Yuav tswj cov ntshav qab zib, ntshav siab, ntshav lipids, thiab Uric acid li cas hauv cov neeg mob raum?

"Cov Lus Qhia rau Kev Ntsuas Thaum Ntxov, Kev Ntsuas thiab Kev Tiv Thaiv Kab Mob Raum Hniav (2022 Edition)" [1] (tom qab no hu ua "Cov Lus Qhia Suav") yog hais txog kab mob raum ntev (CKD) nrog rau lub raum txawv txav lossis ua haujlwm> 3 lub hlis. Qhov ntawd yog, raws li cov cim qhia ntawm lub raum puas thiab / lossis qhov txo qis hauv glomerular filtration rate (GFR), CKD tuaj yeem kuaj tau yog tias lub sijhawm ntev tshaj 3 lub hlis; raws li qhov kwv yees GFR (eGFR), CKD tuaj yeem muab faib ua theem 1-5.

Nyem rau ntawm cov organic cistanche rau mob raum

Qhov kev pheej hmoo stratification ntawm CKD tau ua raws li eGFR staging thiab tso zis albumin thiab muab faib ua qib 1 (tsis tshua muaj kev pheej hmoo), qib 2 (kev pheej hmoo nruab nrab), qib 3 (muaj kev pheej hmoo siab), thiab qib 4 (muaj kev pheej hmoo siab heev). Nyob rau hauv daim ntawv no, ua ke nrog Suav cov lus qhia, cov kev txhim kho tshiab ntawm kev kho tshuaj CKD hauv tsev thiab txawv teb chaws nyob rau xyoo tas los no raug tshuaj xyuas rau kev siv tshuaj kho mob.

tswj ntshav siab

Tam sim no muaj peb txoj kev xav txog kev sib raug zoo ntawm cov ntshav siab thiab CKD. Ib qho yog tias ntshav siab ua rau lub raum arteriolar sclerosis nqaim lub lumen, uas ua rau cov organic puas tsuaj rau lub raum [2]. Qhov thib ob yog tias ntshav siab tsis yog qhov ua rau muaj kab mob ntawm CKD. Hloov chaw, CKD tej zaum yuav ua rau mob ntshav siab [3]. 80 feem pua ​​​​mus rau 100 feem pua ​​​​ntawm cov neeg mob CKD yuav ua ke nrog cov ntshav siab nyob rau theem tom qab, uas ua rau cov mob hnyav ntxiv los txhawb cov lus no [4]. Nws ntseeg tau hais tias cov dej thiab sodium retention los ntawm lub raum lesions yog lub pathological ua rau ua rau los yog ua rau mob ntshav siab [5]. Qhov thib peb yog tias ntshav siab thiab CKD yog qhov ua rau thiab cuam tshuam rau ib leeg [6]. Cov lus ntawd yog kev tshawb fawb ntau dua thiab tseem xav tau kev nthuav qhia ntxiv.

The Chinese guidelines emphasize that CKD patients should set the blood pressure control target value according to the urinary albumin-to-creatinine ratio (UACR) level: when UACR≤30mg/g, maintain blood pressure≤140/90mmHg; when UACR>30mg / g, tswj ntshav siab tsawg dua lossis sib npaug ntawm 130/90mmHg; 80 mmHg. Kev xaiv cov tshuaj antihypertensive yuav tsum coj mus rau hauv tus account qhov muaj lossis tsis muaj proteinuria. Txhawm rau txhim kho tus nqi kom ncav cuag lub hom phiaj ntshav siab, nws raug nquahu kom siv cov tshuaj ib ntsiav tshuaj sib xyaw lossis kev npaj ua ke, thiab cov neeg mob ntshav siab tuaj yeem xaiv 3 lossis ntau dua cov tshuaj tiv thaiv kab mob rau kev kho mob ua ke.

tswj ntshav qab zib

Hauv xyoo tas los no, ntau yam tshuaj hypoglycemic tshiab tau pom zoo rau kev lag luam, suav nrog sodium-glucose cotransporter 2 (SGLT2) inhibitors thiab glucagon-zoo li peptide-1 (GLP-1) ntsig txog cov tshuaj, tom kawg yog kuj tau faib rau hauv Nws yog GLP-1 receptor agonist thiab dipeptidyl peptidase-4 (DPP-4) ​​inhibitor. Lawv muab cov kev xaiv tshiab rau kev tiv thaiv thiab kho mob raum mob ntshav qab zib mellitus (DKD). Ntau qhov kev sim tsiaj thiab kev tshawb fawb soj ntsuam tau pom tias ntxiv rau kev tswj cov ntshav qab zib kom zoo, GLP-1- cov tshuaj muaj feem xyuam kuj tuaj yeem cuam tshuam qhov ua kom lub zog ntawm renin-angiotensin-aldosterone system, inhibit inflammatory reactions thiab oxidative stress, thiab lwm yam. effect [7].

Xyoo 2020, American Diabetes Association cov lus qhia [8] pom zoo GLP-1 receptor agonists rau kev kho mob ntawm cov neeg mob DKD. Nyob rau tib lub xyoo, 2020 cov lus qhia txog kev kho mob [9] tawm los ntawm Lub Koom Haum Ntiaj Teb Cov Kab Mob Hauv Lub Ntiaj Teb (KDIGO) kuj tau pom zoo tias rau cov neeg mob ntshav qab zib hom 2 thiab CKD uas cov ntshav qab zib tseem tsis tuaj yeem ncav cuag lub hom phiaj tom qab kev kho mob nrog metformin thiab SGLT2. inhibitors, kev kho ntxiv tuaj yeem siv tau. GLP-1 receptor agonist kho.

Cov lus qhia Suav tau taw qhia tias kev hloov pauv ntawm lub raum hemodynamic thiab metabolic abnormality tshwm sim los ntawm hyperglycemia yog lub hauv paus pathological ntawm lub raum puas, thiab nws tau pom zoo tias lub hom phiaj tus nqi ntawm glycosylated hemoglobin tau teeb tsa qis dua 7.0 feem pua. SGLT2 inhibitors thiab GLP-1 receptor agonists raug pom zoo los txhim kho lub raum. Ua tib zoo saib xyuas cov qib eGFR thaum siv metformin thiab SGLT2 inhibitors, thiab kho cov koob tshuaj lossis tsis siv sijhawm yog tias tsim nyog.

kev tswj cov lipids

Cov kev tshawb fawb pom tau hais tias statins muaj txiaj ntsig zoo hauv kev txo qis kev pheej hmoo ntawm cov hlab plawv hauv cov neeg mob me me mus rau nruab nrab CKD. Piv txwv li, ib qho kev soj ntsuam ntawm 28 randomized tswj kev sim pom tau hais tias statins kho cov kev txo qis hauv qis lipoprotein cholesterol (LDLC) qib Statins tuaj yeem txo qhov kev pheej hmoo ntawm atherosclerotic cardiovascular disease (ASCVD) hauv cov neeg mob CKD theem 2-3 [ 10], tab sis feem ntau cov kev tshawb fawb tam sim no tau pom tias statins tsis tuaj yeem txo cov kab mob plawv hauv cov neeg mob uas muaj kab mob hauv lub raum kawg (ESRD).

Tsis tas li ntawd, qee qhov kev cog lus tshiab kho rau lipid-txo qis, xws li proprotein convertase subtilisin 9 inhibitors, phenoxide, Omega-3 fatty acid npaj [11], angiotensin receptor blockers [12], thiab lwm yam. tsis tshua muaj kev txwv, thiab nws cov txiaj ntsig thiab kev tiv thaiv kab mob plawv yuav tsum tau lees paub ntxiv. Hauv kev xaus, muaj qhov nyuaj thiab sib txawv ntawm CKD-txog dyslipidemia thiab kab mob plawv (CVD). Kev tshawb fawb ntxiv yog xav tau los txheeb xyuas thiab siv tau cov kev kho mob lipid-txo qis.

Suav cov lus qhia taw qhia tias dyslipidemia yog ib qho tseem ceeb uas txhawb txoj kev loj hlob ntawm CKD thiab tseem yog ib qho kev pheej hmoo tseem ceeb uas kho cov kab mob plawv thiab paj hlwb, lub raum atherosclerosis, thiab lub hom phiaj kev puas tsuaj hauv cov neeg mob CKD. Nws raug pom zoo tias cov hom phiaj kho mob raug txiav txim siab raws li kev ntsuas kev pheej hmoo ntawm tus kab mob es tsis yog qib lipid. LDL-C qib ntawm cov neeg mob tau soj ntsuam tias muaj kev pheej hmoo siab heev yuav tsum yog<1.8 mmol/L and the LDL-C level of other patients should be <2.6 mmol/L. Statins are the first choice for lowering LDL-C levels, but some statins need to be dosed according to eGFR.

Kev tswj hwm ntawm hyperuricemia

Cov kws tshawb fawb yav dhau los ntseeg tias qhov tsis zoo ntawm cov tshuaj urate-txo qis tsis sib haum nrog lawv cov txiaj ntsig kho mob, thiab kev kho mob ntawm cov neeg mob asymptomatic hyperuricemia tsis pom zoo. Txawm li cas los xij, nyob rau xyoo tas los no, ntau thiab ntau cov pov thawj tau pom tias uric acid-txo txoj kev kho muaj txiaj ntsig zoo rau CKD nrog hyperuricemia, thiab kev cuam tshuam ntxov tuaj yeem txhim kho lub raum ua haujlwm.

Ib 6-hli ob-dig muag, randomized, placebo-tswj sim tau pom tias piv nrog cov placebo, febuxostat ncua kev poob qis hauv eGFR hauv cov neeg mob asymptomatic hyperuricemia hauv CKD theem 3-4 [13]. Kev kho mob ntev ntev nrog allopurinol tuaj yeem ua rau qeeb ntawm cov kab mob hauv lub raum thiab txo qis kev pheej hmoo ntawm kev raug mob plawv [14].

Ib qhov chaw ib leeg, sib luag-pab pawg, randomized soj ntsuam kuaj pom tau tias benzbromarone ua ke nrog febuxostat tuaj yeem txo cov ntshav uric acid thiab tswj lub raum ua haujlwm zoo hauv cov neeg mob CKD nrog eGFR 20-60 ml / min / 1.73m2[15]. Ntxiv rau cov neeg laus, febuxostat kuj tau qhia txog cov teebmeem renoprotective hauv cov menyuam yaus lub raum tsis txaus.

Suav cov lus qhia taw qhia tias hyperuricemia thiab lub raum tsis ua haujlwm txhawb nqa ib leeg thiab ua kom muaj kev loj hlob ntawm CKD. Rau cov neeg mob uas muaj urate nephropathy, cov ntshav uric acid tswj lub hom phiaj yog<360 µmol/L, and for patients with gout attacks, the control target is <300 µmol/L. Drug therapy includes drugs that inhibit uric acid synthesis and drugs that increase uric acid excretion. For patients with hyperuricemia secondary to CKD, CKD should be actively treated. Intervention is only recommended when serum uric acid is >480 μmol / L. Txawm hais tias uric acid-txo txoj kev kho tuaj yeem ncua kev loj hlob ntawm CKD tseem tsis paub meej.

Kev tswj hwm ntawm hyperkalemia

Hyperkalemia is one of the main complications of electrolyte disturbance in CKD patients, which can lead to electrophysiological disturbance, severe clinical symptoms, and even death. A study showed that compared with normal serum potassium, serum potassium levels >5.

Cov lus qhia Suav tau taw qhia tias ib zaug hyperkalemia tshwm sim hauv cov neeg mob CKD, nws yog ib qho yooj yim uas yuav rov zoo dua, thiab kev tswj xyuas cov kua qaub rau lub sijhawm ntev yuav tsum tau ntxiv dag zog. Kev ntsuas kev kho mob suav nrog kev noj zaub mov uas tsis muaj cov poov tshuaj tsawg, kho cov tshuaj renin-angiotensin-aldosterone system inhibitors, cov tshuaj tiv thaiv kab mob hauv qhov ncauj, thiab siv cov tshuaj potassium-sparing diuretics raws li qhov tsim nyog. Rau cov mob hyperkalemia uas tswj tsis tau los ntawm cov tshuaj, kev kho mob sai sai yog pib. Feem ntau siv cov tshuaj tua kab mob hauv qhov ncauj muaj xws li SPS, calcium polystyrene sulfonate (CPS), thiab SZC. SZC tuaj yeem siv rau kev kho cov tshuaj potassium-txo cov mob hyperkalemia, thiab tseem tuaj yeem siv rau kev tswj xyuas ntev ntev ntawm cov mob hyperkalemia.

cov ntaub ntawv:

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