Kev txo qis kev ua haujlwm hauv lub raum poob qis hauv cov neeg mob nrog CKD: Cov Ntawv Kawm Tub Ntxhais Kawm 2021

Yog xav paub ntxiv:Ali.ma@wecistanche.com

Teresa K. Chen, Christopher J. Sperati, Sumeska Thavarajah, thiab Morgan E. Grams

Nyem rau Cistanche NZ rau kab mob raum

Kwv yees li ntawm 8 mus rau 16 feem pua ​​​​ntawm cov neeg hauv ntiaj teb muajmob raumkab mob, txhais los ntawm qhov qis glomerular pom tus nqi lossis albuminuria. Kev loj hlob ntawm cov kab mob raum ntev yog txuam nrog cov txiaj ntsig tsis zoo, nrog rau qhov xwm txheej rau lub raum tsis ua haujlwm nrog kev hloov kho, ceev cov kab mob plawv, kev tsis taus, thiab kev tuag. Yog li ntawd, qeebraum muaj nuj nqiKev poob qis yog qhov tseem ceeb hauv kev tswj hwm tus neeg mob uas muaj kab mob raum ntev. Kev txheeb xyuas qhov ua rau mob raum yog thawj kauj ruam tseem ceeb thiab tuaj yeem yuam cov kev kho mob tshwj xeeb. Cov kev siv tau zoo uas siv rau feem coob ntawm cov neeg mob uas muaj kab mob raum muaj xws li kev ua kom zoo ntawm cov ntshav siab thiab thaiv cov kab mob renin-angiotensin-aldosterone, tshwj xeeb tshaj yog tias muaj albuminuria. Cov kev tshawb fawb tsis ntev los no qhia tias sodium / glucose cotransporter 2 inhibitors yog cov kev kho mob zoo heev rau cov neeg mob ntshav qab zib thiab / lossis albuminuria. Rau cov neeg mob ntshav qab zib hom 2, kev tswj glycemic tseem ceeb hauv kev tiv thaiv kev txhim kho ntawm cov teeb meem microvascular, thiab glucagon-zoo li peptide 1receptor agonists tuaj yeem pab txo qis albuminuria. Lwm cov tswv yim suav nrog kev kho cov kab mob metabolic acidosis, tswj lub cev qhov hnyav, ua raws li cov zaub mov uas tsis muaj sodium thiab tsiaj protein, thiab zam cov nephrotoxins xws li nonsteroidal anti-inflammatories, proton-pump inhibitors, thiab iodinated contrast.

Taw qhia

Mob raum mob(CKD) cuam tshuam ntau dua 697 lab tus tib neeg thoob ntiaj teb thiab cuam tshuam nrog kev mob hnyav ntxiv thiab kev tuag. Hauv xyoo 2017, 1.2 lab tus neeg tuag thiab 35.8 lab tus neeg xiam oob khab-hloov lub neej-xyoo raug ntaus nqi rau CKD. Ntawm cov neeg tau txais txiaj ntsig Medicare hauv Uni ted States, kev siv nyiaj txhua xyoo rauraum ua tsis tiavnrog kev hloov kho (KFRT) thiab cov theem ua ntej ntawm CKD tau tshaj $ 120 billion. Txawv ua rauraumkab mobtej zaum yuav xav tau cov kev kho mob tshwj xeeb xws li kev siv tshuaj tiv thaiv kab mob. Txawm li cas los xij, qee cov tswv yim los ncua kev nce qib ntawm CKD rau KFRT yog siv tau rau cov neeg mob feem ntau. Kev tshawb pom ntxov thiab kho kom qeebraummuaj nuj nqiKev poob qis yog qhov tseem ceeb rau kev txhim kho cov txiaj ntsig ntawm cov neeg mob CKD. Cov cim tseem ceeb ntawm CKD kev tswj hwm suav nrog kev tswj ntshav siab thiab hyperglycemia, inhibition ntawm renin-angiotensin-aldosterone system (RAAS), kho cov metabolic acidosis, hloov kho txoj kev ua neej, thiab kev zam ntawm nephrotoxins. Ob chav kawm tshiab ntawm cov tshuaj, sodium / glucose cotransporter 2 (SGLT2) inhibitors, thiab glucagon-zoo li peptide 1 (GLP-1) receptor agonists, kuj txhim kho.raumCov txiaj ntsig ntawm cov neeg mob ntshav qab zib thiab / lossis albuminuria.

Nyeem ntxiv

➢ GBD ChronicLub raumKab mob sib koom tes. Ntiaj teb no, lub regional, thiab lub teb chaws lub nra hnyavraumkab mob, 1990-2017: ib qho kev tshuaj ntsuam xyuas rau Lub Ntiaj Teb Burden of Disease Study 2017. Lancet. 2020; 395:{4}}.

➢ Saran R, Robinson B, Abbott KC, thiab al. US Renal Data System 2019 cov ntaub ntawv qhia txhua xyoo: kev kis mob ntawmraumkab mob hauv Tebchaws Meskas. Am JLub raumDis. 2020; 75(1)(suppl 1): S1-S64.

Kev tswj ntshav siab

Case 1: Ib tug 60-xyoo-laus txiv neej nrog CKD glomerular filtration rate qeb 3b (G3b) thiab albuminuria qeb 2 (A2, sib xws rau cov zis albumin-creatinine ratio [UACR] ntawm 30-300 mg/g ), kub siab, thiab ruaj khov angina rov qab mus ntsib. Nws kwv yees glomerular filtration rate (eGFR) tau poob ntawm 57 mus rau 44 mL / min / 1.73 m2 nyob rau hauv 13 xyoo dhau los. Nws cov ntshav siab (BP) nruab nrab yog 135/72 mm Hg ntawm kev tswj hwm ntawm valsartan ntawm 320 mg txhua hnub, amlodipine ntawm 5 mg txhua hnub, thiab indapamide ntawm 1.25 mg txhua hnub.

Nqe Lus Nug 1: Raws li cov txiaj ntsig ntawm SPRINT, uas ib qho ntawm cov nqe lus hauv qab no yog qhov tseeb tshaj plaws txog lub hom phiaj systolic BP ntawm<120 versus=""><140 mm="">

a) Txhua-ua rau kev tuag raug txo

b) CKD nce qeeb qeeb ntawm lub hom phiaj qis BP

c) Qhov xwm txheej ntawm KFRT siab dua ntawm lub hom phiaj qis BP

d) Qhov tshwm sim ntawm kev hloov lub raum yog qis dua ntawm lub hom phiaj qis BP

Nqe Lus Nug 2: Tus neeg mob twg hauv qab no yuav tsim nyog tshaj plaws rau lub hom phiaj qis BP los pab ua kom qeeb ntawm CKD?

a) CKD G3aA1 nrog UACR ntawm 10 mg / g

b) CKD G4A1 nrog qhov tseem ceeb ntawm ob sab lub raum hlab ntsha stenosis

c) CKD G3bA3 nrog UACR ntawm 3,000 mg/g

d) CKD G3bA3 nrog UACR ntawm 1,200 mg / g thiab keeb kwm ntawm kev poob rov qab

Rau cov lus teb rau cov lus nug, saib cov ntawv hauv qab no.

AHA/ACC pom zoo lub hom phiaj BP<130 0="" mm="" hg="" for="" all="" patients="" with="" ckd,="" whereas="" the="" kdigo="" guidelines="" recommend="" a="" target="" of="" ≤140/90="" mm="" hg="" when="" the="" uacr="" is=""><30 mg/d="" and="" ≤130/80="" mm="" hg="" when="" the="" uacr="" is="" ≥30="" mg/d="" (table="" 1).="" the="" kdigo="" recommendations="" are="" based,="" in="" part,="" on="" 2="" landmark="" randomized="" controlled="" trials.="" the="" aask="" trial="" randomized="" participants="" without="" diabetes="" to="" a="" mean="" arterial="" pressure="" (map)="" goal="" of="" ≤92="" versus="" 102-="" 107="" mm="" hg.="" although="" there="" was="" no="" difference="" in="" the="" rate="" of="" egfr="" decline="" or="" a="" composite="" clinical="" outcome="" (egfr="" decline,="" kfrt,="" or="" death)="" overall,="" participants="" with="" a="" baseline="" urinary="" protein-creatinine="" ratio="" of="">0.22 g / g yog 27 feem pua ​​​​tsis tshua muaj peev xwm tsim tau ob npaug ntawm cov ntshav creatinine, KFRT, lossis kev tuag thaum randomized rau hnyav piv rau tus qauv BP tswj nyob rau theem txuas ntxiv. MDRD Txoj Kev Kawm Randomized cov neeg koom nrog MAP lub hom phiaj ntawm 92 piv rau 107 mm Hg. Ib zaug ntxiv, tsis muaj qhov sib txawv tag nrho, tab sis cov neeg koom nrog cov proteinuria ntau dua lossis sib npaug ntawm 3 g / d muaj GFR tsawg dua hauv pawg tswj hwm BP. Cov no thiab lwm yam kev sim ntawm BP tswj tau sau tseg hauv Table 2.

Tsis ntev los no, SPRINT randomized cov neeg laus uas tsis muaj ntshav qab zib tab sis muaj kev pheej hmoo siab rau cov kab mob plawv mus rau asystolic BP < 120="" mm="" hg="" piv="">< 140="" mm="" hg.="" intensivebp="" tswj="" tau="" cuam="" tshuam="" nrog="" kev="" pheej="" hmoo="" tsawg="" ntawm="" myocardial="" infarction,="" mob="" plawv="" mob,="" mob="" stroke,="" plawv="" tsis="" ua="" hauj="" lwm,="" thiab="" mob="" plawv="" tuag="" (kev="" phom="" sij="" [hr],="" 0.75="" [95="" feem="" pua="" ​​ci,="" 0.="" {6}}.89])="" thiab="" tag="" nrho-ua="" rau="" kev="" tuag="" (hr,="" 0.73="" [95="" feem="" pua="" ​​ci,="" 0.60-0.90]).="" cov="" txiaj="" ntsig="" tau="" zoo="" ib="" yam="" ntawm="" cov="" neeg="" koom="" nrog="" lub="" hauv="" paus="" ckd="" (n="2,646)." intensive="" bpcontrol="" tsis="" tiv="" thaiv="" qhov="" tshwm="" sim="" tsis="" zoo="" rau="" lub="" raum="" (ntau="" dua="" lossis="" sib="" npaug="" rau="" 50="" feem="" pua="" ​​​​egfr="" poob="" lossis="" kfrt).="" ntawm="" cov="" neeg="" koom="" nrog="" yam="" tsis="" muaj="" kab="" hauv="" qab="" ckd="" (n="6,677)," kev="" tswj="" hwm="" bp="" hnyav="" tau="" ua="" rau="" 3.5-fold="" muaj="" kev="" pheej="" hmoo="" siab="" dua="" los="" yog="" sib="" npaug="" li="" 30="" feem="" pua="" ​​​​txo="" hauv="" egfrto="">< 60="" ml/min/1.73="" m2,="" ib="" qho="" kev="" tshawb="" pom="" uas="" yuav="" cuam="" tshuam="" txog="" kev="" hloov="" pauv="" tsis="" zoo="" ntawm="" lub="" raum="" raug="">

Rau nqe lus nug 1, (a) txo qhov kev tuag tag nrho yog cov lus teb raug. Lub hom phiaj ntawm BP qis dua tsis ua rau kev loj hlob ntawm CKD, thiab SPRINT tsis muaj zog los ntsuas KFRT thiab cov xwm txheej hloov raum. Rau nqe lus nug 2, (c) tus neeg mob uas muaj CKD G3bA3 thiab UACR ntawm 3,000 mg/feem ntau yuav tau txais txiaj ntsig los ntawm lub hom phiaj BP qis dua raws li kev tshuaj xyuas pawg los ntawm kev sim tshuaj. Cov neeg mob A1albuminuria, qhov tseem ceeb ntawm ob lub raum lub raum hlab ntsha stenosis, los yog rov qab ntog tsis tshua muaj txiaj ntsig los ntawm lub hom phiaj BP qis lossis tej zaum yuav muaj kev pheej hmoo siab dua ntawm kev kho mob.

Nyeem ntxiv

➢ Appel LJ, Wright JT, Greene T, et al. Intensive ntshav siab tswj nyob rau hauv hypertensive mob raum kab mob. N Engl J Med 2010;363(10):{4}}. ntxiv rau kev nyeem ntawv tseem ceeb

➢ Cheung AK, Rahman M, Reboussin DM, et al. Qhov cuam tshuam ntawm kev tswj hwm BP hauv CKD. J Am Soc Nephrol. 2017; 28(9):{3}}.

➢ Kab mob raum: Txhim kho Cov txiaj ntsig thoob ntiaj teb (KDIGO) CKD Pawg Ua Haujlwm. KDIGO 2012 daim ntawv qhia kev kho mob rau kev ntsuam xyuas thiab kev tswj cov kab mob raum ntev. Raum Int Suppl. 2013; 3(1):{4}}. ntxiv rau kev nyeem ntawv tseem ceeb

➢ Klahr S, Levey AS, Beck GJ, et al. Qhov cuam tshuam ntawm kev txwv kev noj zaub mov protein thiab kev tswj ntshav siab ntawm kev loj hlob ntawm cov kab mob raum ntev. N Engl J Med. 1994; 330(13): 877-884. ntxiv rau kev nyeem ntawv tseem ceeb

➢ Ruggenenti P, Perna A, Loriga G, thiab al. Ntshav-Pressure Control for Renoprotection in Patients With Non-diabetic Chronic Renal Disease (REIN-2): ntau qhov chaw, randomized tswj kev sim. Lancet.2005;365(9463):939-946.

➢ SPRINT Research Group. Ib qho randomized sim ntawm intensive piv rau tus qauv tswj ntshav siab. N Engl J Med. 2015; 373(22):2103-2116. ntxiv rau kev nyeem ntawv tseem ceeb

➢ Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/ AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Cov Lus Qhia rau kev tiv thaiv, nrhiav pom, kev ntsuam xyuas, thiab kev tswj cov ntshav siab hauv cov neeg laus: daim ntawv qhia ntawm American College of Cardiology/American Lub Koom Haum Koom Tes Ua Haujlwm ntawm Lub Koom Haum Saib Xyuas Kev Ua Haujlwm. Ntshav siab. 2018; 71(6): e13-e115.

➢ Wright JT, Bakris G, Greene T, et al. Cov txiaj ntsig ntawm kev txo cov ntshav siab thiab cov tshuaj tiv thaiv kab mob siab rau ntawm kev mob siab rau lub raum: tau los ntawm kev sim AASK. JAMA. 2002; 288(19): 2421-2431.

RAAS Inhibition

Case 2:Tus poj niam muaj hnub nyoog 46- xyoo uas muaj ntshav qab zib hom 2 rov qab los rau nws lub sijhawm teem thib ob. Nws keeb kwm yog qhov tseem ceeb rau retinopathy thiab CKD G3aA3 vim yog mob ntshav qab zib raum. Nws tsis kam muaj cov tsos mob orthostatic lossis mob hauv siab. Nws qhov chaw ua haujlwm automated BP yog 118/75 mm Hg ntawm atenolol thiab chlorthalidone. Kev soj ntsuam hauv chav kuaj pom muaj eGFR ruaj khov (ntawm 55 mL / min / 1.73 m2) nrog UACR ntawm 1,200 mg / g.

Nqe Lus Nug 3: Ib qho twg hauv qab no yuav yog qhov kev kho mob ntshav siab tshaj plaws los pab qeeb CKD kev loj hlob?

a) Tsis muaj kev hloov pauv hauv kev kho mob vim tias nws BP raug tswj hwm rau lub hom phiaj

b) Hloov atenolol rau angiotensin receptor blocker (ARB)

c) Hloov chlorthalidone rau ARB d) Ntxiv ARB rau tam sim no 2- tshuaj noj

Case 3:Ib tus poj niam muaj hnub nyoog 56- xyoo uas muaj CKD G3aA3 vim muaj cov kab mob qog nqaij hlav ntshav qab zib tau pom muaj qhov nruab nrab ntawm BP ntawm 144/83 mm Hg ntawm lisinopril ntawm 20 mg txhua hnub, chlorthalidone ntawm 50 mg. ib hnub, thiab amlodipine ntawm 10 mg ib hnub twg. Nws UACR yog 800 mg / g.

Nqe Lus Nug 4: Ib qho kev cuam tshuam dab tsi hauv qab no yuav tsim nyog tshaj los txo qhov kev pheej hmoo ntawm CKD kev loj hlob?

a) Ntxiv ib qho ARB rau cov txheej txheem tam sim no

b) Hloov lisinopril mus rau ib qho mineralocorticoid receptor antagonist (MRA)

c) Ua kom cov lisinopril ntau npaum

d) Hloov chlorthalidone rau indapamide Rau cov lus teb rau cov lus nug, saib cov ntawv hauv qab no.

The cornerstone of albuminuria management is RAAS inhibition. The KDIGO guidelines recommend that all adults with CKD, hypertension and a UACR of >300 mg/g raug kho nrog angiotensin-hloov enzyme inhibitor (ACEI) lossis ARB. Ntawm cov neeg mob ntshav qab zib thiab UACR> 30 mg / g, kev siv ACEI lossis ARB yuav tsum raug txiav txim siab. RAAS inhibition nyob rau hauv cov neeg mob nrog CKD thiab kub siab kuj tau txais kev txhawb nqa los ntawm tag nrho cov lus qhia kev kub siab loj (Table 1). Ntau qhov kev sim tau pom tias ACEI lossis ARB kev kho mob qeeb CKD kev loj hlob ntawm cov neeg uas muaj albuminuria (Table 3). Kev sim REIN, uas randomized cov neeg mob nrog CKD rau ramipril piv rau cov placebo, qhia tau hais tias txhais tau tias GFR poob qis tseem ceeb hauv pawg ramipril ntawm cov neeg koom nrog cov proteinuria ntau dua lossis sib npaug li 3 g / d. Hauv kev tshawb fawb RENAAL, cov neeg mob uas muaj ntshav qab zib hom 2 thiab CKD randomized rau kev kho mob losartan muaj 16 feem pua ​​​​txo qis ntawm kev tsim cov ntshav creatinine ob npaug, KFRT, lossis kev tuag piv nrog cov placebo pawg. Ib yam li ntawd, IDNT tau tshaj tawm tias kev kho irbesartan tau cuam tshuam nrog kev pheej hmoo tsawg dua ob npaug ntawm cov ntshav creatinine, ntshav creatinine ntau dua lossis sib npaug li 6.0 mg / dL, KFRT, lossis tuag piv nrog amlodipine lossis placebo kev kho mob ntawm cov neeg mob ntshav siab thiab CKD vim yog mob ntshav qab zib hom 2. Thaum kawg, hauv AASK, kev siv ramipril yog tus kheej cuam tshuam nrog 22 feem pua ​​​​thiab 38 feem pua ​​​​ntawm cov kev pheej hmoo tsawg dua ntawm cov txiaj ntsig kev kho mob (GFR poob siab dua lossis sib npaug rau 50 feem pua ​​​​lossis Ntau dua lossis sib npaug li 25 mL / min / 1.73 m2 los ntawm cov hauv paus. , KFRT, lossis tuag) piv nrog metoprolol thiab amlodipine, feem.

Cov ntaub ntawv tam sim no tsis txhawb kev siv ob txoj kev thaiv nrog ACEI thiab ARB hauv cov mob ntshav qab zib raum. VA NEPHRON-D, uas randomized cov qub tub rog uas muaj ntshav qab zib hom 2 thiab CKD G2-G3bA3 rau losartan ntxiv rau lisinopril lossis losartan ib leeg, raug txiav tawm ntxov vim muaj kev txhawj xeeb txog kev nyab xeeb, nrog rau kev sib xyaw ua ke pab pawg muaj kev pheej hmoo siab ntawm hyperkalemia ( . Tsis tas li ntawd, tsis muaj qhov sib txawv tseem ceeb ntawm kev pheej hmoo ntawm lub raum kev ua haujlwm poob qis ntawm 2 pawg kho mob, txawm tias lub sijhawm rov qab los yog luv luv (Table 3).

Kev txo qis sodium kom tsawg tuaj yeem txhim kho cov teebmeem renoprotective ntawm RAAS inhibitors. Ib qho kev soj ntsuam ntawm 11 cov kev tshawb fawb (23 pawg nrog 516 tus neeg koom) tau tshaj tawm tias kev txwv kev noj zaub mov sodium (qhov nruab nrab qis ntawm 92 mmol / d) cuam tshuam nrog 32 feem pua ​​​​ntawm cov zis albumin tso tawm. Qhov txo qis hauv cov zis albumin excretion yog ntau dua nyob rau hauv pawg nrog concomitant RAAS thaiv kev kho dua li cov uas tsis muaj (pooled txhais tau tias sib txawv ntawm −41.9 feem pua ​​thiab −17.2 feem pua, raws li; P=0.01 rau kev sib cuam tshuam), qhia txog kev sib koom ua ke Cov nyhuv ntawm kev noj tsawg sodium nrog RAAS inhibition. Hauv kev soj ntsuam tom qab hoc ntawm 500 tus neeg koom hauv REIN thiab REIN II kev sim tau txais kev kho mob ramipril, kev noj zaub mov nrog > 14 g / d ntsev yog txuam nrog 3.3-fold thiab 2.{17}}fold ntau dua Kev pheej hmoo ntawm KFRT piv nrog cov zaub mov ntawm<7 g/d="" and="" 7="" to="" 14="" g/d="" of="" salt,="" respectively.="" importantly,="" the="" proteinuria-reducing="" effects="" of="" ramipril="" were="" greatest="" in="" the="" low-sodium="" diet="" group.="" in="" another="" post="" hoc="" analysis="" of="" the="" renaal="" study="" and="" idnt="" (n="1,177)," arb="" therapy="" was="" associated="" with="" a="" 43%="" lower="" risk="" of="" a="" renal="" event,="" defined="" as="" a="" doubling="" of="" serum="" creatinine="" or="" kfrt,="" compared="" with="" non-raas="" inhibitor="" therapy="" among="" participants="" in="" the="" lowest="" tertile="" of="" the="" 24-hour="" urinary="" sodium-creatinine="" ratio="" with="" no="" significant="" difference="" in="" risk="" between="" the="" 2="" treatment="" groups="" for="" higher="" tertiles="" of="" sodium="" intake="" (p="" <="" 0.001="" for="" interaction;="" fig="" 1).="" given="" these="" findings,="" patients="" on="" raas="" inhibitors="" for="" the="" treatment="" of="" albuminuria="" should="" be="" encouraged="" to="" follow="" a="" low-sodium="">

For patients intolerant of ACEI/ARB therapy, an MRA can be considered. A recent meta-analysis of 31 randomized controlled trials evaluated the efficacy and safety forms (spironolactone, eplerenone, canrenone, or finerenone) compared with active control or placebo in reducing albuminuria. In the 18 trials (n = 2,036) that examined UACR as an outcome, proportional change in ACR from baseline to end of treatment was 22% lower inMRA treatment compared with active control and placebo. The effect persisted when comparing MRAs to placebo(n = 1,436 in 11 trials) in patients on ACEI/ARB therapy. When comparing MRAs to renin-angiotensin blockers, there was no significant difference in change in albuminuria (n = 201 in 2 trials), but the risk of incident hyperkalemia was 70% higher (n = 855 in 5 trials). Although the reduction in albuminuria is not a universally accepted surrogate endpoint for KFRT, the FIDELIO-DKDtrial of patients with type 2 diabetes and CKD (>98 feem pua ​​​​ntawm concomitant ACEI lossis ARB therapy) tau tshaj tawm tias finerenone tau pom zoo 18 feem pua ​​​​txo qis ntawm cov txiaj ntsig ntawm cov kab mob sib kis (kev poob qis hauv eGFR los ntawm ntau dua lossis sib npaug li 40 feem pua ​​lossis rau<15 ml/min/1.73="" m2,="" kfrt,="" or="" death="" from="" kidney="" causes)="" compared="" with="" placebo.="" thus,="" mras="" reduce="" albuminuria="" and="" may="" also="" slow="" ckd="" progression.="" thesebenefifits,="" however,="" must="" be="" balanced="" against="" the="" potential="" risk="" of="">

Hauv nqe lus nug 3, (b) hloov atenolol rau ARB yog cov lus teb raug. ACEIs thiab ARBs tau pom tias ua rau qeeb ntawm CKD hauv cov neeg mob ntshav qab zib thaum -blockers tsis muaj. Hauv kev tswj cov ntshav siab, -blockers yog ib qho kev kho ntxiv tom qab siv cov tshuaj thawj kab xws li ACEIor ARBs thiab thiazide diuretics. Ntxiv ib qho ARB rau cov kev tswj hwm tam sim no yog qhov xav tau tsawg dua, vim qhov no yuav ua rau muaj kev ntxhov siab hauv tus neeg mob nrog BP twb tau ua rau lub hom phiaj.

Hauv nqe lus nug 4, (c) nce koob tshuaj lisinopril yog cov lus teb zoo tshaj. Kev sib xyaw ua ke ntawm ACEI thiab ARB txoj kev kho yog cuam tshuam nrog kev pheej hmoo ntawm qhov tshwm sim tsis zoo. Txawm hais tias MRA tuaj yeem txo qis albuminuria thaum ua ke nrog ACEI lossis ARB, tsis muaj kev sim tshuaj ntsuam xyuas tau ua los txhawb kev hloov ACEI rau MRA nrog lub hom phiaj ntawm kev ua kom qeeb rau KFRT. Kev hloov chlorthalidone rau indapamide tsis xav tias yuav ua rau qhov kev nce qib no qeeb.

Nyeem ntxiv

➢ Alexandrou ME, Papagianni A, Tapas A, thiab al. Cov teebmeem ntawm mineralocorticoid receptor antagonists nyob rau hauv cov kab mob hauv lub raum proteinuric: kev tshuaj xyuas thiab kev tshuaj xyuas meta-kev soj ntsuam ntawm randomized tswj kev sim. J Hypertens. 2019;37(12):2307-2324. ntxiv rau kev nyeem ntawv tseem ceeb

➢ Bakris GL, Agarwal R, Anker SD, et al. Cov txiaj ntsig ntawm finerenone rau cov kab mob raum ntev tshwm sim hauv hom 2 mob ntshav qab zib. N Engl J Med. 2020; 383(23):2219-2229.

➢ Brenner BM, Cooper ME, De Zeeuw D, et al. Cov teebmeem ntawm losartan ntawm lub raum thiab cov hlab plawv cov txiaj ntsig hauv cov neeg mob ntshav qab zib hom 2 thiab nephropathy. N Engl J Med. 2001; 345(12): 861- 869. ntxiv rau kev nyeem ntawv tseem ceeb

➢ D'Elia L, Rossi G, Schiano di Cola M, et al. Meta-kev soj ntsuam ntawm cov nyhuv ntawm kev noj haus sodium txwv nrog los yog tsis concomitant renin-angiotensin-aldosterone system-inhibiting kev kho mob ntawm albuminuria. Clin J Am Soc Nephrol. 2015; 10(9):{7}}.

➢ Fried LF, Emanuele N, Zhang JH, et al. Ua ke angiotensin inhibition rau kev kho mob ntshav qab zib nephropathy. N Engl J Med. 2013; 369(20): 1892-1903. ntxiv rau kev nyeem ntawv tseem ceeb

➢ GISEN Group (Gruppo Italiano di Studi Epidemiologici hauv Nefrologia). Randomized placebo-tswj sim ntawm cov nyhuv ntawm ramipril ntawm kev poob qis hauv glomerular pom tus nqi thiab kev pheej hmoo ntawm lub raum tsis ua haujlwm hauv cov proteinuria, uas tsis yog mob ntshav qab zib nephropathy. Lancet. 1997; 349(9069):{5}}.

➢ Kab mob raum: Txhim kho Cov txiaj ntsig thoob ntiaj teb (KDIGO) CKD Pawg Ua Haujlwm. KDIGO 2012 daim ntawv qhia kev kho mob rau kev ntsuam xyuas thiab kev tswj cov kab mob raum ntev. Raum Int Suppl. 2013; 3(1):{4}}. ntxiv rau ESENTIAL READING ➢ Lambers Heerspink HJ, Holtkamp FA, Parving HH, thiab al. Kev noj zaub mov zoo sodium potentiates lub raum thiab lub plawv tiv thaiv cov teebmeem ntawm angiotensin receptor blockers. Raum Int. 2012;82(3):330-337.

➢ Lewis EJ, Hunsicker LG, Clark WR, et al. Renoprotective nyhuv ntawm angiotensin-receptor antagonist irbesartan hauv cov neeg mob nephropathy vim hom 2 mob ntshav qab zib. N Engl J Med. 2001; 345(12):{5}}.

➢ Vegter S, Perna A, Postma MJ, thiab al. Sodium intake, ACE inhibition, thiab nce mus rau ESRD. J Am Soc Neph rol.2012;23(1):165-173. ntxiv rau kev nyeem ntawv tseem ceeb

➢ Wright JT, Bakris G, Greene T, et al. Cov txiaj ntsig ntawm kev txo cov ntshav siab thiab cov tshuaj tiv thaiv kab mob siab rau ntawm kev mob siab rau lub raum: tau los ntawm kev sim AASK. JAMA. 2002; 288(19): 2421-2431. ntxiv rau kev nyeem ntawv tseem ceeb