Yuav Ua Li Cas Ntxiv Hlau Rau CKD Raum Ntshav Qab Zib, Koj Puas Tau Txais?

Feem ntau ntawm cov kab mob ntshav qab zib hauv lub raum tsis zoo (CKD) yog siab, nrog ntau dua 50% ntawm cov ntshav ntshav hauv cov neeg tsis tau lim ntshav thiab ntau dua 90% ntawm cov neeg mob ntshav qab zib. Yog li ntawd, lub raum anemia yog ib qho teeb meem tshwm sim hauv cov neeg CKD. Hauv kev kho mob ntawm CKD anemia, txawm hais tias nws yog kev siv cov tshuaj erythropoiesis-stimulating agents (ESAs) los yog hypoxia-inducible factor-prolyl hydroxylase inhibitors (HIF-PHI), qhov yuav tsum tau ua ua ntej yog kho cov hlau tsis txaus, tab sis tam sim no muaj ntau cov hlau. teeb meem nrog kev siv cov khoom siv hlau tam sim no, suav nrog lub sijhawm ntawm kev siv thawj zaug, kev siv cov kev siv thiab ntau npaum li cas, nrog rau cov hom phiaj ntawm cov hlau metabolism yuav tsum tau ua tiav tom qab kev kho cov hlau ntxiv, txhua yam yuav tsum tau tshawb nrhiav ntxiv.

Nyem rau Cistanche rau mob raum

Hlau supplementation kho lub sij hawm thiab txoj kev

Txawm hais tias CKD cov neeg mob ntshav qab zib xav tau kev noj zaub mov ntxiv yuav tsum tau soj ntsuam los ntawm kev txheeb xyuas cov ntsuas cov hlau metabolism. Feem ntau siv cov ntsuas yog ferritin thiab transferrin saturation los soj ntsuam seb cov neeg mob puas muaj hlau tsis txaus thiab hom hlau tsis txaus. Txo cov khw muag khoom hlau thiab hlau txav / thauj khoom yog ob qho tib si tsis muaj hlau tsis txaus; Cov khw muag khoom hlau ib txwm lossis siab siab thiab txo cov hlau txav / thauj mus los yog kev ua haujlwm tsis muaj hlau. Iron supplementation yog pom zoo rau cov neeg mob uas tsis muaj hlau tsis txaus, tab sis kev saib xyuas cov xwm txheej hlau tseem yuav tsum tau saib xyuas. Cov neeg mob uas muaj ntshav qab zib ua ke thiab kev kho mob thawj zaug rau ntshav qab zib yuav tsum tau kuaj ib hlis ib zaug, tshwj xeeb tshaj yog cov neeg mob uas tau txais cov hlau ntxiv. Cov neeg mob uas nyob rau theem kev kho mob lossis uas nws cov hemoglobin ruaj khov yuav tsum tau kuaj tsawg kawg txhua 3 lub hlis.

Xyoo 2021 Suav Cov Kws Kho Mob Cov Lus Qhia rau Kev Ntsuas thiab Kev Kho Mob Raum Ntshav Qab Zib pom zoo SF<100 μg/L and/or TSAT<20% for CKD non-dialysis and peritoneal dialysis patients, and SF<200 μg/L and/or TSAT<20% for hemodialysis patients. Start considering iron supplementation. Oral iron supplementation is recommended for non-dialysis and peritoneal dialysis patients. If oral iron supplementation is intolerable or ineffective, intravenous iron supplementation should be considered, while intravenous iron supplementation is recommended for hemodialysis patients. It should be noted that during iron supplementation treatment, especially for patients taking intravenous iron supplementation, close monitoring of iron status indicators must be strengthened, and blood must be collected 1 week after stopping intravenous iron supplementation to reflect the true level of iron in the body. , provide evidence on whether to continue iron supplementation. If a low response to treatment occurs after regular treatment, it should be re-evaluated whether there are other risk factors that aggravate anemia or other diseases that cause anemia, and corresponding treatment should be given instead of blindly supplementing iron. Blindly excessive iron supplementation may lead to excessive iron load, exceeding iron needs, and deposition of iron in important organs (such as heart, liver, spleen, pancreas, thyroid, etc.), causing structural damage and dysfunction. Therefore, the timing and method of iron supplementation are very important.

Lub hom phiaj ntawm kev kho cov hlau ntxiv

Ntau cov lus qhia yav dhau los tau pom zoo tias qhov txwv siab tshaj ntawm cov hlau ntxiv yog SF<800 μg/L, which has been slightly lowered in recent years to SF<500 μg/L. We know that the most important method for the treatment of renal anemia is to regulate endogenous EPO through HIF-PHI, or to use ESAs to supplement exogenous EPO. The ultimate goal of both methods is to increase EPO levels, but their mechanisms different. In addition to regulating endogenous EPO, HIF-PHI also regulates various aspects of iron metabolism, promoting intestinal absorption of iron, promoting iron release from macrophages, and promoting iron transport to bone marrow cells. Based on this, it also reminds us that the targets of iron supplementation therapy may be different between the two treatment options. Based on current experience, in the real world, iron supplementation is required for patients with absolute iron deficiency regardless of whether they receive ESAs or HIF-PHI. For patients with functional iron deficiency, especially those with ferritin in the normal range but low TSAT, iron supplementation should not be continued, but iron utilization should be promoted. The treatment plan can be changed from ESAs to HIF-PHI to avoid iron overload in the later period. Case.

The PIVOTAL study, the world's first to evaluate intravenous iron supplementation strategies for hemodialysis patients, was published in the New England Journal in 2019. The upper limit of SF in the high-dose group was 700 ug/L, but in terms of safety assessment, RI and other methods were not used to detect the presence of iron. overload, so its conclusions have certain limitations. The multi-center epidemiological survey we initiated in the Jiangsu, Anhui and Jiangxi regions showed that SF>100ug / L tuaj yeem ua tau raws li qhov xav tau ntawm kev kho mob ntshav qab zib hauv cov neeg mob hemodialysis. Raws li kev paub dhau los ntawm kev ua haujlwm hauv chaw kho mob, peb lub chaw teeb tsa lub siab tshaj plaws ntawm cov hlau ntxiv SF rau 400ug / L. Rau cov neeg mob siv txoj kev npaj kho mob HIF-PHI, SF tuaj yeem tswj tau siab dua 200ug / L. Rau cov neeg mob uas siv ESAs txoj kev npaj kho mob, SF tuaj yeem khaws cia ntawm 200-200ug/L. Nyob nruab nrab ntawm 400ug / L, tau kawg, kev sim tshuaj loj loj yuav ua rau kuv lub tebchaws CKD cov pej xeem yav tom ntej los txiav txim siab lub hom phiaj zoo tshaj plaws rau kev ntxiv hlau.

Kev tswj ntawm Iron Deficiency thiab Iron Overload

Thaum kho cov neeg mob CKD anemia, kev saib xyuas yuav tsum tau them rau kev txheeb xyuas qhov ua haujlwm ntawm cov hlau tsis muaj zog. Qee tus neeg mob tuaj yeem tshwm sim nrog ob qho tib si ua haujlwm tsis muaj hlau thiab hlau ntau dhau. Kev ua haujlwm hlau tsis txaus txhais tau hais tias tag nrho lub cev hlau cov ntsiab lus yog qhov qub lossis nce ntxiv. Vim hais tias hlau yog khaws cia nyob rau hauv lub reticuloendothelial system xws li lub siab thiab tus po, nws tsis tuaj yeem raug tso tawm thiab thauj mus rau cov pob txha pob txha los koom rau hauv cov qe ntshav liab. Feem ntau hais lus, muaj cov khoom hauv lub tsev khaws khoom, tab sis lub peev xwm thauj khoom tsis txaus thiab tsis tuaj yeem xa tuaj. . Nws tshwm sim raws li qhov tsis muaj cov hlau khaws cia tab sis tsis muaj cov hlau thauj khoom, ua rau cov hlau tsis muaj zog hauv cov ntshav liab. Qhov siab hepcidin yog qhov txuas tseem ceeb hauv kev ua haujlwm tsis muaj hlau.

Nws tuaj yeem ua rau ferroportin ntawm cov cell membrane ntawm plab hnyuv epithelial hlwb thiab reticuloendothelial system, ua rau nws mus rau sab hauv thiab degraded. Hlau tsis tuaj yeem raug xa tawm ntawm cov hlwb thiab raug kaw hauv cov hlwb. . Kev mob hauv CKD thiab cov hlau ntau dhau hauv lub cev yog qhov ua rau muaj kev nce qib hepcidin. Cov hlau ntau dhau raug kaw rau hauv cov kab mob reticuloendothelial, ua rau cov hlau ntau dhau, uas tuaj yeem ua rau lub cev lossis kev ua haujlwm puas tsuaj rau lub plawv, ntsws, daim siab, tus po, pancreas thiab lwm yam kabmob, tawv nqaij pigmentation, thiab lwm yam. , kev tiv thaiv kev ua haujlwm tsis zoo, thiab lwm yam, cuam tshuam rau cov neeg mob.

MRI yog tus qauv kub rau kev kuaj mob hlau overload. Rau kev kho mob ntawm kev ua haujlwm tsis muaj hlau tsis muaj peev xwm, kev txhaj tshuaj ntxiv rau hauv cov hlab ntsha yuav tsum tau nres ua ntej. Lub hom phiaj ntawm kev kho mob yog nce hlau thauj thiab siv. HIF-PHI tuaj yeem siv los txo qis hepcidin, nce kev hloov pauv thiab tag nrho cov hlau khi muaj peev xwm, thiab txo qis ferritin. , txhawb kev siv hlau thiab txo cov hlau ntau dhau. Ntxiv rau HIF-PHI, cov neeg mob uas muaj hemodialysis lossis peritoneal dialysis tuaj yeem ua rau mob ntshav qab zib ntau ntxiv; rau cov hlau hnyav hnyav, siv cov chelators hlau, xws li deferoxamine, deferoxamine, deferasirox dispersible ntsiav tshuaj; hlau overload ua ke nrog hemoglobin insufficiency Cov neeg mob uas tsis muaj ntshav siab tuaj yeem tau txais kev kho ntshav. Hlau overload yog tshwm sim los ntawm iatrogenic yam nyob rau hauv ntau zaus, yog li kev tiv thaiv yuav tsum yog qhov tseem ceeb.

Cov ntsiab lus

Txawm hais tias cov neeg mob ntshav qab zib CKD tau txais kev kho HIF-PHI lossis ESAs, kev siv hlau ntxiv yuav tsum tau ceev faj. Iron supplementation tsuas yog tsim nyog rau cov neeg mob uas tsis muaj hlau tsis muaj peev xwm, tshwj xeeb tshaj yog cov hlau ntxiv rau hauv cov hlab ntsha. Hlau ntsuas cov metabolism yuav tsum tau saib xyuas zoo thaum lub sijhawm ua haujlwm. Hauv CKD anemia, yuav tsum tau saib xyuas kom paub txog kev ua haujlwm tsis muaj hlau. Rau cov neeg mob no, txawm hais tias kev ntxiv hlau tuaj yeem tau txais txiaj ntsig rau qee cov neeg mob ntshav qab zib, nws tseem ua rau muaj kev phom sij ntau dua li qhov zoo. Cov kev taw qhia ntawm kev kho mob yuav tsum yog los txhawb kev siv hlau thiab txheeb xyuas qhov muaj cov hlau ntau dhau thaum ntxov li sai tau. Nrog rau kev ua kom zoo ntawm cov phiaj xwm kev kho mob ntshav qab zib, tshwj xeeb tshaj yog tib neeg txoj kev nkag siab tob txog cov metabolism hauv hlau, lub hom phiaj ntawm cov ntsuas hlau metabolism kuj hloov pauv. Tau kawg, qhov no yuav tsum muaj kev tshawb fawb soj ntsuam ntau ntxiv los muab pov thawj kev txhawb nqa, thiab nws kuj xav kom cov kws kho mob siv nws hauv kev kho mob. Txuas ntxiv mus sau cov kev paub hauv kev xyaum.

Cistanche kho mob raum li cas?

Cistancheyog ib hom tshuaj suav tshuaj ntsuab siv rau ntau pua xyoo los kho ntau yam mob, suav nrograumkab mob. 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 rauraumnoj 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 tshuab.

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.