeb kom paub txog cov ntsiab lus sib txawv rau HTN nrog rau txhua txoj hauv kev txhawm rau tswj hwm BP tom qab hloov lub raum.
A 24-h ABPM muab qhov nruab nrab ntawm ob hnub thiab hmo ntuj nyeem BP. Physiological txo nyob rau hauv nocturnal BP ntxiv cov neeg mob rau hauv dippers, non-dippers, thiab rov qab dippers. Lee et al. (129) tau pom qhov txo qis hauv qhov txo qis hauv SBP (1SBP) tom qab hloov lub raum.
Tsis tas li ntawd, qhov txo qis hauv 1SBP tau cuam tshuam nrog kev ua haujlwm qis rau lub raum allograft. Hauv txoj kev tshawb no, qhov txhais tau tias OBP thiab 24-h ABPM tsis hloov ntawm 1- xyoo tom qab hloov pauv thaum piv rau BP ntsuas ua ntej hloov lub raum. Txawm li cas los xij, lawv pom tias feem pua ntawm cov neeg mob uas tau noj cov tshuaj tiv thaiv hypertensive thiab cov naj npawb ntawm cov tshuaj antihypertensive yuav tsum tau txo qis tom qab hloov lub raum.
A 24-h ABPM tuaj yeem hais thiab pab nrog qhov tsis zoo ntawm HTN kuaj pom ib txwm muaj los ntawm OBP lossis HBPM. Piv nrog OBP, ib qho 24-h ABPM ua rau 61 feem pua ntawm kev tsis pom zoo hauv kev kuaj mob (58 feem pua thiab 3 feem pua ntawm cov npog ntsej muag thiab lub tsho dawb HTN, feem) (130).
Txawm hais tias ib tug 24-h ABPM tuaj yeem muab cov ntaub ntawv tseem ceeb los kuaj xyuas cov qauv ntawm HTN zoo li lub tsho dawb thiab npog HTN, OBP thiab HBPM feem ntau siv hauv kev kho mob. Txij li thaum hloov lub raum allografts yog qhov nkag siab zoo rau BP hemodynamic hloov pauv, HBPM zoo li yog ib qho kev siv feem ntau ntawm kev ua raws li BP tom qab hloov lub raum. Ib txoj kev tshawb fawb hauv cov neeg mob uas muaj hnub nyoog 1-10 xyoo tom qab hloov lub raum tau qhia tias muaj kev sib raug zoo dua ntawm 24-h ABPM thiab HBPM tshaj 24-h ABPM thiab OBP (131).
Txawm hais tias qhov nce siab hauv nruab hnub thiab hmo ntuj SBP tau txais los ntawm 24-h ABPM tau cuam tshuam nrog kev pheej hmoo ntawm kev ua haujlwm ntawm lub raum allograft, thiab kev nce siab thaum hmo ntuj hauv SBP tau nthuav tawm lub koom haum muaj zog (132). Kev nce siab 24-h nruab nrab SBP tau cuam tshuam nrog qhov kawg ntawm kev poob qis, cov xwm txheej hauv plawv, thiab kev tuag dhau ntawm 5- xyoo rov qab mus rau cov neeg tau txais kev hloov hauv lub raum nrog ntshav qab zib, qis eGFR, proteinuria, cov hluas, thiab leej twg yog poj niam (133). Qhov nruab nrab (hnub thiab hmo ntuj) 24-h DBP nruab nrab ntawm 65 thiab 80 mmHg tau cuam tshuam nrog kev muaj sia nyob ntev dua thaum lub sijhawm 9- xyoo rov qab tom qab hloov lub raum thaum piv rau cov neeg uas muaj DBP nruab nrab<65 or="">80 mmHg (134).
Txawm hais tias HBPM muaj dav, muaj kev sib raug zoo dua rau 24-h ABPM, thiab zoo dua rau OBP thaum kwv yees cov txiaj ntsig nyuaj, peb siv HBPM nrog rau OBP rau peb cov neeg mob hloov lub raum kom txo qis misclassication ntawm HTN kev kuaj mob, saib xyuas lub tsho dawb lossis npog HTN, thiab kho cov tshuaj antihypertensive.
Kev tswj ntshav siab
Cov kev cuam tshuam tsis yog tshuaj kho mob, xws li kev noj zaub mov, kev tawm dag zog, thiab txo kev ntxhov siab, yuav tsum yog ib feem ntawm kev kho HTN. Txij li feem ntau ntawm cov neeg tau txais kev hloov hauv lub raum tau hloov ua ntej HTN xav tau cov tshuaj tiv thaiv kab mob siab (HTN tsis tu ncua) thiab tsuas yog cov neeg mob tsawg zuj zus tsis muaj cov tshuaj ntshav siab (rov qab HTN), kev cuam tshuam tshuaj tshuaj tseem yog lub hauv paus ntawm BP tswj hauv cov pejxeem. Tsis tas li ntawd, lwm yam kev cuam tshuam tshwj xeeb rau qee yam kev tiv thaiv HTN, xws li hloov lub raum hlab ntsha angioplasty stenting thiab kho OSA, yuav tsum tau ua. Lub raum sympathetic denervation ntawm cov neeg lub raum los ntawm ob tog neeg nephrectomy los yog catheter ablation kuj yog ib txoj kev kho mob rau resistant HTN nyob rau hauv cov pejxeem no (Table 2). Hauv qhov kev tshuaj xyuas no, peb tsom mus rau cov tshuaj tiv thaiv kab mob ntshav siab thiab tshuaj xyuas luv luv ob tog neeg nephrectomy thiab RDN ntawm cov neeg lub raum.
PHARMACOLOGICAL MANAGEMENTS
Kev siv cov tshuaj Antihypertensive
Ib qho kev soj ntsuam rov qab tsis ntev los no los ntawm ib qho chaw hloov pauv hauv tebchaws Poland tau tshaj tawm cov qauv ntawm kev siv tshuaj tiv thaiv ntshav siab ntau hauv lawv cov neeg tau txais kev hloov pauv raum tshaj 14 xyoo. Lawv tau tshuaj xyuas cov ntaub ntawv kho mob ntshav siab los ntawm cov neeg tau txais kev hloov pauv thawj zaug mus ntsib kws kho mob los ntawm 2001, 2006, 2011, thiab 2014 (135). Beta-blockers yog cov tshuaj tiv thaiv kab mob siab tshaj plaws uas siv hauv pawg no ua raws li calcium channel blockers. Kev siv ACEI, diuretics, thiab alpha-blockers yog tib yam. Kev kho ARB tau siv tsawg kawg nkaus. Tus naj npawb nruab nrab ntawm cov tshuaj tiv thaiv kab mob ntshav siab xav tau yog 2.24 1.03–2.{13}}.25. Qhov no yog me ntsis qis dua qhov tau tshaj tawm rau cov neeg mob CKD uas qhov nruab nrab xav tau 3.5 tshuaj (136). Tus naj npawb ntawm cov tshuaj tiv thaiv kab mob ntshav siab qis dua yuav tshwm sim los ntawm kev rov ua kom lub raum ua haujlwm tom qab hloov pauv thiab txhim kho cov kua dej tshem tawm, suav nrog ntsev thiab ntim tawm los ntawm lub raum allograft.
Kev tswj ntshav siab thaum lub sijhawm
PERI-TRANSPLANT PERIOD
Cov tshuaj Antihypertensive
Feem ntau ntawm cov neeg mob CKD thiab ESRD siab heev muaj HTN. Volume overload yog qhov ua rau ntau tshaj plaws ntawm kev tswj tsis tau BP hauv cov neeg mob ESRD (137). Hauv lub sijhawm hloov pauv tam sim ntawd, tshwj xeeb tshaj yog nyob rau hauv kev hloov pauv lub raum tuag thaum cov kev phais feem ntau tau tshwm sim tshwm sim (138), BP tuaj yeem tswj tsis tau tshwj xeeb yog tias tus neeg mob yuav tsum tau lim ntshav thaum lub sijhawm phais. Volume-dependent HTN yog tswj nrog kev tshem tawm uid thaum lim ntshav. Txawm li cas los xij, nws yog ib qho kev coj ua kom tshem tawm tsawg dua ntawm cov neeg mob uas tab tom yuav hloov pauv, ua rau lawv muaj qhov hnyav tom qab lim ntshav me ntsis saum lawv qhov hnyav qhuav hauv kev mob siab rau kom tsis txhob muaj kev sib txuam thiab tom qab kev ua haujlwm hypotension. Tsis tas li ntawd, ACEI thiab ARB feem ntau tuav tom qab hloov pauv. Ib qho alpha2 agonist zoo li clonidine, txawm li cas los xij, yuav tsum tau txuas ntxiv mus rau lub sijhawm hloov pauv hloov pauv kom tsis txhob thim rov qab HTN.
Cov kws kho mob saib xyuas cov neeg tau txais kev hloov hauv lub raum muaj kev xav sib txawv thaum xaiv cov tshuaj tiv thaiv kab mob ntshav siab thaum lub sijhawm peri- thiab tom qab hloov pauv. Lawv qhov kev txiav txim siab feem ntau yog tsav los ntawm cov kev cai lossis kev coj ua raws li lawv cov chaw hloov raum. Cov ntaub ntawv tshwj xeeb ntsig txog kev hloov lub raum yuav tsum qhia txog kev xaiv cov tshuaj tiv thaiv hypertensive, tab sis, zoo li lwm yam xwm txheej, nws yog qhov tsim nyog rau kev tswj hwm BP tus kheej rau qee tus neeg tau txais kev hloov hauv lub raum.
Diuretics
Diuretics feem ntau tsis yog siv los ua thawj kab tshuaj tiv thaiv hypertensive hauv cov neeg tau txais kev hloov hauv lub raum. Lawv tuaj yeem ua rau lub ntim depletion, electrolyte cuam tshuam, thiab ua rau lub raum allograft ua haujlwm tsis zoo. Txawm li cas los xij, lawv tau qhia thiab yuav tsum tsis txhob zam rau qee tus neeg mob hauv lub sijhawm hloov pauv hloov pauv.
Loop Diuretics
Kev tswj ntim ntau dua li kev tswj hwm BP yog qhov qhia txog lub voj diuretics hauv cov neeg tau txais kev hloov hauv lub raum, tshwj xeeb tshaj yog nyob rau lub sijhawm tam sim thiab ntxov tom qab hloov pauv. Cov neeg tau txais kev hloov hauv lub raum feem ntau tau txais peri-transplant IV uid kom khaws cov zis tso zis ntau ntxiv los ntawm lub raum ua haujlwm tshiab. Volume overload nthuav tawm nrog peripheral edema, pulmonary congestion, los yog HTN yuav tshwm sim thaum lub lag luam ntawm allograft muaj nuj nqi lags qab lub ntim resuscitation muab. Diuretics tuaj yeem siv los tswj cov ntim thiab BP hauv qhov xwm txheej no.
Kuj tseem muaj pov thawj tias lub voj diuretics muaj cov nyhuv vasodilator thiab tuaj yeem txo qis edema, congestion, thiab oxygen xav tau. Raws li txoj cai, lawv tuaj yeem txo cov mob raum ischemic thiab kev pheej hmoo ntawm DGF hauv cov neeg tau txais kev hloov raum. Txawm li cas los xij, txawm tias lawv feem ntau siv hauv kev kho mob, tsis muaj cov ntaub ntawv zoo ib yam los txhawb kev siv lub voj diuretic kom tso zis ntau ntxiv thiab tiv thaiv DGF. Tsis tas li ntawd, tsis muaj pov thawj muaj zog uas qhia txog kev sib koom ua ke ntawm lub voj diuretic thiab kev txhim kho nyob rau hauv thawj zaug lossis mus sij hawm ntev graft muaj nuj nqi (139). Ntawm qhov tod tes, kev siv lub voj diuretic tau cuam tshuam nrog kev pheej hmoo ntawm UTI hauv thawj 5 xyoo tom qab hloov lub raum (140). Qhov no yog vim hais tias lawv siv depletes medullary NaCl gradient (140), uas yog paub los hloov kho lub cev tiv thaiv kab mob hauv lub cev (141). Lub raum medullary myeloid mononuclear cell phagocytes yog cais raws li pro-inflammatory (M1) thiab reparative / profibrotic (M2) hlwb. Txo M1 / M2 piv los ntawm kev hloov lub raum medullary NaCl gradient nrog lub voj diuretics impairs lub ntuj antibacterial tswv teb teb (142- 144).
Furosemide yog qhov feem ntau siv lub voj diuretic. Nws tau raug siv los kwv yees kev nce qib ntawm AKI nrog lub npe hu ua furosemide stress test (FST) hauv cov neeg mob tsis hloov pauv (145,146). Loop diuretics tseem tuaj yeem muab cov txiaj ntsig zoo txog kev ua haujlwm rau lub raum allograft hauv lub sijhawm tam sim tom qab hloov pauv. Cov lus teb tsis txaus, tso zis tso zis<350ml within="" 4h,="" to="" a="" single="" iv="" furosemide="" dose="" of="" 1.5="" mg/kg="" given="" 3h="" after="" renal="" allograft="" anastomosis="" predicts="" increased="" risk="" of="" dgf="">
Muab ntau yam txaus ntshai thiab cov txiaj ntsig nrog lub voj diuretics, cov kws kho mob yuav tsum ua kom lawv tus kheej siv rau cov neeg tau txais kev hloov pauv. Ntxiv RCTs yuav tsum tau txiav txim siab qhov ua tau zoo thiab kev nyab xeeb ntawm lub voj diuretic hauv cov neeg tau txais kev hloov hauv lub raum.
Thiazides
Thiazide diuretics feem ntau siv cov tshuaj tiv thaiv hypertensives hauv cov pej xeem. Txawm li cas los xij, lawv tsis tshua muaj tshwm sim hauv kev tswj hwm cov neeg tau txais kev hloov hauv lub raum vim lawv cov kev mob tshwm sim hauv metabolic uas suav nrog hyperglycemia, hyperuricemia, hypercalcemia, thiab hyponatremia (147,148).
Thiazides, txawm li cas los xij, tuaj yeem tswj hwm CNI-induced HTN. Txij li thaum CNI-induced HTN yog ntsev-rhiab heev (59, 149) los ntawm kev ua kom lub WNK-SPAK-NCC txoj kev (63,150), thiazides, uas inhibit Na-Cl co-transporter, yuav tsum tswj CNI-induced HTN. Ib qho kev sib tw uas tsis yog kev sib tw sib tw sib piv cov txiaj ntsig ntawm chlorthalidone thiab amlodipine hauv cov neeg mob raum hloov pauv cov neeg tau txais kev noj tacrolimus pom tau tias chlorthalidone tsis qis dua amlodipine hauv kev tswj BP (147). Muab cov vasodilator nyhuv ntawm calcium channel blockers, lawv tau nquag siv cov tshuaj tua kab mob hauv lub raum hloov cov neeg tau txais kev npaj los tiv thaiv cov kab mob thiab lub raum vasoconstrictive nyhuv ntawm CNI ntawm endothelin I (151-153). Txawm li cas los xij, lawv cov kev mob tshwm sim, suav nrog peripheral edema thiab proteinuria, tuaj yeem ua rau thiazides ib qho kev xaiv tsim nyog rau kev tswj hwm BP, tshwj xeeb tshaj yog rau cov neeg uas muaj peripheral edema (147).
Txawm hais tias lub voj diuretics feem ntau nyiam tshaj thiazide diuretics rau kev tswj lub ntim, lawv tuaj yeem ua rau ntxiv rau lub raum magnesium nkos. Thiazides tuaj yeem txiav txim siab hauv cov neeg mob hloov pauv uas twb muaj lwm yam laj thawj rau thiab feem ntau tawm tsam nrog hypomagnesemia. Txawm li cas los xij, vim tias CNI thiab lub voj diuretics ua rau cov txheej txheem ua kom qis luminal electro-positivity txo qis paracellular magnesium reabsorption, siv lub voj diuretic hauv kev hais kwv txhiaj nrog CNI yuav tsis ua rau cov zis magnesium ntxiv (154). Kev tshawb nrhiav rov qab rau hauv cov neeg tau txais kev hloov lub plawv noj CNI tau pom tias cov pab pawg tau txais lub voj diuretics tsis muaj cov tshuaj magnesium qis dua lossis xav tau cov tshuaj magnesium ntau dua piv rau cov pab pawg tsis tau txais lub voj diuretics (154). Thiazide diuretics, ntawm qhov tod tes, nce ntshav magnesium thaum siv nrog CNI. Hauv cov neeg mob uas tsis hloov pauv tsis muaj CNI, kev siv thiazide diuretic mob tshwm sim ua rau muaj zog magnesium reabsorption. Txawm li cas los xij, kev siv thiazide diuretic mus sij hawm ntev tuaj yeem ua rau cov zis magnesium nkos thaum muaj concomitant hypokalemia (154). Cov neeg tau txais kev hloov pauv ntawm CNIs feem ntau muaj hyperkalemia, thiab, yog li ntawd, thiazide diuretics yuav tsis ua rau hypomagnesemia los ntawm CNI tab sis hloov mus nce qib magnesium. Cov kev tshawb fawb yav dhau los tau qhia tias cov neeg hloov lub plawv tau txais thiazide diuretics muaj cov ntshav magnesium ntau dua thiab yuav tsum tau hloov magnesium tsawg dua piv rau cov uas tsis nyob hauv thiazides (154). Yog li ntawd, nyob rau hauv kev teeb tsa ntawm ntim ntau dhau thiab concomitant hypomagnesemia, thiazide diuretic tuaj yeem siv los txo cov nyhuv hypomagnesemia ntawm CNI therapy (154).
Thiazides yuav raug txiav txim siab rau cov neeg tau txais kev hloov hauv lub raum nrog CNI-induced ntsev-sensitive HTN thiab hypomagnesemia.
Mineralocorticoid Receptor Antagonists
Mineralocorticoid receptor antagonists (MCRA) muaj cov txiaj ntsig ntawm CV (155, 156) thiab cov tshuaj tiv thaiv kab mob, tab sis tsis yog siv cov tshuaj tiv thaiv kab mob hauv lub raum hloov pauv, tshwj xeeb tshaj yog cov neeg uas muaj lub raum tsis ua haujlwm allograft. Hyperkalemia yog ib qho kev mob tshwm sim ntawm MCRA thiab nws yuav ua rau mob raum hloov cov neeg tau txais txiaj ntsig uas muaj CNI-induced hyperkalemia.
One pilot study evaluating the antiproteinuric effect of spironolactone 25 mg/day given to 11 kidney transplant recipients whose mean proteinuria was 4.4 1.4 g/day on both ACEI and ARB. Proteinuria was decreased more than 50% with a mean reduction of 85% in nine patients after 6 months on spironolactone. Renal allograft function slightly decreased with GFR, changing from 52 12.7 to 48 14.2 mg/dL, and serum potassium did not significantly increase (4.6 0.4–5 0.62 mEq/L) (157). Another study looked at the safety of eplerenone in kidney transplant recipients with eGFR between 30 and 50 mL/min/ 1.73 m2. After 8 weeks of eplerenone 25 mg/d, nine out of 31 patients had serum potassium of >5 mmol/l, and one patient had serum potassium of >5.5 mmol/l. Mean baseline eGFR was 41 (26–59) ml/min/1.73 m2 after 8 weeks of eplerenone therapy and was not significantly different between patients who did and did not develop hyperkalemia (36.0 [95% CI 26.0–53.0] vs. 44.5 [95% CI 26.0–59.0], p = 0.17). Having a baseline serum potassium >4.35 mmol/l was associated with increased serum potassium of >5 mmol / l ib zaug pib eplerenone (158).
CNIs tuaj yeem ua rau vascular vasoconstriction los ntawm kev ua kom cov mineralocorticoid receptor nyob rau hauv cov leeg du ua rau lub raum tsis ua haujlwm allograft. MCRAs khi mineralocorticoid receptors nyob rau hauv lub hauv paus ntsiab lus hlwb ntawm kev sau ducts thiab muaj peev xwm reno-tiv thaiv los ntawm blunting lub raum vascular tsis kam induced los ntawm CNI txoj kev kho (159).
Spironolactone txo qis plawv sab laug ventricular ntim thiab loj, tab sis kev tshawb fawb yuav tsum tau txiav txim siab nws cov txiaj ntsig hauv cov neeg tau txais kev hloov raum (160). Tsis tas li ntawd, tsis muaj pov thawj hais txog CV thiab cov txiaj ntsig kev tuag hauv cov neeg tau txais kev hloov hauv lub raum.
Nrog qee cov pov thawj rau cov nyhuv antiproteinuric thiab lawv tsim kev nyab xeeb hauv cov neeg txais kev hloov pauv txawm tias thaum ua ke nrog ACEI lossis ARB, MCRA yuav yog ib qho kev xaiv tshiab rau BP tswj cov neeg uas muaj CNI-induced HTN thiab proteinuria.
Beta-Blockers
Cov teebmeem cardioprotective thiab kev muaj sia nyob ntawm beta-blockers ua rau lawv cov tshuaj nyiam nyob rau hauv dav dav (161) thiab ESRD cov pejxeem (162-165). Hauv cov neeg tau txais kev hloov hauv lub raum, kev tshawb fawb rov qab tsis ntev los no los ntawm 2001 txog 2014 tau pom tias beta-blockers yog cov tshuaj tiv thaiv ntshav siab tshaj plaws (135). Tsis tas li ntawd, Aftab et al. (166) tau ua ib qho kev tshawb nrhiav ib-chaw rov qab rau hauv 321 rau cov neeg tau txais kev hloov hauv lub raum hauv lub sijhawm 10 4 xyoo rov qab thiab pom tias cov neeg uas tau siv cov tshuaj beta-blockers muaj txiaj ntsig tseem ceeb ntawm kev ciaj sia piv rau cov uas tsis tau. Ntxiv mus, cov kws sau ntawv tau pom tias beta-blocker muaj qhov cuam tshuam ntxiv rau ACEI lossis ARB nrog kev muaj sia nyob ntau dua hauv cov neeg mob hloov lub raum ntawm qhov sib xyaw no piv rau cov uas tau txais cov tshuaj ib leeg lossis tsis yog. Lub peev xwm tiv thaiv kev tiv thaiv ntawm beta-blocker yog los ntawm kev txo qis ntawm lub paj hlwb, uas yog txhawb nqa hauv lub raum tsis ua haujlwm (167-169). Tsis tas li ntawd, beta-blockers txo qis proinflammatory cytokines, uas paub tias yuav ua rau muaj kev pheej hmoo rau atherosclerosis (170).
Txawm hais tias beta-blockers muab kev ciaj sia nyob rau hauv cov neeg tau txais kev hloov hauv lub raum, lawv tuaj yeem ua rau muaj kev cuam tshuam metabolic, suav nrog proteinuria, hyperkalemia, thiab npog cov tsos mob hypoglycemic. Yog li ntawd, ceev faj yuav tsum tau siv thaum siv beta-blockers nyob rau hauv lub raum hloov pauv cov neeg tau txais kev pheej hmoo los tsim cov kev mob tshwm sim no.
Calcium Channel Blockers
Calcium channel blockers inhibits cov calcium nkag mus rau hauv vascular du leeg hlwb, ua rau vascular vasodilation (171). Txij li cov nyhuv vasoconstrictive ntawm CNIs ua rau tom qab hloov HTN (172), calcium channel blockers tau xav tias yog tus neeg sawv cev tsim nyog rau kev hloov HTN tom qab. Theoretically lawv cov vasodilatory nyhuv tuaj yeem tiv thaiv cov nyhuv vasoconstrictive ntawm CNIs thiab txhim kho BP tswj (171,173,174).
Ntxiv nrog rau kev tswj ntshav siab, calcium channel blockers kuj tseem tiv thaiv kev raug mob tom qab hloov cov tubular raug mob (ATI) lossis DGF. Ib qho kev sim yav tom ntej tau saib ntawm kev siv diltiazem hauv cov neeg mob uas tau txais kev hloov pauv lub raum tuag (DDRT). Cov neeg koom nrog tau randomized rau lub raum uas tau muab diltiazem (Euro-collin's tov (20} mg / l) thaum lub sij hawm pub dawb nephrectomy; lub sijhawm no, cov neeg tau txais kev txhaj tshuaj bolus ntawm diltiazem (0.28 mg. /kg) ua ntej ua haujlwm raws li kev txhaj tshuaj 0.0022 mg / min / kg rau 2 hnub ua ntej hloov mus rau qhov ncauj diltiazem vs. pawg tswj hwm, uas tsis tau txais diltiazem tab sis txwv tsis pub tau txais tib txoj kev tiv thaiv kab mob tiv thaiv kab mob CsA. Qhov tshwm sim qis dua ntawm ATI, GFR siab dua nrog lub luag haujlwm tseem ceeb, thiab qis dua qhov tshwm sim ntawm kev tsis lees paub ntawm 1 lub hlis tom qab hloov pauv, txawm li cas los xij, lawv muaj CsA ntau dua piv rau pawg tswj hwm, tag nrho CsA xav tau qis dua hauv pawg diltiazem, raws li qhov xav tau, Txhawm rau kom ua tiav cov qib CsA sib piv ntawm ob pawg.Qhov qis dua tom qab hloov pauv ATI hauv pawg diltiazem tau muab tso rau hauv qhov thib ob kom txo qis ischemic puas hauv lub raum allograft thiab txo CNI nephrotoxicity (175). th tag nrho ntawm 724 tus neeg koom kuj tau xaus lus tias peri-operative calcium channel blocker txo qis qhov tshwm sim tom qab hloov ATI thiab DGF. Tsis muaj qhov sib txawv ntawm kev poob qis, kev tuag, lossis kev xav tau rau hemodialysis, tab sis tsis muaj pov thawj txaus los txiav txim siab txog cov tshuaj tsis zoo (176). Muaj lwm txoj kev tshawb fawb randomized placebo tswj kev sib piv rau lub raum allograft cov txiaj ntsig ntawm cov neeg mob uas tau txais kev hloov pauv ua ntej isradipine vs. cov neeg tau txais cov placebo. Cov pab pawg qub tau ua haujlwm ntau dua rau lub raum allograft piv rau yav tas los. Txawm li cas los xij, tus nqi ntawm DGF thiab biopsy-pov thawj mob tsis lees paub tsis txawv hauv txoj kev tshawb no (177).
Txawm hais tias calcium channel blockers muab kev ua haujlwm zoo rau lub raum allograft, ntau qhov kev tshawb fawb pom tias tsis muaj qhov sib txawv ntawm BP tswj thaum siv verapamil piv rau enalapril lossis doxazosin (178). Tsis muaj qhov sib txawv hauv GFR, qib creatinine hauv cov ntshav, protein ntau tawm, lossis BP thaum nitrendipine lossis nifedipine piv rau cov placebo (179). Ntxiv mus, ib qho kev tshawb nrhiav rov qab tau pom 2.26 lub sij hawm muaj kev pheej hmoo ntau dua ntawm cov kab mob plawv ischemic hauv cov neeg mob raum hloov pauv uas tau txais dihydropyridine calcium channel blockers (180).
Cov pov thawj rau cov txiaj ntsig ntawm calcium channel blockers zoo li tsis sib xws; Txawm li cas los xij, kev tshuaj xyuas tsis ntev los no thiab kev tshuaj ntsuam meta-kev soj ntsuam ntawm 60 kev sim suav nrog 3,802 cov neeg mob tau pom tias, piv rau cov placebo lossis tsis muaj kev kho mob, calcium channel blockers txo qis graft poob [kev pheej hmoo piv (RR ) ntawm 0.75, 95 feem pua ntawm kev ntseeg siab (CI) 0.57–0.99] thiab nce GFR [qhov txawv (MD) 4.5 mL / min, 95 feem pua CI 2.2–6.7]. Piv rau ACEIs, cov neeg mob kho nrog calcium channel blockers zoo li muaj
siab dua GFR; Txawm hais tias muaj cov ntaub ntawv tsis txaus ntseeg txog kev poob ntawm kev poob ntawm ob pawg no (181). Muab cov ntaub ntawv muaj, calcium channel blockers tseem yog tus neeg saib xyuas kev noj qab haus huv rau cov neeg tau txais kev hloov hauv lub raum txwv tsis pub muaj kev qhia tshwj xeeb rau lwm cov tshuaj tiv thaiv ntshav siab lossis contraindications rau calcium channel blocker therapy.
Cov tshuaj tiv thaiv tsis zoo thiab tshuaj yeeb-tshuaj sib cuam tshuam ntawm calcium channel blockers thiab lwm yam tshuaj uas nquag siv yuav tsum tau muab coj los xav. Calcium channel blockers tuaj yeem ua rau peripheral edema thiab cov leeg tsis muaj zog tshwj xeeb tshaj yog thaum siv nrog cov tshuaj steroids. Cov pos hniav hyperplasia kuj muaj ntau dua thaum siv calcium channel blockers nrog CsA (171). Txawm hais tias dihydropyridine calcium channel blockers tsis inhibit cytochrome P450 (CYP) 3A4 isoenzyme, lawv tau metabolized los ntawm CYP3A4 isoenzyme thiab tuaj yeem sib tw nrog CNI.
Qhov no ua rau muaj kev nce ntxiv ntawm calcium channel blocker thiab CNI raug. Non-dihydropyridine calcium channel blockers inhibit CYP3A4 isoenzyme thiab nce qib CNI.
Angiotensin-Hloov Enzyme Inhibitors
(ACEI) thiab Angiotensin II Receptor
Blockers (ARB)
Txij li cov proteinuria yog ib qho cim rau tus kab mob raum, txo qis proteinuria yog ib lub tswv yim kom qeeb kev loj hlob ntawm CKD. ACEIs thiab ARBs yog cov tshuaj tiv thaiv hypertensive uas paub txog cov tshuaj tiv thaiv kab mob. ACEIs inhibit angiotensin-hloov enzyme, uas hloov renin rau angiotensin. ARBs ua rau angiotensin II receptors thiab tom qab ntawd inhibit RAAS txoj hauv kev.
Kev tshuaj xyuas cov txheej txheem thiab kev tshuaj ntsuam meta ntawm 21 qhov kev sim tshuaj, suav nrog 1,549 tus neeg mob, qhia tias tsis muaj qhov sib txawv ntawm MAP hloov ntawm ACEI lossis ARB pawg thiab pawg tswj hwm. Serum potassium kuj tsis txawv ntawm ob pawg. Txawm li cas los xij, ACEI lossis ARB pawg tau txo qis hauv proteinuria, eGFR, thiab hematocrit thaum piv rau pawg tswj hwm. Muaj cov ntaub ntawv tsis txaus hais txog cov txiaj ntsig ntawm ACEI lossis ARB kev kho mob raws li tus neeg mob lossis lub raum allograft survival (182). Hauv cov lus hais los saum toj no kev tshuaj xyuas thiab kev tshuaj ntsuam meta, eGFR hauv pawg ACEI tsis txawv ntawm qhov ntawd hauv pawg placebo tab sis qis dua cov calcium channel blocker pawg. Kev sib piv ntawm cov ntaub ntawv hais txog kev poob qis ntawm ACEI thiab calcium channel blocker therapy yog qhov tsis txaus ntseeg (181).
RAAS kev ua kom muaj feem cuam tshuam nrog interstitial fibrosis thiab tubular atrophy (IF / TA), ib qho ntawm feem ntau ua rau lub raum allograft poob (183,184). ACEI perindopril tau pom tias tiv thaiv cortical interstitial expansion, ib qho cim ntawm fibrosis hauv CKD cov neeg mob uas muaj ntshav qab zib nephropathy (185). Ib qho RCT hauv cov neeg tau txais kev hloov hauv lub raum uas tau txais losartan 100mg txhua hnub hauv 3 lub hlis tom qab hloov pauv thiab txuas ntxiv nws rau 5 xyoos piv rau cov placebo tswj kev sib raug zoo tsis tau qhia txog benet ntawm ARB txoj kev kho nyob rau hauv cov nqe lus ntawm kev txo qis hauv kev sib xyaw interstitial expansion lossis ESRD los ntawm IF / TSI (186).
ACEIs thiab ARBs tuaj yeem ua rau txo qis ntawm LVH hauv cov neeg tau txais kev hloov hauv lub raum (187, 188), tab sis cov kev tshawb fawb tib yam no tsis tau pom tias muaj kev txhim kho hauv txhua qhov kev tuag (189). Kev tshuaj xyuas tsis ntev los no thiab kev tshuaj ntsuam xyuas meta tau pom tias muaj sia nyob nrog ACEI lossis ARB kev kho mob hauv cov neeg tau txais kev hloov hauv lub raum tab sis tsuas yog los ntawm cov kev tshawb fawb sib koom ua ke thiab tsis yog RCTs (190).
Txawm hais tias ACEIs thiab ARBs muab cov nyhuv antiproteinuric, lawv feem ntau tsis yog cov tshuaj xaiv thaum lub sijhawm tam sim thiab ntxov tom qab hloov pauv. Qhov no feem ntau yog vim lawv paub tias txo GFR. Cov kev mob tshwm sim no thim rov qab, tab sis nws ua rau tsis meej pem thaum ntxov ntawm kev sib txawv ntawm lawv lub luag haujlwm los ntawm lwm yam ua rau lub raum allograft tsis ua haujlwm thiab tuaj yeem ua rau muaj kev ua haujlwm tsis tsim nyog, suav nrog kev tshawb nrhiav, xws li hloov lub raum biopsy.
Txawm hais tias tsis muaj pov thawj zoo rau CV lossis kev muaj sia nyob zoo nrog kev siv ACEIs, ARBs, thiab MCRAs, cov tshuaj tiv thaiv ntshav siab no yuav raug txiav txim siab. Lawv yuav raug txiav txim siab hauv cov neeg tau txais kev hloov pauv, tshwj xeeb yog cov neeg muaj LVH, mob plawv tsis ua haujlwm, thiab proteinuria.
Alpha1-Cov neeg tawm tsam
Alpha1-cov antagonists tsis tshua siv los ua thawj zaug lossis ib qho tshuaj tiv thaiv kab mob siab hauv cov neeg tau txais kev hloov raum. Txawm hais tias lawv txo BP los ntawm kev txo qis peripheral vasoconstriction thiab theoretically yuav tsum tawm tsam nrog cov nyhuv vasoconstrictive ntawm CNI, tsis muaj pov thawj tias alpha1- antagonists muab cov nyhuv antihypertensive zoo dua lossis qeeb qhov kev loj hlob ntawm lub raum allograft tsis ua haujlwm thaum piv rau lwm cov tshuaj antihypertensive. . Ib txoj kev tshawb fawb nrog kev soj ntsuam mus sij hawm ntev hauv 88 tus neeg mob ntshav siab hloov lub raum uas tau muab faib ua peb pawg, verapamil, enalapril, thiab doxazosin, tau qhia tias doxazosin muab tib yam nkaus hauv BP tswj piv nrog lwm tus thaum tswj kev nyab xeeb zoo. Txawm li cas los xij, txog li 38 feem pua ntawm cov neeg mob hauv pawg doxazosin xav tau cov tshuaj tiv thaiv ntshav siab ntxiv piv rau tsuas yog 8 thiab 13 feem pua ntawm cov pab pawg verapamil thiab enalapril, raws li (178). Alpha1-antagonist tej zaum yuav muaj lub luag hauj lwm raws li ib tug adjunctive therapy es tsis yog thawj-line antihypertensive tus neeg saib xyuas nyob rau hauv cov neeg tau txais kev hloov.
Alpha2 Agonists
Centrally acting alpha2 agonists ua hauj lwm ntawm presynaptic alpha2 adrenoceptors nyob rau hauv lub hauv paus paj hlwb thiab suppress central sympathetic kev ua si (191). Tshwj xeeb, ua kom cov alpha2A receptors ua rau muaj kev sib haum xeeb-inhibitory nyhuv thiab txo BP. Txawm li cas los xij, stimulating alpha2A receptors hauv cov hlab ntsha ua rau peripheral vasoconstriction (192). Ntawm qhov tod tes, alpha2B receptor activation ua rau muaj kev xav-excitatory nyhuv (192).
Ob ntawm cov laus tshaj plaws alpha2 agonists, methyldopa thiab clonidine, tau ntev tau siv rau BP tswj (193). Clonidine yog tam sim no feem ntau siv alpha2 agonist. Thaum siv raws li kev kho mob monotherapy, methyldopa yog txuam nrog kev tiv thaiv kab mob siab, edema, thiab qhov hnyav nce. Clonidine kuj tseem cuam tshuam nrog qhov hnyav nce thiab nce ntxiv nrog kev siv txuas ntxiv. Kev siv ntev tsis cuam tshuam nrog sodium thiab dej tuav lossis lub cev uid ntim nthuav dav (193). Nws hloov pauv ua rau txo qis hauv lub cev hloov pauv ntawm sodium thiab plasma ntim, uas tej zaum yuav yog lwm yam tshuaj tiv thaiv kab mob ntawm clonidine (194).
Zoo ib yam li lwm pab pawg ntawm cov tshuaj antihypertensive, clonidine muaj kev cuam tshuam rau lub raum hemodynamics thiab txo qis lub raum vascular tsis kam. Ib txoj kev tshawb fawb hauv 13 tus neeg mob ntshav siab tseem ceeb uas tau txais clonidine mus ntev tau pom tias nws txo qis cov ntshav renin kev ua haujlwm, hloov kho lub raum vascular tsis kam, thiab tom qab ntawd txo qis MAP (195). Kev tshawb fawb ntawm cov nyhuv ntawm clonidine ntawm lub raum hemodynamics tau ua nyob rau hauv rau
Cov neeg tau txais kev hloov hauv lub raum uas pib tau txais furosemide rau 2 lub lis piam ua ntej qhov sib ntxiv ntawm clonidine titrated rau BP tswj tau pom tias GFR thiab lub raum zoo ntshav ow ntsuas los ntawm inulin thiab amino-hippurate sodium clearances tsis hloov pauv (196).
Clonidine yog ib qho tshuaj tiv thaiv kab mob siab. Ntau tus neeg mob ESRD uas nyob rau hauv lub raum hloov cov npe tos muaj HTN uas tsis tau tswj hwm thiab nyob rau ntawm clonidine ntxiv rau lawv lwm cov tshuaj tiv thaiv kab mob siab. Txawm li cas los xij, raws li tau hais yav dhau los, rov qab HTN yog qhov tshwm sim tom qab txiav tawm ntawm clonidine, thiab cov neeg mob uas nyob rau ntawm clonidine ua ntej hloov lub raum yuav muaj kev tswj tsis tau HTN uas tshwm sim los ntawm qhov tshwm sim rov qab. Hauv cov neeg mob no, clonidine feem ntau rov pib dua thiab tau tapered o thaum lub sijhawm hloov pauv thaum ntxov. Yog li ntawd, clonidine tsis tshua siv los ua ib tus neeg saib xyuas ntshav siab tom qab hloov lub raum.
Hauv cov ntsiab lus, tsis muaj tshuaj xaiv rau kev tswj BP tom qab hloov lub raum. Ob peb yam tseem ceeb tau koom nrog hauv kev xaiv cov tshuaj tiv thaiv kab mob uas tsim nyog suav nrog cov tshuaj tiv thaiv kab mob thiab cov tshuaj tiv thaiv tsis haum nrog rau lub sijhawm tom qab hloov lub raum.
Sib txawv ntawm cov neeg tsis hloov pauv CKD, beta-blockers thiab calcium channel blockers yog cov feem ntau siv ua ke hauv cov neeg tau txais kev hloov hauv lub raum. Beta-blockers muab cov txiaj ntsig cardioprotective rau cov neeg mob hloov lub raum, uas yuav muaj hauv qab CAD (166). Calcium channel blockers muaj cov nyhuv vasodilatory uas tawm tsam cov nyhuv vasoconstrictive ntawm CNIs (197). ACEIs thiab ARBs, ntawm qhov tod tes, tsis niaj hnub siv cov tshuaj tiv thaiv kab mob siab hauv cov neeg tau txais kev hloov raum. Qhov no yog qhov tseeb tshwj xeeb tshaj yog thaum lub sijhawm hloov pauv thaum ntxov thaum lub raum lub raum allograft ua haujlwm tsis zoo. Txawm li cas los xij, lawv tuaj yeem txiav txim siab thaum muaj qhov qhia tshwj xeeb rau lawv siv, xws li proteinuria thiab posttransplant erythrocytosis. Kev nce ntshav creatinine los ntawm ACEI lossis ARB txoj kev kho, txawm tias rov qab los, yog qhov laj thawj tseem ceeb uas lawv raug zam. Qhov kev hloov pauv hauv cov ntshav creatinine tuaj yeem ua rau nyuaj rau kev sib txawv ntawm lwm yam ua rau lub raum ua haujlwm tsis zoo, tshwj xeeb tshaj yog mob raum allograft rejection, ua rau tsis tsim nyog workups thiab tej zaum yuav tsis tsim lub raum allograft biopsies. Zoo ib yam li ACEIs thiab ARBs, diuretics feem ntau tsis siv los ua thawj kab rau kev tswj BP hauv cov neeg tau txais kev hloov hauv lub raum. Nws tuaj yeem siv rau kev tswj ntim ntawm tam sim lossis ntxov tom qab hloov pauv.
Los ntawm cov yam ntxwv, cov txiaj ntsig kev kho mob, thiab cov txiaj ntsig tshwm sim ntawm cov tshuaj tiv thaiv kab mob siab, peb niaj hnub siv dihydropyridine calcium channel blockers thiab / lossis beta-blockers ua thawj kab tshuaj tiv thaiv ntshav siab. Txij li feem ntau ntawm cov neeg mob tsis ua tiav BP tswj lub sijhawm tam sim lossis ntxov tom qab hloov pauv, kev sib xyaw ntawm dihydropyridine channel blockers nrog beta-blockers feem ntau siv hauv peb qhov chaw hloov pauv. Thaum lub raum allograft ua haujlwm tau tsim thiab ruaj khov, peb txiav txim siab ntxiv lossis hloov ACEI lossis ARB rau dihydropyridine channel blockers thiab beta-blockers yog tias muaj cov lus qhia tsim nyog, xws li proteinuria lossis post-transplant polycythemia.
Table 3 qhia txog cov yam ntxwv ntawm cov tshuaj tiv thaiv kab mob siab tshaj plaws thiab cov laj thawj rau kev xaiv txhua cov tshuaj BP hauv cov neeg tau txais kev hloov raum (154, 175, 176,198–204).
BLOOD Pressure GUIDELINE RAUKIDNEY TRANSPLANT RECIPIENTS
BP lub hom phiaj tau yog ib lub ntsiab lus tsis sib haum xeeb tsis yog nyob rau hauv cov pej xeem tsis hloov pauv, tab sis kuj yog cov neeg tau txais kev hloov hauv lub raum. Ntau lub koom haum tshaj lij los ntawm ntau lub teb chaws tau tsim cov txheej txheem kho mob nrog qee qhov sib xws thiab qhov sib txawv (Table 4) (26, 27, 205-212).
Txog thaum muaj cov ntaub ntawv pov thawj muaj txiaj ntsig zoo hauv cov ntsiab lus ntawm CV, cov neeg mob, lossis lub raum allograft ciaj sia, BP lub hom phiaj yuav tsum yog tus kheej, suav nrog cov tshuaj tiv thaiv kab mob thiab tsis muaj tshuaj tiv thaiv kab mob uas ua rau HTN hauv txhua tus neeg tau txais kev hloov hauv lub raum.
Lwm txoj kev tswj ntshav ntshavNYIAJ
Native Nephrectomy
Hauv ESRD cov neeg mob uas tiv thaiv HTN, txhais tau tias tsis muaj kev tswj hwm BP nrog tsawg kawg peb cov tshuaj tiv thaiv hypertensive uas ib qho yog diuretic, theem nrab HTN yuav tsum tau txiav txim siab. Sib nrug los ntawm renovascular thiab hormonal ua rau theem nrab HTN, lub raum ua tsis tiav tuaj yeem ua rau HTN lossis ua rau HTN tsis tswj hwm hauv ESRD cov neeg mob. Hauv ESRD thib ob rau ADPKD, cov txheej txheem ntawm HTN los ntawm ob lub raum ua tsis tiav yog cuam tshuam nrog rau lub raum renin es tsis txhob siv lub cev renin (213, 214). Hauv kev hloov lub raum, qhov muaj lub raum tsis ua haujlwm hauv lub raum yog txuam nrog tom qab hloov pauv-tiv thaiv HTN. Qhov no yog suav tias yog ib feem cuam tshuam nrog cov nyhuv ntawm angiotensin II (215). Hauv cov neeg tau txais kev hloov lub raum nrog HTN, ACEIs thiab cov neeg mob ntshav qab zib hom 2 yuav tsum tau txiav txim siab.
Muaj pov thawj tias cov neeg tau txais kev hloov hauv lub raum nrog ua ntej lossis tom qab hloov pauv ib txwm muaj nephrectomy tau txo qis BP thaum piv rau cov neeg tsis muaj nephrectomy (Table 5) (216- 221). Feem ntau ntawm cov kev tshawb fawb no tau ua tshwj xeeb hauv cov neeg mob ADPKD uas yog qhov ua rau ESRD.
Native Renal Sympathetic Denervation
Sib nrug los ntawm txoj kev angiotensin II, sympathetic overactivity los ntawm lub raum tsis ua hauj lwm yog lwm yam uas ua rau HTN resistant. Lub raum thiab systemic sympathetic hyperactivity pab txhawb rau lub pathophysiology ntawm resistant HTN. Cov nyhuv ntawm RDN ntawm BP tswj tau tsim (222). Hauv cov neeg tau txais kev hloov hauv lub raum nrog lub raum tsis ua haujlwm, kev ua siab zoo ntawm lub paj hlwb ua haujlwm los ntawm qhov tsis muaj teeb meem ntawm lub raum ib txwm tau khaws cia (223).
Surgical Renal Denervation by Bilateral
Native Nephrectomy
Ua kom tiav RDN tuaj yeem ua tau los ntawm ob tog neeg nephrectomy. Kev tshawb nrhiav rov qab hauv 32 lub raum hloov pauv
Cov neeg tau txais kev hloov pauv ua ntej ob tog neeg nephrectomy qhia tawm qis dua SBP, ntau cov tshuaj tiv thaiv kab mob siab, sab laug ventricular mass Performance index thiab sab laug atrial volume index tab sis siab dua sab laug ventricular diastolic dysfunction piv rau qhov sib npaug (hnub nyoog, poj niam txiv neej, qib creatinine, eGFR, kev kho tshuaj tiv thaiv kab mob, thiab lub sijhawm kho lub raum hloov) pawg tswj hwm (221). Cov ntaub ntawv no txhawb nqa cov txiaj ntsig ntawm RDN raws li kev kho mob rau HTN hauv cov pejxeem.
Txawm hais tias haiv neeg nephrectomy tuaj yeem txhim kho kev hloov HTN, ob qho tib si ua ntej thiab tom qab hloov pauv tom qab tus neeg mob nephrectomy tuaj yeem ua rau muaj teeb meem kev phais, uas tuaj yeem ua rau lub raum tsis ua haujlwm. Yog li ntawd, ib txwm nephrectomy rau lub hom phiaj ntawm BP tswj nyob rau hauv cov neeg tau txais kev hloov hauv lub raum yuav tsum tau ua hauv cov neeg mob uas tsis muaj kev tswj hwm tsis zoo tom qab hloov HTN uas, tsis muaj kev kho mob, yuav muaj kev cuam tshuam ntawm lub raum allograft ua haujlwm lossis muaj kev pheej hmoo ntawm CV teeb meem. Cov neeg mob uas tau txais ob tog neeg nephrectomy rau lwm qhov kev qhia xws li kev kis tus kab mob rov qab, tsis xis nyob los ntawm lub raum loj polycystic, lossis cov qog nqaij hlav hauv lub raum tsis zoo tuaj yeem muaj cov txiaj ntsig ntxiv ntawm kev txhim kho BP.
Catheter Ablative Renal Denervation
Ib nrab reinnervation ntawm tib neeg lub raum transplanted tau pom histologically. Axonal regeneration hauv tib neeg lub raum pib ntawm 28 hnub mus rau 5 lub hlis tom qab hloov lub raum thiab ua tiav hauv 8-12 lub hlis mus rau 2 xyoos (224, 225). Kev ua haujlwm ntawm lub raum cov hlab ntsha uas rov ua dua lub raum cov hlab ntsha, txawm li cas los xij, yuav tsis zoo ib yam li qhov tshwm sim hauv cov hlab ntsha hauv lub raum (226, 227). Ib txoj kev tshawb fawb ntawm lub raum hemodynamics, sodium excretion, thiab tubular muaj nuj nqi tom qab noradrenaline infusion (2 µg h 1 kg 1) thiab qis lub cev tsis zoo siab (27 mmHg) hauv 25 tus neeg tau txais kev hloov pauv raum thiab 10 cov kev kawm ib txwm tau xaus lus tias cov hlab ntsha hauv lub raum tsis zoo hauv lub raum. tib neeg hloov lub raum yog tseem tseem ceeb functionally denervated (228). Txij li thaum ua tiav RDN los ntawm ob tog neeg nephrectomy hauv cov neeg tau txais kev hloov hauv lub raum yog qhov cuam tshuam thiab ua rau muaj kev pheej hmoo ntawm kev ua haujlwm ntxiv, haiv neeg RDN yog lwm txoj kev xaiv, thiab nws yuav tsum tau tshwj tseg rau cov neeg mob xaiv.
Ob tus neeg tau txais kev hloov lub raum nrog HTN resistant tau txhim kho BP tswj tom qab RDN ntawm cov neeg raum (229, 230). Tus neeg tshawb nrhiav-pib, yav tom ntej, ib-chaw RCT nrog rau 6- hli tom qab ntawm 18 lub raum hloov pauv cov neeg tau txais kev tiv thaiv HTN piv qhov ua tau thiab kev ua tau zoo ntawm lub raum sympathetic denervation piv rau kev kho mob ib leeg. Cov pab pawg qub tau poob qis dua ib zaug SBP ntawm 23.3 14.5 mmHg thiab ntau dua ntawm cov neeg mob uas hloov los ntawm cov tsis yog dippers mus rau dippers. Nocturnal BP sau nrog 24-h ABPM, tab sis tsis yog nruab hnub BP, kuj qis dua 10.38 12.8 mmHg hauv pawg RDN, txawm tias qhov no tsis yog qhov tseem ceeb. Cov ntsiab lus kev nyab xeeb suav nrog kev hloov pauv hauv lub raum allograft muaj nuj nqi thiab cov teeb meem renovascular tsis txawv ntawm 2 pawg (231). Txawm hais tias haiv neeg RDN muaj txiaj ntsig zoo hauv kev tswj BP, RCTs loj dua nrog kev tswj tsis zoo yuav tsum tau ua.
Cov lus xaus
HTN yog ib yam kab mob ntau heev hauv CKD thiab ESRD thiab tseem nyob tom qab hloov lub raum. Lub pathogenesis ntawm post-transplant HTN yog complex. Kev ntsuas BP tseem yog qhov teeb meem tseem ceeb rau kev kuaj mob kom raug thiab ua raws hauv HTN kev tswj hwm. A 24-h ABPM, txawm tias tus qauv kub, tsis yooj yim thiab tsis siv wildly. Kev xaiv cov tshuaj antihypertensive xav tau tus kws kho mob kom hloov pauv thiab cov tshuaj tiv thaiv kab mob rau hauv kev saib xyuas. Kev tswj hwm rau OSA thiab kev cuam tshuam rau HTN resistant, xws li hloov lub raum hlab ntsha angioplasty stenting, ob tog neeg nephrectomy, thiab haiv neeg RDN, tseem muaj kev xaiv rau resistant HTN hauv cov neeg tau txais kev hloov lub raum. Tsis muaj qhov tseeb BP lub hom phiaj rau cov pej xeem no thiab cov hom phiaj kho mob yuav tsum tau ua tus kheej. Kev tshawb fawb ntxiv los txhim kho lub cev muaj zog ntawm cov pov thawj rau cov kab mob tom qab hloov HTN thiab qhia cov kws kho mob txog kev ntsuas BP tsim nyog, siv cov tshuaj tiv thaiv kab mob siab, kev phais lossis cov txheej txheem, thiab tsim BP lub hom phiaj rau cov neeg tau txais kev hloov hauv lub raum.
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