Kev Tswj Cov Ntshav Qab Zib hauv Cov Neeg Mob Mob Raum Ntshav Qab Zib: Cov ntsiab lus ntawm Lub Koom Haum Koom Tes ntawm British Clinical Diabetologists Thiab UK Kidney Association (ABCD-UKKA) Cov Lus Qhia 2021
Jul 08, 2022
Diabetic kidney disease (DKD) accounts for >40 feem pua ntawm cov neeg mob raum mob ntev (CKD) thoob ntiaj teb. Ntshav siab yog ib qho tseem ceeb ntawm kev pheej hmoo rau kev loj hlob ntawm DKD thiab qhov tshwm sim siab ntawm cov kab mob plawv thiab kev tuag ntawm cov neeg no. Kev tswj xyuas kom zoo ntawm kev kub siab yog, yog li ntawd, tseem ceeb heev kom txo qis kev loj hlob ntawm DKD thiab txo qis kev pheej hmoo ntawm cov hlab plawv. Randomized tswj cov pov thawj sib txawv hauv hom 1 thiab hom 2 mob ntshav qab zib thiab nyob rau theem sib txawv ntawm DKD raws li lub hom phiaj ntshav siab (BP). Renin-angiotensin thaiv cov neeg ua haujlwm txo qis ntawm DKD thiab cov xwm txheej hauv plawv hauv ob hom ntshav qab zib hom 1 thiab hom 2, txawm tias txawv raws li theem ntawm CKD. Muaj cov pov thawj tshwm sim rau cov txiaj ntsig ntawm sodium-glucose cotransporter 2, nonsteroidal xaiv mineralocorticoid antagonists, thiab endothelin-A receptor antagonists hauv kev ua kom qeeb thiab txo cov xwm txheej hauv plawv hauv DKD. Qhov no UK cov lus qhia, tsim ua ke los ntawm cov kws kho mob ntshav qab zib thiab cov kws kho mob nephrologist, tau tshuaj xyuas tag nrho cov pov thawj tam sim no hais txog kev tswj cov ntshav siab hauv DKD los tsim cov txheej txheem qhia txog tus kheej rau kev tswj hwm BP thiab kev siv cov tshuaj tiv thaiv kab mob raws li hnub nyoog, hom ntshav qab zib, thiab theem ntawm CKD (https://ukkidney.org/sites/renal.org/fifiles/Management-of-hypertension-and-RAAS-blockade-in-adults-with-DKD.pdf). Cov ntsiab lus luv luv ntawm cov lus qhia, suav nrog ib qho infographic, tau nthuav tawm ntawm no.
Nyem rau Cistanche bioflavonoids ntsiav tshuaj rau mob raum
Cov neeg mob ntshav qab zib mellitus thiab CKD muaj kev pheej hmoo ntawm kev mob ntxov ntxov thiab tuag taus piv nrog cov tsis muaj cov mob no; Feem ntau muaj feem cuam tshuam nrog cov xwm txheej ntawm cov hlab plawv, xws li mob plawv, mob plawv, thiab mob stroke, uas, kub siab yog ib qho kev pheej hmoo hloov pauv tau.1 Cov kab mob hauv lub raum kawg yog lwm qhov teeb meem, kho hauv ib feem los ntawm kev kub siab, thiab cuam tshuam nrog cov neeg pluag. Lub neej zoo, ntau lub tsev kho mob nkag, thiab lub nra hnyav ntxiv rau cov kev kho mob uas twb muaj lawm thoob plaws ntiaj teb.2,3
Debasish Banerjee 1, Peter Winocour 2, Tahseen A. Chowdhury 3, Parijat De 4, Mona Wahba5, Rosa Montero 6, Damian Fogarty 7, Andrew Frankel 8, Gabrielle Goldet 8, Janaka Karalliedde9, Patrick B. Mark10, Dipesh Pokraj1111 , Adnan Sharif13, Sagen Zac-Varghese2, Stephen Bain14, thiab Indranil Dasgupta13; sawv cev ntawm lub koom haum ntawm British Clinical Diabetologists thiab UK raum Association
1 St. George's Hospitals NHS Foundation Trust, London, UK; 2 ENHIDE, East thiab North Hertfordshire NHS Trust, Stevenage, UK; 3 Royal London Tsev Kho Mob, London, UK; 4 Lub Tsev Kho Mob Hauv Nroog, Birmingham, UK; 5 St. Helier Tsev Kho Mob, Carshalton, UK; 6 King's College, London, UK; 7 Belfast Health and Social Care Trust, Belfast, UK; 8 Imperial College Healthcare NHS Trust, London, UK; 9 Guy's and St Thomas' Hospital, London, UK; 10University of Glasgow, Glasgow, UK; 11Royal Free London NHS Foundation Trust, London, UK; 12West Hertfordshire Tsev Kho Mob, Hertfordshire, UK; 13 Department of Renal Medicine, Heartlands Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK; thiab 14Swansea University Medical School, Swansea; UK
Nrog rau kev nce thoob ntiaj teb kev mob ntshav qab zib hom 2, DKD tau tshwm sim los ua ib qho tseem ceeb rau lub nra ntawm cov kab mob thoob ntiaj teb.4 Qhov no tau nyiam kev tshawb fawb nrog cov neeg ua haujlwm tshiab xws li sodium-glucose co-transporter 2 inhibitors thiab nonsteroidal mineralocorticoid receptor antagonists nyob rau xyoo tas los no. . Cov neeg sawv cev tshiab no tau pom los txhim kho cov txiaj ntsig cardiorenal nrog rau cov nyhuv BP-txo qis.5,6
Lub hom phiaj ntawm kev kho thiab cov neeg sawv cev siv rau kev tswj hwm BP hauv cov neeg nrog DKD tau hloov zuj zus hauv 40 xyoo dhau los. Cov neeg ua haujlwm uas inhibit renin-angiotensin-aldosterone system (RAAS) tau pom tias yuav txo qis qhov tshwm sim tsis zoo ntawm cov hlab plawv thiab dhau ntawm BP-txo cov nyhuv.7 Txawm li cas los xij, kev tswj hwm BP hnyav (systolic BP.<120 mm="" hg)="" has="" not="" been="" found="" to="" be="" associated="" with="" better="" outcomes="" than="" standard="" control="" (systolic="" bp=""><140 mm="" hg)="" in="" people="" with="" diabetes.8="" people="" with="" dkd="" are="" often="" old,="" frail,="" and="" multimorbid.="" as="" such,="" lower="" bp="" targets="" are="" likely="" to="" be="" associated="" with="" increased="" adverse="" events,="" including="" symptomatic="" postural="" hypotension,="" falls,="" fractures,="" acute="" kidney="" injury,="" and="">
Cov lus qhia hais txog qhov tseem ceeb ntawm kev ntsuas BP kom raug thiab saib xyuas, kev tswj xyuas tsis yog tshuaj, kev siv cov tshuaj uas tsim nyog, thiab BP lub hom phiaj raws li cov pov thawj muaj (Daim duab 111,12 thiab Table 1).
Txoj kev
Cov lus pom zoo yog raws li kev tshuaj xyuas cov ntaub ntawv pib thaum Lub Kaum Hli 2013 txog Lub Kaum Ob Hlis 2016 thiab kev tshuaj xyuas ntxiv kom ntxaws txog lub Plaub Hlis 2021 rau qhov hloov tshiab tam sim no. Peb tshawb fawb PubMed/MEDLINE, Cochrane Library, EMBASE, thiab Google Scholar thiab siv cov ntsiab lus tseem ceeb hauv qab no: hom 1 mob ntshav qab zib, hom 2 mob ntshav qab zib, kub siab, albuminuria, microalbuminuria, microvascular teeb meem, nephropathy, CKD, angiotensin-hloov enzyme inhibitors (ACEI) , angiotensin receptor blockers (ARBs), thiab mineralocorticoid antagonists. Cov qib kev pom zoo muaj txij li 1 (kev pom zoo) mus rau 2 (kev pom zoo tsis muaj zog), thiab cov ntaub ntawv pov thawj zoo yog raws li hauv qab no: A (cov pov thawj zoo), B (cov pov thawj tsis zoo), C (cov pov thawj tsis zoo), thiab D (cov pov thawj tsis zoo heev). Hauv thaj chaw uas tsis muaj pov thawj txaus los txhawb kev pom zoo, kev tshawb fawb ntxiv tau tawm tswv yim (Kev Tshawb Fawb Pom Zoo).
Tsis yog Pharmacological Management
Cov lus qhia pom zoo kom txo cov ntsev kom tsawg,<90 mmol="" of="" sodium="" daily=""><2 g="" of="" sodium="" or=""><5 g="" of="" sodium="" chloride="" daily),="" alcohol=""><2 units="" daily="" for="" men="" and="" 1="" unit="" daily="" for="" women,="" and="" regular="" exercise="" of="" at="" least="" 30="" minutes="" daily="" for="" 5="" days="" a="" week,="" and="" to="" maintain="" a="" body="" mass="" index="" between="" 20="" and="" 25="" kg/m2.="" these="" recommendations="" are="" based="" on="" observational="" studies="" in="" people="" with="" type="" 2="" diabetes="" and="" require="" regular="" reinforcement="" at="" each="" patient="">
Cov lus pom zoo rau kev tswj ntshav siab hauv cov neeg mob ntshav qab zib hom 1 thiab CKD G1 txog 5 (Nondialysis)
1. Hauv cov neeg mob ntshav qab zib hom 1 thiab cov zis albumin-to-creatinine ratio (ACR) ntawm #3 mg/mmol), peb pom zoo kom muaj qhov pib rau BP kev kho mob ntawm ib qho kev pheej hmoo siab (sab lossis sawv) BP uas yog $ 140/90 mm. Hg (1B)*
In children and adolescents with type 1 diabetes, the threshold for high BP is an average systolic BP and/or diastolic BP greater than the 95th percentile for the person's sex, age, and height on >3 lub sijhawm (1B).**
2. Peb pom zoo tias kev kho ACEI yuav tsum tau siv los ua ib tus neeg saib xyuas thawj zaug rau kev txo qis BP thiab, yog tias kev kho ACEI yog contraindicated los yog tsis zam ARBs yuav tsum raug txiav txim siab (1B).
3. In most adults with type 1 diabetes mellitus and persistent ACR >3 mg/mmol, we recommend that ACEI therapy should be considered irrespective of BP and that the target upright BP should be #130/ 80 mm Hg in younger adults (1B), but #140/90 mm Hg for those aged >65 xyoo (2D). Peb pom zoo tias koob tshuaj ACEI yuav tsum tau titrated rau qhov siab tshaj plaws (1B).
4. Tsis muaj pov thawj tam sim no los txhawb lub luag haujlwm ntawm ACEI kev kho mob rau BP tswj lossis kev tiv thaiv raum rau cov neeg mob ntshav qab zib hom 1 uas tsis muaj zog thiab muaj zis ACR #3 mg/mmol (1C).
5. Muaj qee cov pov thawj los txhawb kev siv candesartan los tiv thaiv kev txhim kho lossis kev loj hlob ntawm retinopathy hauv cov neeg mob ntshav qab zib hom 1 uas tsis muaj zog thiab muaj zis ACR #3 mg / mmol (1C).
6. Tsis muaj pov thawj ruaj khov los txhawb lub luag haujlwm ntawm ob qhov thaiv ntawm RAAS hauv cov neeg mob ntshav qab zib hom 1 (1C).
7. Peb pom zoo kom cov neeg mob ntshav qab zib hom 1 yuav tsum tau qhia kom tuav cov tshuaj RAAS-thaiv thaum lub sijhawm muaj mob hnyav (1C).
8. Peb pom zoo kom cov poj niam uas muaj hnub nyoog yug me nyuam yuav tsum tau txhawb kom tuav cov tshuaj RAAS-txhim kho ua ntej txiav txim siab cev xeeb tub (1B).
The guideline recommends tight control of BP in those with signifificant proteinuria. Proteinuria in type 1 diabetes is strongly associated with progression to stage G3 CKD (32% in 10 years) and end-stage kidney disease (16% in 10 years); treatment of hypertension slows progression and alongside glycemic control can induce regression of proteinuria with a decreased risk of declining glomerular filtration rate.14 The recommended BP target in people with type 1 diabetes with ACR >3 mg / mmol yog<130 0="" mm="" hg,="" whereas="" the="" target="" is=""><140 0="" mm="" hg="" when="" acr="" is="" #3="" mg/mmol.="" the="" threshold="" for="" treatment="" and="" targets="" in="" children="" is="" lower,="" as="" illustrated="" in="" figure="" 1.="" the="" results="" of="" the="" pittsburgh="" edc="" study's="" 25-year="" follow-up="" study="" support="" a="" target="" bp="" of="" 120/80="" mm="" hg="" in="" childhood-onset="" type="" 1="" diabetes.15="" nevertheless,="" for="" older="" adults,="" the="" targets="" are="" higher="" at="" 130="" to="" 139="" mm="" hg="" systolic.16="" on="" the="" basis="" of="" the="" evidence="" from="" short-term="" randomized="" controlled="" trials,="" the="" guideline="" recommends="" acei="" as="" the="" initial="" treatment="" of="" hypertension="" and="" for="" proteinuria="" without="" hypertension="" and="" arbs="" if="" acei="" are="" not="" tolerated.17="" acei="" should="" not="" be="" used="" in="" normotensive="" individuals="" without="" proteinuria="" nor="" during="" pregnancy="" and="" needs="" to="" be="" temporarily="" withheld="" during="" an="" acute="" illness.="" there="" is="" no="" evidence="" to="" support="" the="" use="" of="" acei="" and="" arb="" together.="" control="" of="" bp="" long-term="" is="" more="" critical="" than="" the="" use="" of="" a="" specific="" raas-blocking="">
Cov lus pom zoo rau kev tswj ntshav siab thiab RAAS Inhibitor hauv cov neeg mob ntshav qab zib hom 2 thiab CKD G1 txog 3
1 Hauv cov neeg mob ntshav qab zib hom 2 thiab ntshav siab, peb pom zoo kom noj ntsev<90 mmol="" per="" day=""><2 g="" per="" day="" of="" sodium—equivalent="" to="" 5="" g="" of="" sodium="" chloride)="">
2. Hauv cov neeg uas muaj hom 2 mob ntshav qab zib mellitus, CKD, thiab zis ACR # 3 mg / mmol, peb xav kom lawv lub hom phiaj ncaj ncees BP yuav tsum yog<140 0="" mm="" hg,="" using="" antihypertensive="" therapy="" in="" the="" maximum="" tolerated="" doses="">
3. In people with type 2 diabetes mellitus, CKD, and urine ACR >3 mg / mmol, peb xav kom tsom mus rau lub hom phiaj upright BP uas tsis tu ncua<130 0="" mm="" hg,="" using="" antihypertensive="" therapy="" in="" the="" maximum="" tolerated="" doses="">
4. Tsis muaj pov thawj los txhawb ACEI lossis ARB txoj kev kho raws li thawj kab BP-txo cov kab mob hauv kev sib piv nrog lwm cov tshuaj tiv thaiv kab mob hauv cov neeg mob ntshav qab zib hom 2, lub raum ua haujlwm tsis zoo, thiab cov zis ACR (# 3 mg / mmol) ( 1A).
5. We suggest that ACEIs (or ARBs if ACEIs are not tolerated) should be preferentially used in people with type 2 diabetes mellitus and CKD who have urine ACR >3 mg / mmol. Peb pom zoo tias koob tshuaj ACEI (los yog ARB) yuav tsum tau titrated rau qhov siab tshaj plaws (2D).
6. Tam sim no tsis muaj pov thawj los txhawb lub luag haujlwm hauv tsev lossis kev saib xyuas BP hauv cov neeg mob ntshav qab zib hom 2 thiab CKD theem G2 thiab G3 (1D).
7. Tam sim no tsis muaj pov thawj los txhawb lub luag haujlwm ntawm ob qhov thaiv ntawm RAAS hauv cov neeg mob ntshav qab zib hom 2 thiab CKD theem G1 txog G3 (1B).
8. Upright BP lub hom phiaj yuav tsum tau teem rau tsis muaj<150 0="" mm="" hg="" in="" those="" with="" type="" 2="" diabetes="" mellitus="" who="" are="" aged="" $75="" years="">
9. Peb pom zoo kom cov neeg uas muaj hom 2 mob ntshav qab zib mellitus yuav tsum tau qhia kom tuav RAAS-thaiv cov tshuaj thaum lub sij hawm muaj mob hnyav thiab rov pib dua 24 mus rau 48 teev tom qab rov zoo los ntawm tus kab mob (1C).
Cov lus pom zoo rau kev tswj ntshav siab thiab RAAS Inhibitor hauv Cov Neeg Mob Ntshav Qab Zib Hom 2 thiab CKD G4 thiab 5 (Nondialysis)
1 We recommend initiation of antihypertensive agents in people with diabetes, CKD stages G4 and G5, and ACR #3 mg/mmol when BP is >140/90 mm Hg thiab tsom rau BP ntawm<140 0="" mm="" hg="" during="" therapy="">
2. We suggest initiation of antihypertensive agents in people with diabetes, CKD stages G4 and G5, and ACR >3 mg/mmol when BP is >130/80 mm Hg thiab tsom rau lub hom phiaj BP<130 0="" mm="" hg="">
3. Peb pom zoo kom siv ACEI (ARB yog tias tsis kam rau ACEI) ua tus thawj xaiv BP-txo tus neeg sawv cev rau cov neeg mob ntshav qab zib, CKD theem 4 thiab 5, thiab micro/ macroalbuminuria (1B).
4. Peb tsis pom zoo kom siv kev sib txuas ntawm ACEIs thiab ARBs hauv cov neeg mob ntshav qab zib thiab CKD theem G4 thiab G5 (2B).
5. Peb muab tswv yim txog kev noj haus, kho cov kua qaub, thiab kho cov kab mob diuretic kom txo cov poov tshuaj hauv cov ntshav raws li qhov tsim nyog rau cov neeg mob ntshav qab zib mellitus thiab CKD theem G4 thiab G5 rau kev siv ACEI (lossis ARB) zoo (tsis suav).
6. Xav txog kev siv cov tshuaj potassium binders tshiab rau cov neeg mob ntshav qab zib thiab CKD theem G3b txog G5 (nondialysis) yog tias qib poov tshuaj yog 6 mmol / l lossis siab dua, rau kev siv ACEi (lossis ARB), txuas ntxiv thiab nyab xeeb rau cov neeg. tsis noj lossis tsuas yog noj cov tshuaj RAAS nkaus xwb vim yog hyperkalemia (tsis suav).
Cov lus pom zoo rau CKD theem G1 txog G3 thiab G4 thiab G5 (nondialysis) zoo ib yam, nrog qhov sib txawv me me raws li tau hais dhau los. Rau cov neeg uas muaj ACR # 3 mg / mmol, peb pom zoo kom lub hom phiaj BP ntawm<140 90="" mm="" hg="" and=""><130 0="" mm="" hg="" if="" the="" acr="" is="">3 mg/ mmol. There is no good evidence for tighter BP control, though such evidence exists in people without diabetes.8,18 The guideline suggests the use of ACEI or ARB as the fifirst-choice antihypertensive agent in the presence of signifificant proteinuria, that is, ACR >3 mg/ mmol titrating to maximum dose tolerated,19 but not in the absence of signifificant proteinuria.20 Nevertheless, the guideline recommends against the use of dual ACEI and ARB therapy owing to evidence suggesting the absence of benefits and the risk of potential harm mainly owing to hyperkalemia.21 For older people (>75 xyoo) nrog DKD, uas feem ntau qaug zog thiab raug kev txom nyem ntau dua ntawm kev kho mob ntshav siab, lub hom phiaj yog<150 mm="" hg="" systolic,="" which="" is="" supported="" by="" evidence="" from="" the="" stop="" hypertension="" trial.20,22="" hyperkalemia="" is="" common="" in="" patients="" with="" ckd="" with="" diabetes,="" particularly="" when="" in="" raas="" blockade.23="" the="" novel="" potassium="" binders="" may="" be="" used="" in="" patients="" with="" dkd="" with="" hyperkalemia="" related="" to="" raas="" blockade.="" in="" people="" with="" diabetes="" and="" ckd="" stages="" 3="" to="" 4,="" on="" raas="" blockade="" (acei/arb="" ="" spironolactone),="" the="" use="" of="" a="" novel="" potassium="" binding="" polymer,="" patiromer,="" resulted="" in="" a="" signifificant="" decrease="" in="" serum="" potassium="" maintained="" in="" 52="">
Cov lus pom zoo rau kev tswj ntshav siab thiab RAAS Inhibitor hauv cov tib neeg muaj ntshav qab zib nyob ntawm Dialysis
1 Peb pom zoo tias yuav tsum siv qhov ntsuas BP hauv tsev lossis kev ntsuas BP los saib xyuas BP hauv cov neeg mob ntshav qab zib mellitus (1C).
2. Yog tias kev ntsuas BP hauv tsev lossis hauv tsev tsis muaj peev xwm saib xyuas BP hauv cov neeg mob ntshav qab zib mellitus, peb xav kom siv cov kev ntsuas BP ua ntej, intra-, thiab post-dialysis standardized BP rau cov neeg uas nyob rau hauv hemodialysis thiab siv standardized clinic BP. Kev ntsuas rau cov neeg uas nyob rau hauv peritoneal dialysis (2D).
3. Peb pom zoo kom ntim ntim raws li kev tswj hwm thawj kab txhawm rau txhim kho BP tswj cov neeg mob ntshav qab zib mellitus (1B).
4. Peb xav kom ntsev txwv rau<5 g="" per="" day="" to="" optimize="" bp="" control="" in="" people="" with="" diabetes="" who="" are="" on="" dialysis="">
5. Peb xav kom lub hom phiaj upright interdialytic BP ntawm<140 0="" mm="" hg="" for="" people="" with="" diabetes="" who="" are="" on="" dialysis.="" individualization="" of="" the="" bp="" target="" may="" be="" indicated="" in="" other="" people="" who="" are="" burdened="" with="" multiple="" comorbidities="" to="" reduce="" adverse="" events="" of="" bp="" lowering="">
6. Peb pom zoo tias yuav tsum zam kom tsis txhob muaj ntshav qab zib intradialytic hauv cov neeg mob ntshav qab zib mellitus (1B).
7. Peb xav kom siv ACEIs lossis ARBs (tab sis tsis ua ke), beta-blockers, thiab calcium channel blockers kom txo tau cov kab mob plawv hauv cov neeg mob ntshav qab zib thiab ntshav siab uas tau lim ntshav (2B).
8. Peb pom zoo kom siv cov tshuaj diuretics kom tshem tawm cov kua dej thiab kev tswj BP hauv cov neeg mob ntshav qab zib mellitus uas tau lim ntshav thiab muaj lub raum tsis ua haujlwm (2C).
randomized tswj cov pov thawj los qhia kev tswj BP hauv cov neeg mob ntawm kev lim ntshav, tshwj xeeb tshaj yog cov neeg mob ntshav qab zib, yog qhov tsis txaus. Yog li ntawd, ntau cov lus pom zoo nyob rau hauv nqe lus no tsis muaj zog thiab raws li cov ntaub ntawv pov thawj qis-rau-zoo heev. Kev saib xyuas BP kom raug yog qhov nyuaj rau cov neeg mob ntshav qab zib ntawm kev lim ntshav vim qhov hloov pauv ntawm cov xwm txheej thiab muaj cov kab mob autonomic neuropathy hauv ntau. Cov ntaubntawv povthawj siv tau zoo tshaj plaws uas cuam tshuam nrog 24- teev BP kev soj ntsuam yog interdialytic home BP recordings.25 Li no, cov lus qhia pom zoo kom siv BP hauv tsev rau kev saib xyuas nrog interdialytic BP lub hom phiaj ntawm<140 0="" mm="" hg.="" meticulous="" fluid="" volume="" management="" is="" suggested="" as="" the="" fifirst="" step="" in="" the="" management="" of="" hypertension="" in="" patients="" on="" dialysis.="" a="" randomized="" controlled="" trial="" of="" 150="" patients="" on="" hemodialysis="" randomized="" to="" an="" additional="" ultrafiltration="" group="" (40="" of="" 100="" had="" diabetes)="" or="" control="" group="" (19="" of="" 50="" had="" diabetes)="" revealed="" improved="" bp="" with="" volume="" control.26="" the="" guideline="" advises="" avoidance="" of="" intradialytic="" hypotension="" as="" it="" is="" associated="" with="" increased="" mortality="" in="" patients="" on="" hemodialysis.27="" there="" is="" insufficient="" evidence="" from="" randomized="" controlled="" trials="" to="" make="" firm="" recommendations="" on="" the="" choice="" of="" antihypertensive="" medication.="" beta-blockers,="" raas-blocking="" agents,="" and="" dihydropyridine="" calcium="" channel="" blockers="" are="" all="" reasonable="" choices.="" diuretics="" may="" be="" used="" in="" the="" patients="" to="" help="" with="" fluid="" removal="" in="" those="" individuals="" with="" residual="" renal="" function28="" (table="">
Cov Lus Qhia Tseem Ceeb Tshawb Fawb
Cov cheeb tsam hauv qab no tsis muaj pov thawj zoo rau kev tswj cov ntshav siab hauv cov neeg nrog DKD thiab yog li kev tshawb fawb ntxiv yog tsim nyog.
1. Puas muaj lub luag haujlwm rau kev saib xyuas BP hauv tsev lossis kev saib xyuas BP hauv kev kuaj mob thiab tswj cov ntshav siab hauv cov neeg mob ntshav qab zib hom 1, tshwj xeeb tshaj yog rau cov neeg mob ntshav qab zib autonomic neuropathy?
2. Puas yog nruj glycemic tswj thiab BP-txo qis txo qhov tshwm sim ntawm cov neeg tsim cov teeb meem microvascular hauv hom 1 mob ntshav qab zib?
3. Dab tsi yog qhov cuam tshuam rau lub raum ua haujlwm ntawm qis BP lub hom phiaj hauv cov neeg hluas uas muaj ntshav qab zib hom 1 thiab nephropathy?
4. Lub luag haujlwm ntawm aldosterone receptor blockers hauv cov neeg mob ntshav qab zib hom 1 thiab nephropathy yog dab tsi?
5. Dab tsi yog qhov pov thawj-raws li kev txwv qis rau BP txo (<130 0="" mm="" hg)="" in="" people="" with="" type="" 2="" diabetes="" who="" have="" ckd="" in="" terms="" of="" cardiovascular="" and="" renal="">
6. Dab tsi yog qhov zoo tshaj plaws thib ob thiab thib peb cov kab mob BP-txo qis hauv cov neeg mob ntshav qab zib hom 2 uas muaj CKD thiab proteinuria?
7. Puas yog kev kho mob ntshav siab thaum pw tsaug zog txhim kho cov hlab plawv thiab lub raum hauv cov neeg mob ntshav qab zib hom 2 thiab CKD?
8. Qhov kev ntsuas BP twg yuav tsum tau siv los kwv yees tus mob sab laug ventricular hypertrophy thiab kev tuag ntawm cov neeg mob ntshav qab zib uas tau lim ntshav: predialysis, pre-dialysis, tsev, lossis ambulatory BP ntsuas?
9. Dab tsi yog qhov zoo tshaj plaws upright BP lub hom phiaj rau cov neeg mob ntshav qab zib uas tau lim ntshav?
10. Puas yog kev kho mob nrog ACEIs, ARBs, beta-blockers, lossis calcium channel blockers kom txo BP hauv cov neeg mob ntshav qab zib uas tau lim ntshav txo cov hlab plawv thiab kev tuag?
11. Puas yog ntsev txwv (<5 g="" per="" day)="" in="" people="" with="" diabetes="" who="" are="" on="" dialysis="" influence="" bp="" control="" or="" cardiovascular="">
Xaus
Cov lus pom zoo hauv Lub Koom Haum Koom Tes ntawm British Clinical Diabetologists thiab UK Lub Koom Haum Raum Cov Txheej Txheem muab cov lus qhia uas txhawb nqa kev kho tus kheej nrog BP lub hom phiaj uas txawv raws hnub nyoog, hom ntshav qab zib, thiab theem ntawm CKD. Lub Koom Haum Koom Haum Koom Tes ntawm British Clinical Diabetologists thiab UK Lub Koom Haum Koom Haum Cov Lus Qhia yog ua raws li cov ntaub ntawv pov thawj zoo tshaj plaws txawm tias muaj pov thawj tsawg dua muaj rau qib siab ntawm CKD vim muaj qhov tsis txaus ntawm cov kev sim tshuaj ntsuam xyuas. Cov lus qhia txhawb nqa kev xa cov neeg mob hauv kev saib xyuas hauv kev teeb tsa lub hom phiaj, uas muab cov neeg mob tau txais txiaj ntsig zoo tshaj plaws thaum tswj hwm lub neej zoo.
Yog xav paub ntxiv:Ali.ma@wecistanche.com
