Empagliflozin nyob rau hauv Cov Neeg Laus Nrog Mob Raum Kab Mob (CKD): Cov pov thawj tam sim no thiab qhov chaw hauv kev kho mob

Abstract:Mob raum mobcov txheej txheem thiab kho kab mob-hloov kho tau pom qhov hloov pauv loj hauv 5 xyoo dhau los. SGLT2 inhibitor chav kawm ntawm cov tshuaj tau raug catapulted los ntawm cov tshuaj tswj hwm hyperglycemia mus raukab mob plawv thiab raumtxhim kho kev kho mob. Ntau qhov kev sim saib ntawm kev mob siab raucov hlab plawv thiab lub raum endpointstau ua rau muaj txiaj ntsig zoo. Qhov kev tshuaj xyuas no yuav tsom rau empagliflozin thiab txoj kev taug kev zoo siab uas nws tau ua raws li txoj kev no. Empagliflozin tau kawm rauhyperglycemia, mob plawv, thiablub raum hard outcome endpoints. Ob leegcov neeg mob ntshav qab zibthiab tsis tau kawm nruj me ntsis thiab pom cov txiaj ntsig xav tsis thoob. Qhov cuam tshuam loj rau cov neeg mob ntawm empagliflozin yuav tshwm sim. Cov kev tshawb fawb yav tom ntej thiab cov lus qhia tau cia siab tias yuav ntxiv rau kev paub txog kev loj hlob ntawm SGLT2 inhibitor chav kawm, nrog rau kev tshawb pom muaj peev xwm ua rau cov kab mob tshiab tau txais txiaj ntsig los ntawm empagliflozin.

Ntsiab lus: empagliflozin, SGLT2,mob raum mob, kab mob plawv, ntshav qab zib, kab mob raum kawg

NYEEM NTXIV RAU HAUV QHOV CHAW UA HAUJ LWM TSHIAB NTAWM CISTANCHE FOR CKD TREATMENT

Taw qhia

Hyperfiltrationyog lub zog tsav tsheb uas ua rau nephrons mus rau glomerulosclerosis thiab nws thiaj li ua raumob raum mob(CKD) thiab theem kawgkab mob raum(ESKD). Nws tau yog li ntawd tau intuitive tias txo qis hyperfiltration yog lub ntsiab lus tseem ceeb rau kev ua kom qeeb ntawm CKD.

Me ntsis dhau 2 xyoo dhau los, peb tau pom thawj zaug ntawm qhov kev sim tshuaj uas muaj cov chav kawm ntawm cov tshuaj, renin-angiotensin-aldosterone inhibitors (RAASi) uas tau hais txog qhov kev coj ua no thiab tau nthuav qhia txoj hauv kev uas peb tau tswj cov neeg mob ntshav qab zib raum (DKD) , raws li ib qho kev ua kom qeeb ntawm CKD. Txij thaum ntawd los, qhov chaw no tau tuag ntsiag to txog thaum tsis ntev los no qhia txog cov chav kawm tshiab ntawm kev kho mob, sodium-glucose co-transporter 2 inhibitors (SGLT2i). Teb Chaws AsmeskasFood and Drug Administration(FDA) tau pom zoo thawj SGLT2ii thaum ntxov 2013, ua raws li tsab ntawv ceeb toom ntawm qhov yuav tsum tau ua kom muaj kev nyab xeeb ntawm cov hlab plawv. Zuag qhia tag nrho, cov kev sim tau tshaj tawm rau hnub tim qhia tias SGLT2i tsis ua rau muaj kev pheej hmoo siab plawv (CV). Ob peb ntawm SGLT no-2Kuv tau cuam tshuam nrog kev txo qis hauv cov xwm txheej hauv plawv loj (MACE) thiab CV tuag. Txhua qhov kev txo qis hauv kev tuag tau tshwm sim los ntawm empagliflozin, thiab lwm yam kev sim kev nyab xeeb SGLT2i qhia txog kev txo qis hauv lub plawv tsis ua haujlwm (CHF). Hauv cov kev sim no, muaj qhov txo qis hauv kev pheej hmoo rau lub raum nyuaj kawg (ESKD, xav tau kev lim ntshav lossis ob npaug ntawm cov ntshav creatinine [DSC], lossis tuag), nrog cov txheeb ze kev pheej hmoo txo ​​qis ntawm 40% thiab 24%.1,2 Cov no. Kev txo qis, nrog rau cov teebmeem ntawm SGLT2i ntawm cov txiaj ntsig ntawm lub plawv, muaj ntau dua li cov tau txais nrog RAASi. Hauv kev sim kev nyab xeeb CV yav dhau los, lub raum qhov kawg yog qhov thib ob lossis kev tshawb nrhiav nkaus xwb. Ntau qhov kev sim tau luam tawm txij li thaum, saib ntawm lub raum tshwj xeeb endpoints.1,2 Kev tshuaj xyuas no yuav qhia txog cov tshuaj, kev nyab xeeb thiab kev ua tau zoo, thiab cov kev tshawb pom tseem ceeb ntawm kev sim SGLT2i tsis ntev los no tshwj xeeb, Empagliflozin, thiab cov kev txhim kho tshiab kawg.

Pharmacology ntawm Sodium-Glucose Cotransporter (SGLT)

Lub raum glomeruli feem ntau lim li 120-180 grams qabzib los ntawm cov ntshav txhua hnub tab sis tsawg dua 0.5 grams raug tso tawm hauv cov zis. Glucose paub tias yog lim dej dawb hauv lub glomerulus thiab tom qab ntawd rov ua dua nyob rau hauv qhov sib thooj convoluted tubule (PCT). Qhov siab tshaj plaws lub raum qabzib reabsorptive muaj peev xwm (TmG) yog xam ntawm 375 mg / min thiab cov piam thaj yog lim ntawm 125 mg / min lossis 180 mg / hnub, hauv tib neeg nruab nrab (xws li kwv yees li ib txwm kwv yees glomerular filtration rate (eGFR)). Tsis tas li ntawd, glucosuria tshwm sim thaum glycemia ntau dua 180 mg / dL hauv cov neeg mob uas muaj hom 1 lossis hom 2 mob ntshav qab zib mellitus thiab qhov tshwm sim no tshwm sim vim tias cov piam thaj lim dej ntau dua TmG ua rau glucosuria.

Hauv lub raum physiology, cov piam thaj tsis tuaj yeem rov qab los ntawm cov phab ntsa ntawm PCT, yog li nws xav tau kev pab cuam ntawm cov piam thaj thauj los ntawm cotransporters uas muaj nyob hauv PCT. Sodium glucose co-transporters, SGLT1 thiab SGLT2 yog cov tswv cuab ntawm tsev neeg SLC5 gene, subdivision ntawm sodium cotransporters. SGLT1 feem ntau qhia nyob rau hauv cov hnyuv me thiab tsawg dua nyob rau hauv ob lub raum, tshwj xeeb tshaj yog nyob rau hauv lub cortex, whereas SGLT2 muaj nyob rau hauv lub raum cortex.3 SGLT2 muaj nyob rau hauv thawj thiab thib ob ntu (S1 thiab S2) ntawm PCT thiab Nws yog lub luag haujlwm rau 90% ntawm cov piam thaj reabsorption. SGLT1 feem ntau yog tam sim no nyob rau hauv lub luminal membrane ntawm S3 ntu.4 Cov cotransporter hauv S1 no muaj peev xwm / tsawg affinity whereas nyob rau hauv S2 thiab S3, nws muaj ib tug high-affinity thiab low-capacity qabzib / galactose co-transporter. Cov SGLT cov proteins koom nrog Na / K ATPase twj tso kua mis nyob rau hauv lub basolateral daim nyias nyias uas ua rau ib tug poob nyob rau hauv lub intracellular sodium concentration ua tiav ib tug sodium gradient uas generates ib tug downhill gradient mus thauj ib qabzib molecule tawm tsam uphill qabzib gradient nyob rau hauv lub apical membrane ntawm PCT. . Qhov sib piv ntawm sodium rau qabzib cotransport nyob rau hauv lub cell yog 1: 1 thiab 2: 1 rau SGLT2 thiab SGLT1, feem. lub PCT.

SGLT2i yog ib chav kawm ntawm cov tshuaj uas txhawb nqa lub raum tso ntshav qabzib los ntawm kev ua kom cov piam thaj txo qis, txo TmG thiab qhov pib rau cov piam thaj reabsorption, thiab txawm hais tias lawv tsis yog thawj cov neeg ua haujlwm rau kev kho mob ntshav qab zib hom 2, lawv tau dhau los ua ib qho tseem ceeb. tivthaiv hauv kev tswj cov neeg mob ntshav qab zib, nrog rau cov neeg mob plawv tsis ua haujlwm thiab CKD, raws li tau piav qhia hauv qab no

SGLT2 intercedes nyob rau hauv lub reabsorption ntawm 90% ntawm lim piam thaj, txawm li cas los xij, SGLT2i tsuas yog nce glucosuria los ntawm kwv yees li 50% ntawm cov kua nplaum lim dej. Qhov tshwm sim no tshwm sim vim tias SGLT1 nyob rau hauv feem ntau hauv S2 thiab S3, ua haujlwm qis dua nws lub peev xwm thauj khoom siab tshaj plaws tau muab qhov tseeb tias SGLT2 twb tau rov ua dua 90% ntawm cov kua nplaum uas lim dej.4 Yog li, thaum SGLT2 yog inhibited, qhov no ua rau cov khoom xa tuaj. loj load ntawm qabzib mus rau SGLT1 transporter uas nyob rau ntawm lub sij hawm ntawd, yog nyob rau ntawm nws tag nrho reabsorptive muaj peev xwm, uas yuav piav qhia yog vim li cas peb pom tsawg tshaj li 50% ntawm cov kua nplaum lim nyob rau hauv cov zis. Tam sim no, SGTL2i cov chav kawm tshuaj tsis raug pom zoo siv rau cov neeg mob uas muaj hom 1 mob ntshav qab zib mellitus. Muaj kev ntshai ntawm metabolic acidosis thiab muaj peev xwm ketoacidosis nrog SGLT2i raug. Cov neeg mob no tsis tau suav nrog hauv qhov kev sim loj thiab cov ntaub ntawv tsis tuaj yeem raug ntxiv rau pawg no.

Empagliflozin Pharmacology Cov yam ntxwv

Empagliflozin is an SGLT2 inhibitor with a higher selectivity for SGLT2 over SGLT1 (over >2500 ib.). Nws bioavailability nyob ib ncig ntawm 75% thiab yog absorbed sai sai tom qab kev tswj qhov ncauj. Empagliflozin muaj Tmax ntawm 1.5 teev thiab khi rau cov proteins los ntawm 86% thiab nws lub neej ib nrab (T1/2) yog 13 teev thiab raug tshem tawm feem ntau los ntawm fecal (40%) thiab raum (55%) txoj kev. .5.

Tom qab pib SGLT2i feem ntau muaj kev poob qis hauv eGFR, ib qho kev cuam tshuam uas rov qab los ntawm lub sijhawm lossis tom qab noj tshuaj. Ntau tus qauv ntawm cov ntshav qab zib muaj feem xyuam nrog hyperfiltration tau pom tias muaj kev cuam tshuam ntau ntxiv rau cov macula densa activates tubuloglomerular tawm tswv yim, zoo li los ntawm cov txheej txheem ntsig txog adenosine, txawm li cas los xij, qhov no tau sib cav los ntawm lwm qhov kev tshawb pom qhia tias cov txiaj ntsig tseem ceeb yog post-glomerular vasodilation, es tsis yog preglomerular vasoconstriction.6 Qhov no tuaj yeem piav qhia txog kev txo qis microalbuminuria uas pom nrog cov chav kawm tshuaj no. Lwm cov txiaj ntsig zoo rau lub sijhawm ntev tuaj yeem piav qhia los ntawm kev txo qis hauv intraglomerular siab.7

Hauv cov tib neeg noj qab haus huv, empagliflozin tau pom tias tau nqus sai sai tom qab siv qhov ncauj. Kev nce ntxiv hauv cov zis albumin tshwm sim yog qhov sib npaug ntawm cov koob tshuaj empagliflozin (0.5–800 mg). Cov kev tshawb pom zoo sib xws tau tshaj tawm nrog cov koob tshuaj ntawm 1 thiab 100 mg hauv cov neeg mob noj qab haus huv Nyij Pooj.8 Cov kev tshawb pom no tuaj yeem piav qhia raws li cov neeg Nyij Pooj feem ntau muaj qhov hnyav dua. Nws kuj tseem tau pom tias thaum empagliflozin tau noj nrog zaub mov, muaj kev nqus qeeb me ntsis, txawm hais tias Cmax qis dua nyob rau hauv kev noj zaub mov ntau dua li thaum cov tshuaj tau muab rau hauv kev yoo mov, cov kev tshawb pom no tau tshwm sim tsis yog kev kho mob tseem ceeb, thiab cov tshuaj. tuaj yeem muab nrog zaub mov.

Plasma concentrations ntawm empagliflozin ntawm cov koob tshuaj ntau dua xws li 100 mg, tau tshaj tawm tias tuaj yeem kuaj pom tau ntev txog 72 teev. Tsis tas li ntawd, FDA thiab raws li International Conference on Harmonization (ICH) cov lus qhia, 9 pom zoo tias kev sim tshuaj siv cov tswv yim thiab sau cov ntaub ntawv hauv ib cheeb tsam los txiav txim seb puas muaj qhov sib txawv ntawm haiv neeg hauv lwm cheeb tsam. Piv txwv li, tsis muaj qhov sib txawv ntawm cov tshuaj pharmacokinetic ntawm cov neeg Iyiv thiab cov neeg German dawb thiab tsis muaj kev hloov kho koob tshuaj hauv cov neeg no 10 thaum noj 25 mg ntawm empagliflozin.

Kev tshawb fawb hyperglycemia rau Empagliflozin

Hauv nruab nrab 2010s, SGLT2i suav nrog empagliflozin tau txais kev sim tshuaj raws li kev kho mob hyperglycemic. Thaum lub sijhawm ntawd, cov neeg mob uas muaj CKD siab heev tau raug tshem tawm los ntawm Theem 1 kev sim uas cuam tshuam txog kev nyab xeeb thiab kev zam txim.11 Peb tau xaiv qhov kev sim ua pov thawj uas pab tsim kom muaj kev siv tau, kev nyab xeeb, thiab kev ua tau zoo ntawm empagliflozin. 2013 EMPA-REG MONO Phase 3 qhov kev sim tshuaj ntsuam xyuas randomized cov neeg laus nrog glycosylated hemoglobin (HbA1c) 7-10% ntawm tsis muaj kev kho ua ntej rau cov placebo, sitagliptin, lossis 10 lossis 25mg koob ntawm empagliflozin. Piv nrog rau cov placebo, empagliflozin txo A1c los ntawm 0.74 thiab 0.85% nyob ntawm qhov koob tshuaj, uas yog qhov sib txawv tseem ceeb piv rau 0.73% qhov sib txawv pom nrog sitagliptin. Raws li qhov kawg ntawm qhov kev ua tau zoo thib ob, cov kws tshawb nrhiav pom tias cov ntshav siab systolic tau txo qis los ntawm qhov nruab nrab ntawm 3.7mmHg thiab lub cev hnyav tau txo los ntawm qhov nruab nrab ntawm 2.5kg (hauv pawg 25mg ntau npaum li cas) uas yog qhov tseem ceeb piv rau sitagliptin thiab placebo.12 Qhov kev tshawb pom ntawm qhov txo qis. qhov hnyav tau zoo ib yam nyob rau xyoo 2014 EMPA-REG MET sim, uas empagliflozin tau ntxiv rau metformin, nrog kev txo qis zoo sib xws hauv qhov hnyav ntawm 2.5kg hauv pawg 25mg.13 Hauv qhov kev sim no, systolic ntshav siab raws li kev tshawb nrhiav tau txo qis los ntawm ib qho. Qhov nruab nrab ntawm 4.8 mmHg hauv pawg koob tshuaj 25 mg.

Tom qab EMPA-REG MONO thiab EMPA-REG MET, kev sim ntxiv tau pom qhov ua tau zoo ntawm empagliflozin raws li kev kho ntxiv rau metformin thiab sulfonylurea (EMPA-REG METSU14) thiab pioglitazone (EMPA-REG PIO15), ua rau SGLT2i zoo tshaj plaws. xaiv cov tshuaj thib ob thiab thib peb rau cov neeg mob ntshav qab zib. Qhov tseem ceeb, qhov sib ntxiv ntawm empagliflozin rau sulfonylurea nce qhov tshwm sim ntawm cov xwm txheej hypoglycemia, tab sis qhov tshwm sim ntawm hypoglycemia tsis tau nce ntxiv thaum ua ke nrog pioglitazone. Ob qhov kev sim no tau pom tias txo qis systolic ntshav siab thiab lub cev hnyav hauv cov neeg mob siv empagliflozin piv rau sulfonylurea lossis pioglitazone ib leeg.

Zaj dab neeg ua tiav zaum kawg rau empagliflozin raws li kev kho mob hyperglycemia yog 2015 tshaj tawm ntawm EMPA-REG BASAL trial.16 Txoj kev tshawb no tau tso npe rau cov neeg mob uas muaj ntshav qab zib mellitus (HbA1c> 7%) txawm tias basal insulin thiab, hauv qee qhov Cov neeg mob, kev siv cov tshuaj metformin los yog sulfonylurea concomitant. Hauv cov neeg mob cuv npe ntawm 18 lub lis piam, HbA1c txo qis los ntawm 0.7% nrog ntxiv ntawm empagliflozin 25mg piv rau 0.1% hauv cov placebo. Cov nyhuv no tau txo qis me ntsis los ntawm lub lim tiam 78, raws li cov kws tshawb fawb tau tso cai kom nce cov tshuaj insulin yog tias xav tau tom qab lub lim tiam 18, tab sis qhov kev txhim kho tseem ceeb hauv A1c tseem tau sau tseg. Raws li hauv kev tshawb fawb ua ntej, qhov sib ntxiv ntawm empagliflozin tau pom qhov txo qis hauv lub cev hnyav ntawm 10 lossis 25 mg koob, txawm li cas los xij, qhov txo qis hauv systolic ntshav siab tsuas yog pom nrog koob tshuaj 10 mg.

Zuag qhia tag nrho, empagliflozin tau tshwm sim los ua qhov kev xaiv kho mob tsim nyog rau cov neeg mob ntshav qab zib, xws li kev kho mob monotherapy, kev kho tsis yog insulin ntxiv, lossis ntxiv rau kev kho tshuaj insulin. Lub koom haum American Diabetes cov lus pom zoo tau nthuav dav hauv xyoo 2020 kom qhia meej tias cov neeg mob uas muaj hom 2 mob ntshav qab zib nrog cov kab mob atherosclerotic plawv lossis kab mob raum yuav tsum muaj SGLT2i lossis GLP-1 agonist ua ib feem ntawm lawv cov tswv yim txo cov piam thaj. Nws yuav tsum raug sau tseg, txawm li cas los xij, cov lus pom zoo no tau ntxiv los ua cov lus teb rau cov kev sim siab (sib tham tom qab) ua rau pom tias muaj kev pheej hmoo ntawm lub plawv thiab lub raum hauv cov neeg mob no.

Feem ntau cov kev sim no tau ua kom pom qhov tshwm sim ntawm cov kab mob tso zis lossis qhov chaw mos nrog kev siv empagliflozin, uas yog qhov kev thuam loj ntawm SGLT2i. Nws yog ib qho tseem ceeb uas yuav tsum nco ntsoov tias cov neeg mob nrog eGFR<30mL/min/m2 were excluded from these earlier hyperglycemia trials. When comparing the different SGLT2i medications, the side effects do appear to be a class effect and all patients need to be warned of potential infection risk and hypovolemia.17

Lub raum Studies rau SGLT2i thiab Empagliflozin

Cov txiaj ntsig ntawm lub raum ntawm SGLT2i tau tshawb pom ua ntej hauv txhua qhov kev tshawb fawb ntawm cov hlab plawv, raws li cov txiaj ntsig thib ob (EPMA REG, CANVAS18) thiab yuav tau tham tom qab hauv kab mob plawv ntawm qhov kev tshuaj xyuas no. Thawj qhov kev sim hais txog qhov tshwm sim ntawm lub raum raws li qhov tshwm sim thawj zaug yog CREDENCE kev sim hauv 2{{20}}19.1 CREDENCE randomized 4401 cov neeg mob uas muaj T2DM, CKD (eGFR 30- tsawg dua los yog sib npaug rau 90 mL/min/1.73 m2 ) thiab albuminuria (300-5000 mg/g), uas tau ruaj khov ntawm renin– angiotensin system blockade rau 4 lub lis piam lossis ntau dua kom tau txais Canagliflozin 100 mg lossis placebo. Txoj kev tshawb no tau nres thaum ntxov tom qab kev soj ntsuam ib ntus nrog kev soj ntsuam nruab nrab ntawm 2.62 xyoo. Canagliflozin ua rau muaj 30% kev pheej hmoo txo ​​qis ntawm cov txiaj ntsig tseem ceeb (ESKD, ob npaug ntawm cov ntshav creatinine, lossis tuag los ntawm lub raum lossis mob plawv). Cov pab pawg canagliflozin kuj muaj 31% qis dua ntawm cov hlab plawv tuag, myocardial infarction, lossis mob stroke (HR 0.80; 95% CI, 0.67 txog 0.95; P=0.01) thiab pw hauv tsev kho mob rau lub plawv tsis ua haujlwm (HR 0.61; 95 % CI, 0.47 txog 0.80; P <0.001).

Nrog rau cov txiaj ntsig ntawm lub raum ntshiab ntawm Canagliflozin ntawm albuminuric CKD cov neeg mob nrog T2DM, qhov thib ob raum cov txiaj ntsig tau sim siv dapagliflozin tau luam tawm hauv 2020. DAPA-CKD randomized 4304 cov neeg mob CKD (eGFR 25–75 mL/min/1.73m2), nrog lossis tsis muaj ntshav qab zib, albuminuria (200} rau 5{{ 49}}00 mg/g), uas tau ruaj khov ntawm renin-angiotensin system blockade rau 4 lub lis piam lossis ntau dua kom tau txais dapagliflozin 10 mg lossis placebo.2 Ib zaug ntxiv, txoj kev tshawb no tau raug tso tseg ua ntej vim muaj kev ua tau zoo. Cov pab pawg Dapagliflozin muaj 44% txheeb ze kev pheej hmoo txo ​​qis ntawm qhov tseem ceeb ntawm kev poob qis hauv qhov kwv yees GFR tsawg kawg yog 50%, ESKD, lossis tuag los ntawm lub raum lossis mob plawv (HR 0.56, 95% CI, 0.45 txog 0.68; P <0.001). Cov txiaj ntsig ntawm cov hlab plawv ntawm dapagliflozin, lossis chav kawm SGLT2i, tau pom meej meej nrog 29% kev pheej hmoo txo ​​qis ntawm kev sib xyaw ntawm kev tuag los ntawm cov hlab plawv lossis mus pw hauv tsev kho mob rau lub plawv tsis ua haujlwm. Cov nyhuv ntawm dapagliflozin kuj zoo ib yam li cov neeg mob CKD uas muaj lossis tsis muaj ntshav qab zib. Kev sim loj nrog qhov sib txawv SGLT2i tuaj yeem pom hauv daim duab 1. Lwm qhov kev sim tiag tiag hauv ntiaj teb saib cov txiaj ntsig ntawm lub raum nrog SGLT2i siv yog CVD-REAL 3.19 Qhov kev soj ntsuam kev soj ntsuam no pom tias kev siv SGLT2i cuam tshuam nrog kev txo qis eGFR (qhov sib txawv ntawm txoj kab nqes rau SGLT2i vs. Lwm cov tshuaj txo qis ntshav qabzib 1.53 mL / min / 1.73 m2 ib xyoos twg, 95% CI 1.34–1.72, p < 0.0001) thiab qis dua ntawm lub raum loj (kev phom sij piv 0.49, 95% CI 0.35–0.67; p <10). . Ib yam li ntawd, cov kev tshawb pom no tau zoo ib yam thoob plaws pawg sub thiab ntau thaj chaw thoob plaws ntiaj teb.

Empagliflozin-tshwj xeeb rau lub raum kev sim tau raug luam tawm tsis ntev los no (EMPA-KIDNEY).

The EMPA-KIDNEY is the third of the kidney outcome trials for the SGLT2i class. EMPA-KIDNEY randomized 6609 patients to empagliflozin 10mg, versus placebo, to test its effect on kidney disease progression (ESKD, a sustained eGFR below 10mL/min/1.73m2, kidney death, or a sustained ≥40% decline in eGFR) and cardiovascular death.20 EMPA-KIDNEY included patients with more advanced CKD without albuminuria (eGFR > 45 down to 20mL/min/1.73m2 ) or patients with CKD stage 1–3a (eGFR 45->90 mL/min/ 1.73m2 ) nrog rau cov zis albumin: creatinine ratio Ntau dua los yog sib npaug rau 200 mg/g (los yog protein: creatinine ratio Ntau dua los yog sib npaug rau 3 {{30}}0 mg/g). Lub hnub nyoog nruab nrab yog 63.8 xyoo, 54% tsis muaj keeb kwm ntawm DM, thiab qhov nruab nrab eGFR yog 37.5 mL / min / 1.73 m2. Nrog rau qhov nruab nrab ntawm 2.0 xyoo tom qab, kev loj hlob ntawm cov kab mob raum lossis tuag los ntawm cov hlab plawv tau tshwm sim hauv 432 ntawm 3304 tus neeg mob (13.1%) hauv caj npab empagliflozin thiab hauv 558 ntawm 3305 tus neeg mob (16.9%) hauv cov placebo caj npab (kev phom sij. piv, 0.72; 95% kev ntseeg siab lub sijhawm [CI], 0.64 txog 0.82; P < 0.001). Cov txiaj ntsig kuj tseem zoo ib yam ntawm cov neeg mob uas muaj thiab tsis muaj ntshav qab zib. Cov ntaub ntawv no tau muab piv rau yav dhau los cov txiaj ntsig nyuaj ntawm kev sim canagliflozin thiab dapagliflozin. Cov ntaub ntawv no tau nthuav tawm ntawm American Society of Nephrology Raum Lub Limtiam lub rooj sib tham 2022 nrog kev zoo siab thiab kev zoo siab.

Daim duab 1 Xaiv cov kev sim tshuaj ntsuam xyuas ntawm SGLT2 inhibitors hauv CVD thiab CKD. * Qhov tseem ceeb rau CV tuag lossis HHF tab sis tsis yog rau MACE. Nrog kev tso cai los ntawm Jefferson Triozzi. Muaj los ntawm: https://www.grepmed.com/images/12169/ebm-table-inhibitors-cvd-visualabstract. Cov ntawv luv: ASCVD, atherosclerotic cardiovascular kab mob; T2DM, hom 2 mob ntshav qab zib mellitus; CKD, mob raum mob; eGFR, kwv yees glomerular pom tus nqi; CV, mob plawv; MI, myocardial infarction; SCr, ntshav creatinine; ESKD, kawg xeev kab mob raum; HF, lub plawv tsis ua hauj lwm; GDMT, kev qhia qhia kev kho mob; MACE, cov xwm txheej mob plawv loj; HHF, tsev kho mob rau lub plawv tsis ua hauj lwm.

SGLT2 inhibitors tau dhau los ua thiab yuav tsum yog thawj kab kev kho mob, ua ke nrog RAAS blockers, rau kev tswj hwm cov neeg mob nrog CKD muab lawv cov txiaj ntsig cardiorenal. Lawv txoj kev nyab xeeb txuas ntxiv tau lees paub nrog ntau qhov kev sim loj randomized. Tshwj xeeb, qhov teeb meem ntawm kev txiav thiab tawg uas ua ntej tau pom hauv CANVAS mus sib hais, tam sim no nyob rau hauv txoj kab nrog cov placebo hauv DAPA-CKD thiab EMPA-KIDNEY mus sib hais. Cov kab mob mycotic thiab urinary kab mob tseem yog ib qho teeb meem, tab sis kev tshuaj xyuas zoo dua thiab kev saib xyuas nrog kev siv lub ntiaj teb tiag tiag yuav tsum ua rau cov teeb meem no tsis tshua muaj.

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