Summary and Inventory Of Chronic Kidney Disease Treatment Progress and Guidelines hauv 2023

Mob raum mob (CKD) cuam tshuam txog li 10% ntawm lub ntiaj teb cov pej xeem, muab lub nra hnyav rau lub ntiaj teb thiab tib neeg. Cov kws kho mob thiab cov kws tshawb fawb thoob plaws ntiaj teb tau txhawj xeeb txog qhov no thiab siv sijhawm ntau, lub zog, thiab nyiaj txiag kawm txog kev kho mob CKD txhua xyoo, thiab xyoo no tsis muaj kev zam.

Nyem rau Cistanche rau mob raum

Thaum kawg ntawm 2023, BMJ tau tshaj tawm cov ntsiab lus nthuav dav ntawm CKD kev kho mob nce qib hauv 2023, suav nrog cov ntsiab lus thiab ua rau CKD, cov hom phiaj kho mob, cov txheej txheem kho mob, thiab kev tshawb fawb txog kev kho mob.

Txhais thiab ua rau CKD

Ua ntej qhia meej txog kev kho mob ntawm CKD, cov ntsiab lus thiab cov khoom ntawm CKD yuav tsum tau qhia ua ntej. Tam sim no, CKD tau txhais tias yog qhov txawv txav ntawm lub raum qauv lossis kev ua haujlwm uas nyob ntev dua 3 lub hlis, tshwm sim los ntawm qhov qis glomerular filtration rate (GFR) lossis muaj cov cim ntawm lub raum puas. Cov txheej txheem kuaj mob tshwj xeeb rau CKD yuav tsum muaj tsawg kawg yog ib qho ntawm cov hauv qab no:

CKD cov txheej txheem kuaj mob

Urinary albumin rau creatinine ratio (UACR) Ntau dua lossis sib npaug li 30mg / g;

Albumin excretion hauv 24 teev Ntau dua lossis sib npaug rau 30mg;

GFR 60 ml / min / 1.73㎡;

urinary sediment, raum histology, los yog imaging abnormalities;

Electrolyte los yog lwm yam txawv txav tshwm sim los ntawm lub raum tubular teeb meem;

Keeb kwm ntawm kev hloov raum.

Feem ntau hais lus, etiology ntawm CKD yog qhov nyuaj. Cov kws kho mob yuav tsum txiav txim siab qhov laj thawj los ntawm kev yees duab, kev tshwm sim ntawm lub cev, biomarkers, lub raum biopsy, thiab lwm yam. Kev faib tawm etiological feem ntau nyob ntawm seb tus neeg mob puas muaj kab mob, xws li kev rog, ntshav qab zib, ntshav siab, lossis kab mob autoimmune, thiab qhov chaw tshwj xeeb ntawm lub raum pathology, xws li glomeruli, tubules, lub raum hlab ntsha, lossis cystic / congenital anomalies. Hmoov tsis zoo, rau feem ntau cov neeg mob nrog CKD, qhov ua rau tsis raug txheeb xyuas. Qhov no txwv txoj kev kho CKD. Nws yog ib nqi sau cia hais tias nyob rau hauv xyoo tas los no, phenotyping thiab genetic testing tau nce siv los pab rau kev kuaj mob ntawm qhov ua rau CKD. Ib txoj kev tshawb fawb qhia tias 34% ntawm cov neeg mob CKD yuav muaj lawv qhov laj thawj rov qab lees paub raws li cov txiaj ntsig ntawm kev ntsuam xyuas caj ces. Thaum kawg ntawm xyoo 2022, European Renal Association (ERA) thiab European Rare Kidney Disease Reference Network (ERKDRN) tau sib koom ua ib qho kev pom zoo pom zoo tias cov neeg mob CKD hauv qab no yuav tsum tau txais kev kuaj caj ces:

Cov xwm txheej yuav tsum tau kuaj genetic test

kab mob raum tubular;

Cov kab mob Glomerular, suav nrog congenital nephrotic syndrome, glucocorticoid-refractory nephrotic syndrome, thiab ntau lub cev-resistant glucocorticoid-refractory nephrotic syndrome;

Cov kab mob sib xyaw ua ke, suav nrog kev tiv thaiv kab mob tsis sib haum xeeb mebranoproliferative glomerulonephritis, C3 glomerulonephritis, thiab atypical hemolytic uremic syndrome (aHUS);

Lub raum ciliopathies;

congenital lub raum thiab zis malformations;

Cov neeg mob hnub nyoog qis dua 50 xyoo uas muaj CKD hnyav uas tsis paub txog qhov ua rau;

Patients >50 xyoo, nrog rau qhov pib tshiab CKD, thiab nrog tsev neeg keeb kwm ntawm kab mob raum.

cov hom phiaj kho mob

Muaj ob lub hom phiaj kev kho mob rau CKD: ua rau kev kho mob thiab kho cov tsos mob. Kev kho ntawm qhov ua rau yog tus kheej. Rau cov neeg mob uas nws qhov laj thawj tau raug txheeb xyuas, kev kho mob ntawm qhov laj thawj tuaj yeem txhim kho qhov kev loj hlob ntawm CKD thiab txawm tias xam lub sij hawm kwv yees ntawm kev loj hlob mus rau theem kawg ntawm lub raum kab mob (ESRD), uas muaj txiaj ntsig zoo rau kev tswj tus neeg mob. Kev kho mob yog kev tswj hwm uas txhua tus neeg mob CKD yuav tsum tau txais, xws li kev tswj ntshav siab, tswj ntshav qab zib (yog tias ua ke nrog ntshav qab zib), thiab lwm yam.

01 Kho qhov laj thawj

Kev txiav txim siab qhov ua rau CKD yog qhov tseem ceeb vim tias muaj ntau yam ua rau CKD muaj ntau qhov kev kuaj mob thiab kev kho mob sib txawv. Piv txwv li, autosomal dominant polycystic raum kab mob (ADPKD), feem ntau cov caj ces ua rau CKD, feem ntau mus sai dua lwm yam kab mob. Kev kho mob ntawm ADPKD yog qhov txawv ntawm lwm yam CKD. Hais txog kev noj tshuaj, tolvaptan yuav tsum tau ntxiv, thiab kev noj zaub mov yuav tsum tau ua kom cov kua dej ntau ntxiv. Immunoglobulin A (IgA) nephropathy yog cov kab mob glomerulonephritis feem ntau hauv cov tebchaws nyob rau sab hnub tuaj Asia thiab Pacific. Qee qhov kev tshawb fawb tsis ntev los no tau qhia tias APOL1-muaj feem cuam tshuam txog cov noob caj noob ces (feem ntau hauv African Asmeskas) tej zaum yuav ua rau qee qhov IgA nephropathy. Ib qho kev tshaj tawm tsis ntev los no theem 2A txoj kev tshawb fawb txog kev kho mob rau APOL1-cov kab mob cuam tshuam tau pom tias muaj kev cuam tshuam rau kev txo qis albuminuria hauv IgA nephropathy cov neeg mob nrog APOL1 gene variants. Tsis tas li ntawd, cov neeg mob uas muaj lupus nephritis yuav tsum tau kho nrog belimumab, thaum cov neeg mob uas muaj hyperoxaluria thawj zaug yuav tsum tau kho nrog lumasiran. Muaj qhov tshwm sim siab tias cov tshuaj saum toj no yuav tsis tshwm sim hauv cov tshuaj ntawm lwm tus neeg mob CKD.

Hauv cov ntsiab lus, kev qhia meej txog qhov ua rau tus kab mob tuaj yeem ua kom cov tshuaj muaj tseeb thiab pab cov kws kho mob tswj cov neeg mob CKD.

02 Kev kho mob

Kev kho cov tsos mob feem ntau yog los kho cov kev pheej hmoo uas ua rau muaj kev loj hlob thiab teeb meem ntawm CKD, xws li kev tswj kev noj zaub mov, ua kom muaj zog, tswj qhov hnyav, tswj ntshav siab, tswj qhov hnyav, thiab tswj lipid.

Ntawm cov kev cuam tshuam thiab kev kho mob saum toj no, plaub lub ntsiab lus tseem ceeb yuav tsum tau saib xyuas tshwj xeeb:

① Kev tswj ntshav siab

Cov pov thawj tam sim no qhia tau hais tias kev tswj ntshav siab hnyav tsis ua rau txo qis ntawm GFR hauv txhua tus neeg mob nrog CKD, tab sis Kev Hloov Kho Kev Noj Qab Haus Huv Hauv Lub Raum Kev Tshawb Fawb (MDRD) pom tias hauv cov neeg mob uas muaj cov proteinuria ntau dua lossis sib npaug li 3 g / d, Kev txo qis ntshav siab tuaj yeem ua rau txo qis ntawm GFR. Qhov no qhia tau tias kev txo qis ntshav siab yuav ua tau zoo dua rau cov neeg mob CKD uas muaj proteinuria loj.

Tsis tas li ntawd, kev tswj ntshav siab yog ib txoj hauv kev tseem ceeb los cuam tshuam qhov tshwm sim thiab kev loj hlob ntawm cov kab mob plawv hauv cov neeg mob CKD. Txoj kev tshawb fawb SPRINT tau qhia tias txawm hais tias tsis muaj qhov sib txawv tseem ceeb ntawm qhov kev pheej hmoo ntawm kev ua rau lub raum sib xyaw ua ke hauv cov neeg mob CKD ntawm systolic ntshav siab (SBP) cov hom phiaj.<140 mmHg and the SBP target group <120 mmHg, patients in the SBP <140 mmHg group experienced composite cardiovascular outcomes and all-cause outcomes. Lower risk of death!

② Kev tswj ntshav qab zib

Hauv cov neeg mob ntshav qab zib thiab CKD, kev tswj ntshav qab zib yog ib feem tseem ceeb ntawm kev kho mob. Txoj kev tshawb fawb ADVANCE tau qhia tias rau 11,140 tus neeg mob ntshav qab zib (19% eGFR<60ml/min/1.73㎡, 31% of patients had proteinuria at baseline), intensive glycemic control was associated with a reduced risk of end-stage renal disease compared with standard glycemic control. 65% correlation (HR=0.35; 95%CI 0.15-0.83).

③ Tsis txhob noj tshuaj nephrotoxic

Ntau cov tshuaj raug tshem tawm los ntawm glomerular filtration lossis tubular secretion. Txo glomerular filtration tus nqi tuaj yeem ua rau tsub zuj zuj ntawm cov tshuaj los yog lawv cov metabolites, ua rau muaj kev phiv tshuaj. Kev saib xyuas tshwj xeeb yuav tsum tau them thaum qee cov tshuaj tiv thaiv kab mob, tshuaj tua kab mob, tshuaj tiv thaiv qhov ncauj, tshuaj tua kab mob, thiab tshuaj ntshav qab zib tau muab rau cov neeg mob CKD, thiab qhov ntau npaum li cas ntawm cov tshuaj saum toj no yuav tsum tau kho raws li eGFR. Lub US Food and Drug Administration (FDA) qhia tias nws tsis pom zoo kom siv creatinine clearance kwv yees los ntawm Cockcroft-Gault equation los kho qhov ntau npaum ntawm cov tshuaj saum toj no.

Cov neeg uas muaj CKD yuav tsum zam lossis txo qis kev siv qee yam tshuaj los txo qhov kev pheej hmoo ntawm lub raum ua haujlwm tsis zoo. Nonsteroidal anti-inflammatory tshuaj (NSAIDs) yuav tsum zam thaum cov neeg mob CKD tau kho nrog angiotensin-hloov enzyme inhibitors (ACEi) lossis angiotensin II receptor blockers (ARB) + diuretics. Tsis tas li ntawd, proton twj tso kua mis inhibitors (PPIs) tuaj yeem ua rau mob hnyav lossis mob ntev nephritis. Txawm hais tias tus txheej txheem tsis paub, feem ntau cov kws tshaj lij ntseeg tias PPIs yuav tsum tau siv nrog ceev faj rau cov neeg mob CKD.

④ Lipid tswj

Txoj kev tshawb fawb SHARP tau qhia tias statins tuaj yeem muaj kev nyab xeeb thiab txo qis lipids hauv cov neeg mob CKD (33% tau txais kev lim ntshav) nrog qhov nruab nrab eGFR ntawm 27ml / min / 1.73㎡. Piv nrog rau cov placebo, pawg kev cuam tshuam tau ntsib thawj qhov loj atherosclerosis. Qhov kev pheej hmoo ntawm cov xwm txheej tau txo qis los ntawm 17%.

qhia kev kho mob

Cov lus qhia CKD tam sim no feem ntau yog los ntawm Lub Tsev Kho Mob Raum Txhim Kho Ntiaj Teb Cov Txheej Txheem (KDIGO) lub koom haum British National Institute for Health thiab Clinical Excellence (NICE), American College of Cardiology, American Heart Association, European Society of Cardiology, European Society ntawm Hypertension, International High School Blood Pressure Society, American Diabetes Association (ADA).

Cov kws tshaj lij tau sau cov lus qhia saum toj no thiab pom tias 7 lub tswv yim tau pom zoo:

Cov lus pom dav dav

① Cov neeg mob ntshav qab zib yuav tsum tau txais kev kuaj CKD tsawg kawg ib xyoos ib zaug, thiab cov lus ceeb toom tshwj xeeb yuav tsum suav nrog kuaj proteinuria;

②Kuaj ib tus neeg muaj kev pheej hmoo rau CKD, suav nrog cov neeg muaj ntshav siab, kab mob plawv, ntshav qab zib, thiab keeb kwm ntawm mob raum raug mob.

Rau cov neeg mob CKD, kuaj proteinuria yuav tsum tau ua ib xyoos ib zaug;

④ SBP yuav tsum yog<130mmHg, especially if UACR≥70mg/mmol, the blood pressure target is <130/80mmHg.

⑤NICE cov lus qhia thiab KDIGO cov lus qhia pom zoo ACEi/ARB ua thawj kab tshuaj tiv thaiv kab mob rau cov neeg mob uas tsis muaj ntshav qab zib tab sis muaj proteinuria thiab rau cov neeg mob ntshav qab zib thiab CKD theem G1-G4.

⑥KDIGO and ADA guidelines recommend that the first-line treatment drug for all CKD patients with type 2 diabetes (eGFR ≥ 20ml/min/1.73㎡) is a sodium-glucose co-transporter 2 inhibitor (SGLT-2i). NICE guidelines recommend that if UACR is >30 mg/mmol, SGLT-2kuv yuav tsum tau siv. Yog tias UACR nyob nruab nrab ntawm 30 thiab 300 mg / g, SGLT-2 kuv yuav tsum tau txiav txim siab.

⑦KDIGO cov lus qhia ntxiv qhia ntxiv tias ib zaug SGLT-2 kuv pib, txawm tias tus neeg mob eGFR yog<20ml/min/1.73㎡, as long as it is tolerated and renal replacement therapy is not performed, the patient can continue to receive SGLT-2i treatment.

Kev tshawb fawb nce qib ntawm cov tshuaj kho mob

Nyob rau hauv xyoo tas los no, kev tshawb fawb txog tshuaj kho CKD tau nce sai, tab sis 5 cov tshuaj yuav tsum tau saib xyuas tshwj xeeb. Cov kab lus no feem ntau piav qhia lawv cov kev ceev faj txog kev kho mob:

①ACEi thiab ARB

ACEi tuaj yeem txo qhov kev pheej hmoo ntawm kev hloov lub raum los ntawm 30%, ARB tuaj yeem tiv thaiv kev loj hlob ntawm CKD thiab tuaj yeem tiv thaiv kab mob plawv hauv cov neeg mob CKD. Txawm li cas los xij, hauv kev kho mob, cov neeg mob yuav tsum tsis txhob siv ACEi thiab ARB ib txhij los tiv thaiv hyperkalemia thiab mob raum raug mob.

②SGLT-2i

Cov kev tshawb fawb soj ntsuam tsis ntev los no tau pom tias rau hauv paus eGFR<20ml/min/1.73㎡, SGLT-2i can reduce the risk of adverse renal outcomes by approximately 30%. In addition, SGLT-2i can be used in combination with ACEi/ARB, which can be additive in delaying the progression of CKD. Existing data indicate that SGLT-2i has no significant safety risk, but it should be noted that SGLT-2i may lead to a slightly increased risk of genital infection in CKD patients.

③ Glucagon-zoo li peptide -1 receptor agonist

Glucagon-zoo li peptide-1 receptor agonists (GLP-1RA) tau pom tias txhim kho lub raum cov txiaj ntsig hauv cov neeg mob ntshav qab zib hom 2, txo qhov kev pheej hmoo ntawm lub raum tshwm sim (xws li albuminuria) los ntawm 15% mus rau 36% . Txawm li cas los xij, qhov tseeb mechanism uas GLP-1RA ncua eGFR poob thiab/lossis proteinuria txo qis tsis meej.

④ Mineralocorticoid receptor antagonists

Mineralocorticoid receptor antagonists (MRA) tuaj yeem siv los ua kev kho mob rau ACEi lossis ARB, tshwj xeeb tshaj yog rau cov neeg mob albuminuria thiab / lossis ntshav qab zib. Ob hom steroidal nonselective MRAs, spironolactone, thiab eplerenone, ob leeg txo qis albuminuria.

But even more eye-catching is the non-steroidal MRA, fenelinone. Existing evidence suggests that fenelidone reduces the risk of the composite renal outcome by 15-23%. Moreover, for CKD patients with type 2 diabetes, the combined use of fenelidone and SGLT-2i or GLP-1RA will not affect the efficacy of each other, and it is even possible that 1+1>2.

⑤ Endothelin receptor antagonist

Endothelin receptor antagonists tau tshwm sim raws li kev kho tshiab rau ntau yam kab mob raum. Piv txwv li, SONAR txoj kev tshawb fawb tau soj ntsuam qhov cuam tshuam ntawm Atrasentan (tentative translation: Atrasentan) hauv cov neeg mob ntshav qab zib hom 2 thiab pom tias piv nrog cov placebo pab pawg, cov txiaj ntsig ntawm lub raum (ob npaug ntawm cov ntshav creatinine lossis ESKD) hauv pab pawg atrasentan yog. kev pheej hmoo raug txo los ntawm 35%.

Lwm tus endothelin receptor antagonist, Sparsentan (lub npe hu ua: Sparsentan), muaj cov teebmeem tshwj xeeb ntawm IgA nephropathy thiab focal segmental glomerulosclerosis (FSGS), thiab piv nrog irbesartan, nws tuaj yeem txo cov proteinuria muaj zog.

Cistanche kho mob raum li cas?

Cistancheyog ib hom tshuaj suav tshuaj ntsuab siv rau ntau pua xyoo los kho ntau yam mob, suav nrog kab mob raum. Nws yog muab los ntawm qhuav stems ntawmCistanchedeserticola, ib tsob nroj nyob rau hauv cov suab puam ntawm Tuam Tshoj thiab Mongolia. Lub ntsiab active Cheebtsam ntawm cistanche yogphenylethanoidglycosides, echinacoside cov tshuaj, thiabacteoside, uas tau pom tias muaj txiaj ntsig zoo rau lub raum kev noj qab haus huv.

Kab mob raum, tseem hu ua kab mob raum, hais txog ib yam mob uas lub raum ua haujlwm tsis zoo. Qhov no tuaj yeem ua rau muaj cov khoom pov tseg thiab cov co toxins hauv lub cev, ua rau muaj ntau yam tsos mob thiab teeb meem. Cistanche tuaj yeem pab kho mob raum ase los ntawm ntau lub tswv yim.

Ua ntej, cistanche tau pom tias muaj cov nyhuv diuretic, txhais tau tias nws tuaj yeem ua rau cov zis ntau ntxiv thiab pab tshem tawm cov khoom pov tseg ntawm lub cev. Qhov no tuaj yeem pab txo lub nra ntawm lub raum thiab tiv thaiv kev tsim cov co toxins. Los ntawm kev txhawb nqa diuresis, cistanche kuj tseem tuaj yeem pab txo qis ntshav siab, ib qho teeb meem ntawm cov kab mob raum.

Ntxiv mus, cistanche tau pom tias muaj cov teebmeem antioxidant. Kev ntxhov siab oxidative, tshwm sim los ntawm qhov tsis sib xws ntawm kev tsim cov dawb radicals thiab lub cev tiv thaiv antioxidant, ua lub luag haujlwm tseem ceeb hauv kev mob raum. ies pab neutralize dawb radicals thiab txo Oxidative kev nyuaj siab, yog li tiv thaiv lub raum los ntawm kev puas tsuaj. Cov phenylethanoid glycosides pom hauv cistanche tau tshwj xeeb hauv kev tshem tawm cov dawb radicals thiab inhibiting lipid peroxidation.

Tsis tas li ntawd, cistanche tau pom tias muaj cov nyhuv anti-inflammatory. Kev mob yog lwm yam tseem ceeb hauv kev loj hlob thiab kev loj hlob ntawm cov kab mob raum. Cistanche's anti-inflammatory zog pab txo cov zus tau tej cov pro-inflammatory cytokines thiab inhibit qhov ua kom o yuav tsum tau txoj kev, yog li alleviating o nyob rau hauv lub raum.

Tsis tas li ntawd, cistanche tau pom tias muaj cov teebmeem immunomodulatory. Hauv kab mob raum, lub cev tiv thaiv kab mob tuaj yeem ua rau tsis zoo, ua rau muaj kev mob ntau dhau thiab cov ntaub so ntswg puas. Cistanche pab tswj lub cev tiv thaiv kab mob los ntawm kev hloov kho kev tsim khoom thiab kev ua haujlwm ntawm lub cev tiv thaiv kab mob, xws li T hlwb thiab macrophages. Txoj cai tiv thaiv kab mob no pab txo qhov mob thiab tiv thaiv kev puas tsuaj ntxiv rau lub raum.

Ntxiv mus, cistanche tau pom los txhim kho lub raum kev ua haujlwm los ntawm kev txhawb nqa kev tsim kho ntawm lub raum hlab nrog cov hlwb. Lub raum tubular epithelial hlwb ua lub luag haujlwm tseem ceeb hauv kev pom thiab rov nqus cov khoom pov tseg thiab electrolytes. Hauv kab mob raum, cov hlwb no tuaj yeem raug puas tsuaj, ua rau lub raum ua haujlwm puas. Cistanche lub peev xwm los txhawb kev tsim kho ntawm cov hlwb no pab kho lub raum kom zoo thiab txhim kho lub raum tag nrho.

Ntxiv nrog rau cov kev cuam tshuam ncaj qha rau lub raum, cistanche tau pom tias muaj txiaj ntsig zoo rau lwm yam kabmob thiab lub cev hauv lub cev. Txoj hauv kev zoo rau kev noj qab haus huv no tseem ceeb tshwj xeeb hauv cov kab mob raum, vim tias tus mob feem ntau cuam tshuam rau ntau lub cev thiab lub cev. che tau pom tias muaj kev tiv thaiv rau lub siab, lub plawv, thiab cov hlab ntsha, uas feem ntau cuam tshuam los ntawm kab mob raum. Los ntawm kev txhawb nqa kev noj qab haus huv ntawm cov kabmob no, cistanche pab txhim kho lub raum tag nrho thiab tiv thaiv kev mob ntxiv.

Hauv kev xaus, cistanche yog cov tshuaj suav tshuaj ntsuab siv rau ntau pua xyoo los kho mob raum. Nws cov active Cheebtsam muaj diuretic, antioxidant, anti-inflammatory, immunomodulatory, thiab regenerative teebmeem, uas pab txhim kho lub raum ua haujlwm thiab tiv thaiv ob lub raum los ntawm kev puas tsuaj ntxiv. , cistanche muaj txiaj ntsig zoo rau lwm yam kabmob thiab lub cev, ua rau nws txoj hauv kev zoo rau kev kho mob raum.