Ib txoj hauv kev zoo rau Cov Kab Mob Raum Hniav hauv Kev Kho Mob Ntiag Tug Seng Wee Cheo, Qin Jian Ⅱ

3.0 Kev tswj hwm ntawm CKD

3.1 Kev tswj hwm dav dav

Lub hom phiaj ntawm covkev tswj hwm ntawm CKDyog raws li nram no 23: a) ncua lubkev loj hlob ntawm CKDb) Totxo cov hlab plawvc) Totxo lub raum raug mob ntxiv, thiabzam cov tshuaj nephrotoxicd) Txhawm rau txheeb xyuas cov neeg mob uas xav tau kev kho lub raum hloov e) Rautswj cov teeb meem ntawm CKDf) Txhawm rau kho cov tshuaj raws li GFR Feem ntau, kev tswj hwm ntawm CKD nyob ntawm qhovtheem ntawm CKD. Feem ntau theem 1-3 Cov neeg mob CKD tuaj yeem tswj hwm hauv qhov chaw saib xyuas thawj zaug, thaum CKD 4-5 yuav tsum tau tswj hwm hauv tsev kho mob. Hauv CKD 1-3, kev kho mob feem ntau yog tsom rau kev txwv tsis pub muajkev loj hlob ntawm CKD(Table 10).

3.2 CKD kev nce qib

Cov neeg mob uas muaj CKD yuav tsis muaj kev vam meej. Kev nce qib ntawm CKD yog txhais tau tias yog qhov poob qis hauv GFR qeb lossis poob rau hauv qeb GFR nrog 25% lossis ntau dua poob hauv eGFR los ntawm lub hauv paus.10 Cov neeg mob nrog CKD 1-3 yuav tsum tau saib xyuas lawv eGFR tsis tu ncua {{3 }} zaug / xyoo. Ib txoj hauv kev zoo dua ntawm kev ntsuas CKD kev nce qib yog los saib xyuas eGFR trajectory, uas yog, kev hloov pauv txhua xyoo hauv eGFR lossis eGFR txoj kab nqes. Qhov kev coj ua no tuaj yeem txhawb cov kws kho mob thawj zaug kom taug qab eGFR hloov pauv lub sijhawm. Cov neeg mob uas muaj kev pheej hmoo ntawm kev poob qis sai yuav tsum raug txheeb xyuas ntxov, thiab yog tias qhov poob qis sai sai, lawv yuav tsum raug xa mus rau tus kws kho mob nephrologist.

Kev pheej hmoo rau kev nce qib ntawm CKD suav nrog 24:

a) Proteinuria

b) Suboptimal BP tswj

c) Kev tswj hwm glycemic zoo

d) Kev haus luam yeeb

e) Kab mob plawv

f) mob raum mob

g) mob ntshav qab zib

Organic tshuaj ntsuab rau CKD MANAGEMENT

3.3 Kev hloov ua neej nyob

Cov lus qhia dav dav txog kev hloov kho lub neej siv rautag nrho cov theem ntawm CKD. Kev hloov pauv txoj kev ua neej muaj xws li kev haus luam yeeb, txo qhov hnyav, noj ntsev tsawg (<2 g/ day), and avoidance of nephrotoxic agents.13 Patients with CKD should be encouraged to engage in physical activities compatible with cardiovascular health and tolerance (at least 30 minutes, 5 times per week).10 Smoking is associated with a higher rate of CKD progression.25 Smoking cessation will reduce the risk of CKD progression as well as cardiovascular risk. Dietary input from a dietitian may help in providing advice regarding a low-salt and low-potassium diet (Table 11). 

3.4 Ntshav siab thiab proteinuria

Kev tswj hwm BP thiab txo cov proteinuria yog 2 qhov tseem ceeb tshaj plaws hauv kev ncua CKD kev loj hlob thiab txo qis kev pheej hmoo ntawm cov hlab plawv hauv cov neeg mob CKD.20 Tshwj xeeb, kev tswj ntshav siab, uas muaj nyob hauv ntau dua 80% ntawm cov neeg mob CKD, feem ntau tsis zoo rau cov neeg mob no. 14 Ntau qhov kev tshawb fawb thiab cov lus qhia tau tawm tswv yim rau kev tswj hwm BP nruj rau cov neeg mob CKD. Tsis tas li ntawd, BP lub hom phiaj sib txawv rau cov neeg mob ntshav qab zib mellitus thiab cov tsis muaj. Lub hom phiaj BP rau cov neeg mob ntshav qab zib yog<130/80 mmHg, which has been shown to reduce the risk of CKD progression. This finding is supported by the RENAAL study revealing that patients who achieved a systolic BP <130 mmHg had a significantly lower risk of ESRD or mortality26 and further supported by the ADVANCE-ON trial where mortality benefits were observed in diabetic patients treated with BP-lowering therapy.27 For non-diabetic patients with CKD, the target is <140/90 mmHg if the patient's proteinuria is less than 1 g per day and <130/80 mmHg when proteinuria is more than 1 g per day.13 Any antihypertensive can be used to control BP in patients with CKD. 

The most critical issue in prescribing antihypertensive medications is probably medication adherence.28 A renin-angiotensin system (RAS) blockade by way of an angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II receptor blocker (ARB) is the preferred first-line option for those with diabetic kidney disease or those with heavy proteinuria (proteinuria >1 g ib hnub twg).13 RAS blockade tau pom tias txo cov proteinuria thiab muaj cov txiaj ntsig ntawm kev ua kom qeeb ntawm CKD ywj siab ntawm BP tswj.23 qhov txiaj ntsig no tau txais kev txhawb nqa los ntawm RENAAL txoj kev tshawb fawb thiab IDNT kev tshawb fawb. Nco ntsoov tias kev saib xyuas lub raum profile thiab cov tshuaj poov tshuaj nyob rau hauv 2-4 lub lis piam tom qab pib ntawm ACEI lossis ARB lossis 2 lub lis piam ntawm kev nce koob tshuaj yog qhov tseem ceeb. Ntxiv mus, kev sib txuas ACEi thiab ARB tsis pom zoo, vim tias muaj teeb meem ntau dua yam tsis muaj txiaj ntsig meej.1

3.5 Glycemic tswj

Lub hom phiaj tswj glycemic tam sim no yog HbA1C ntawm 6.5% mus rau 7.0%.1,10,13 Kev tswj hwm qhov zoo HbA1c txo qis kev pheej hmoo ntawm cov hlab plawv, nrog rau kev txhim kho albuminuria thiab poob ntawm lub raum ua haujlwm dhau sijhawm.1 Cov txiaj ntsig ntawm kev tswj ntshav qab zib nruj yuav tsum tau ntsuas qhov kev pheej hmoo ntawm hypoglycemia, tshwj xeeb tshaj yog rau cov neeg laus thiab cov neeg mob uas muaj CKD ntau dua. Cov tshuaj yuav tsum tau tshuaj xyuas tsis tu ncua, thiab cov koob tshuaj yuav tsum tau hloov kho raws li eGFR, tshwj xeeb tshaj yog siv sulfonylurea (hypoglycemia) thiab metformin (lactic acidosis).

Tsis ntev los no, SGLT2 inhibitors tau pom tias muaj kev tiv thaiv lub raum. Kev sim 2019 CREDENCE tau pom tias kev kho nrog canagliflozin rau cov neeg mob uas muaj ntshav qab zib hom 2 thiab albuminuric CKD theem 1-3 (qhov nruab nrab eGFR 56 ml / min) tau cuam tshuam nrog kev txo qis ntawm ESRD, txo qis ntawm CKD, thiab qis dua. ntawm cov xwm txheej hauv plawv.25 Qhov kev sim DAPA-CKD kuj tau lees paub cov txiaj ntsig ntawm SGLT2 inhibitors hauv cov neeg mob CKD (nruab nrab eGFR 43 ml / min) txawm hais tias muaj lossis tsis muaj ntshav qab zib. Hauv qhov kev sim no, kev siv dapagliflozin tau pom tias yuav ncua qhov kev loj hlob ntawm CKD thiab txo qhov kev pheej hmoo ntawm ESRD nrog rau kev pheej hmoo ntawm kev tuag los ntawm lub raum lossis cov hlab plawv.29 Ib yam li ntawd, hauv EMPA-REG txoj kev tshawb fawb, kev siv empagliflozin kuj. txhim kho cov txiaj ntsig ntawm cov hlab plawv ntawm cov neeg mob ntshav qab zib mellitus nrog CKD ( nruab nrab eGFR 70-80} ml / min).

3.6 Dyslipidemia

Dyslipidaemia is a major risk factor for a cardiovascular event. All patients with newly diagnosed CKD should have a lipid profile evaluation. In adults aged >50 years with CKD not on RRT, treatment with lipid-lowering therapy is recommended. This suggestion is supported by the SHARP trial, in which statin plus ezetimibe therapy led to a significant 17% reduction in the relative hazard of the primary outcome involving a major atherosclerotic event. In adults aged 18-49 years with CKD not on RRT, lipid-lowering therapy is recommended if the patient has 1 of the following conditions: known coronary artery disease, diabetes mellitus, prior ischaemic stroke, or 10-year risk of cardiovascular event >10%.31 

3.7 Risk rau AKI thiab kab mob

Cov neeg mob nrog CKD muaj kev pheej hmoo siab ntawm kev tsim AKI thiab kis kab mob. Txhua ntu ntawm AKI yuav txo qis tus naj npawb ntawm cov nephrons siv tau thiab ua kom qhov kev loj hlob ntawm CKD. Kev kis kab mob thiab cov tshuaj nephrotoxic yog qhov muaj feem cuam tshuam rau AKI.25 Ib qho kev txiav txim siab tseem ceeb suav nrog kev txheeb xyuas tus neeg mob uas muaj kev pheej hmoo ntawm AKI (hypovolemia, sepsis), kev tswj hwm tshuaj zoo, kev txhaj tshuaj tiv thaiv kab mob, thiab kev saib xyuas ntawm GFR.20 Kev rho tawm metformin, SGLT2 inhibitors, los yog ACEi/ARB raug pom zoo yog tias tus neeg mob muaj kev pheej hmoo ntawm lub cev qhuav dej lossis hypovolaemic, piv txwv li, muaj mob raws plab lossis ntuav, tshwj xeeb tshaj yog tias tus neeg mob yuav tsum tau mus pw hauv tsev kho mob.23 Tshwj tsis yog txwv tsis pub, cov neeg mob CKD yuav tsum tau txhaj tshuaj tiv thaiv kab mob khaub thuas txhua xyoo.

4.0 Kev tswj cov teeb meem ntawm CKD

4.1 Ntshav Qab Zib

Anemia txhais tau tias yog qib hemoglobin<13 g/dl in men and <12 g/dl in women.10 As CKD progresses, patients are at increased risk of developing anemia, as erythropoietin production decreases with a low GFR. It is recommended that patients with stage 3 CKD should have their hemoglobin level measured at least annually or even more frequently as renal function declines. Anemia usually starts to develop when GFR <60 ml/ min/1.73 m2. The treatment of anemia in CKD includes iron supplementation, the use of an erythropoietin-stimulating agent (ESA), and blood transfusion. All CKD patients with iron deficiency should be treated with iron supplementation. Once iron deficiency has been corrected, the use of an ESA can be considered after discussion with a nephrologist. The optimal Hb target in CKD is 10-12 g/dl. 

4.2 Mineral kab mob

CKD-mineral and bone disorder (CKD MBD) yog ib qho teeb meem ntawm CKD. Cov neeg mob uas muaj CKD theem 3 thiab siab dua yuav tsum tsawg kawg muaj cov tshuaj calcium, phosphate, alkaline phosphatase, thiab parathyroid hormone (PTH) ntsuas txhua xyoo - lossis ntau zaus yog tias muaj qhov txawv txav. Lub hauv paus ntsiab lus ntawm kev kho mob rau CKD-MBD yog phosphate theem txo mus rau ib txwm theem.10 Kev kho mob pib pib nrog kev txwv tsis pub noj phosphate thaum phosphate thiab PTH qib pib nce. Kev txwv kev noj zaub mov phosphate kuj suav nrog kev noj zaub mov tsis muaj protein ntau. Cov neeg mob uas tuaj yeem ua raws li kev noj zaub mov tsis muaj protein ntau feem ntau yuav pom cov phosphate qis dua.32 Kev kho tshuaj nrog phosphate binders yuav tsum raug txiav txim siab yog tias tus neeg mob pom tias muaj kev pheej hmoo ntawm hyperphosphatemia txawm tias muaj kev txwv kev noj haus. Tshaj calcium ntxiv thiab vitamin D analog yuav tsum tau zam, vim tias qhov kev sib xyaw ua ke no yuav ua rau muaj kev pheej hmoo ntawm vascular calcification.

4.3 Cov kua dej ntau dhau

Kev loj hlob ntawm CKD ua rau cov neeg mob muaj kev pheej hmoo ntawm kev tsim cov kua dej ntau dhau, feem ntau yog vim txo qis zis. Yog li, kev ntsuas cov kua dej hauv qhov chaw kho mob yog qhov tseem ceeb, nrhiav cov tsos mob thiab cov tsos mob ntawm cov kua dej ntau dhau xws li kev tswj tsis tau BP, tsa jugular venous siab, crepitations hauv ntsws, thiab pedal edema. Cov neeg mob uas muaj cov kua dej ntau dhau tuaj yeem kho nrog cov kua dej thiab ntsev txwv thiab voj diuretics.1

4.4 Kev pheej hmoo mob plawv

Tsawg GFR, proteinuria, thiab CKD-MBD nrog vascular calcifications tag nrho tau cuam tshuam nrog kev mob plawv thiab kev tuag.33 Kev tswj hwm kev pheej hmoo plawv hauv cov neeg mob CKD zoo ib yam li cov uas tsis muaj CKD, suav nrog BP tswj, glycemic tswj, thiab lipid- txo txoj kev kho. Kev kho mob antiplatelet yuav tsum tau muab tsuas yog kev tiv thaiv theem nrab vim tias muaj kev pheej hmoo los ntshav hauv pawg neeg mob no ntau ntxiv. cov kws kho mob. Kev kho mob ntawm CKD ntsig txog metabolic acidosis nrog qhov ncauj alkali tau pom tias yuav ncua CKD kev loj hlob. Piv txwv li, sodium bicarbonate tuaj yeem pib thaum tus neeg mob cov ntshav qab zib tsawg dua 22 mmol / L.1,34.

Kev xaus lus xaus, CKD yog ib qho teeb meem tshwm sim hauv kev saib xyuas thawj zaug uas nws qhov muaj feem yuav nce ntxiv raws li cov neeg laus thiab cov muaj feem cuam tshuam nrog CKD. Tus kab mob no feem ntau asymptomatic nyob rau hauv nws cov theem pib. Cov kws kho mob thawj zaug ua lub luag haujlwm tseem ceeb hauv kev txheeb xyuas thiab tshuaj xyuas cov neeg mob uas muaj kev pheej hmoo, tsim kom muaj qhov ua rau CKD, thiab tswj cov neeg mob thaum ntxov ntawm CKD raws li. Kev xa mus rau tus kws kho mob nephrologist yuav tsim nyog los txheeb xyuas qhov tseem ceeb ntawm CKD rau kev kho mob tshwj xeeb. Cov neeg uas muaj CKD ntau dua yuav tsum raug xa mus rau kev saib xyuas tom tsev tam sim ntawd kom qeeb qhov kev loj hlob mus rau ESRD thiab npaj tus neeg mob rau RRT mus sij hawm ntev.

Kev tsis sib haum xeeb Cov neeg sau ntawv tshaj tawm tias lawv tsis muaj kev tsis sib haum xeeb ntawm kev txaus siab.

Nyiaj txiag Cov neeg sau ntawv tsis tau txais kev pab nyiaj txiag rau qhov kev tshaj tawm no.

Kev lees paub Peb xav ua tsaug rau Tus Thawj Saib Xyuas Kev Noj Qab Haus Huv ntawm Malaysia rau nws qhov kev tso cai los luam tawm tsab xov xwm no.

Cov ntaub ntawv

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2. Hill NR, Fatoba ST, Oke JL, et al. Ntiaj teb no muaj feem ntau ntawm cov kab mob raum mob ib tug systematic tshuaj xyuas thiab meta-analysis. PLoS Ib. Xyoo 2016; 11:e0158765. doi: 10.1371 / phau ntawv journal. ib.0158765

3. Mills KT, Xu Y, Zhang W, et al. Kev txheeb xyuas cov ntaub ntawv thoob ntiaj teb cov pej xeem raws li lub nra hnyav thoob ntiaj teb ntawm cov kab mob raum nyob rau xyoo 2010. Raum Int. 2015; 88:950–957. doi: 10.1038/ki.2015.230

4. Hooi LS, Ong LM, Ahmad G, et al. Ib txoj kev tshawb nrhiav pej xeem ntsuas kev nthuav dav ntawm cov kab mob raum ntev ntawm cov neeg laus hauv West Malaysia. Raum Int. 2013; 84(5):{5}}. doi:10.1038/ ki.2013.220 5. Saminathan TA, Hooi LS, Mohd Yusoff M, et al. Feem ntau ntawm cov kab mob raum ntev thiab nws cov teeb meem cuam tshuam hauv Malaysia; kev tshawb pom los ntawm kev tshawb fawb thoob teb chaws-raws li kev tshawb fawb hla ntu. BMC NPE. Xyoo 2020; 21:344. doi: 10.1186/s12882-020-01966-8.

6. Malaysian Society of Nephrology. Tshooj 2, 26th Tshaj Tawm ntawm Malaysian Dialysis thiab Transplant Registry 2018. National Renal Registry.

7. Lub Tsev Haujlwm Saib Xyuas Kev Noj Qab Haus Huv 2020. National Health and Morbidity Survey (NHMS) 2019: Cov kab mob tsis sib kis, kev xav tau kev noj qab haus huv, thiab kev paub txog kev noj qab haus huv - kev tshawb pom tseem ceeb; Lub Tebchaws Malaysia; 2020. 40 Nws.

8. Surendra NK, Abdul Manaf MR, Hooi LS, et al. Kev txheeb xyuas tus nqi hluav taws xob ntawm kev kho mob raum raum kawg hauv Ministry of Health dialysis centers, Malaysia: hemodialysis tiv thaiv kev mob ntshav qab zib tsis tu ncua peritoneal dialysis. PLoS Ib. 23 Lub Ob Hlis 2019; 14(10):e0218422. doi: 10.1371/journal.pone.0218422

9. Ismail H, Abdul Manaf MR, Abdul Gafor AH, et al. Lub nra nyiaj txiag ntawm ESRD ntawm Malaysian kev saib xyuas kev noj qab haus huv [tso tawm kev kho tshwm sim hauv Raum Int Rep. 2019 Kaum Ob Hlis 03; 4(12): 1770]. Raum Int Rep. 2019 Lub Tsib Hlis 29; 4(9): 1261–1270. doi: 10.1016/j. xov.2019.05.016

10. KDIGO Group. KDIGO 2012 daim ntawv qhia kev kho mob rau kev soj ntsuam thiab kev tswj cov kab mob raum ntev. Raum Int. Xyoo 2013; 3: 1.