Dab tsi yog Autoimmune Renal Diseases?
Mar 15, 2022
Hu rau: Audrey Hu Whatsapp / hp: 0086 13880143964 Email:audrey.hu@wecistanche.com
Cov kab mob autoimmune raum
Mårten Segelmark, Thomas Hellmark ⁎
TSAB NTAWV
Qhov thib ob feem ntau ua rau mob ntevlub raumKev tsis ua haujlwm yog glomerulonephritis, uas yog ib lo lus siv los siv rau ntau yam kab mob nrog cov kab mob sib txawv ntawm cov kab mob histological.lub raumo emanating los ntawm glomerular tuft. Txawm hais tias txhua hom glomerulonephritis yuav tsum raug suav hais tias yog kab mob autoimmune yog qhov sib cav, tab sis kev tiv thaiv kab mob tseem ceeb hauv txhua tus. Qhov kev tshuaj xyuas no tsom mus rau plaub hom kev piav qhia zoo ntawm thawj glomerulonephritis: Goodpasture's lossis anti-GBM kab mob,IgAnephritis, membranous nephropathy, thiab membranoproliferative glomerulonephritis. Cov autoantibodies raug coj mus rau cov molecules nyob rau hauv lub glomeruli, xws li lub glomerular qab daus daim nyias nyias nyob rau hauv anti-GBM kab mob, thiab mus rau lub podocytes nyob rau hauv membranous glomerulonephritis, los yog rau lub Cheebtsam ntawm lub cev tsis muaj zog xws li C3 convertase nyob rau hauv membranoproliferative glomerulonephritis thiab IgA. . Qhov sib txawv ntawm kev kuaj mob thiab kev faib tawm cov kev tsis sib haum xeeb tsis pom kev sib piv cov kev tshawb fawb txog kab mob sib kis, tab sis zoo li muaj qhov sib txawv loj ntawm cov xwm txheej ntawm cov teb chaws, thiab dhau sij hawm, ob qho tib si caj ces thiab kab mob zoo li muaj teeb meem tab sis cov lus qhia muaj zog rau lub luag haujlwm ntawm lwm yam ib puag ncig tseem tsis muaj. .
Ntsiab lus
Anti-GBM kab mob,IgA nephritis, Membranousnephropathy, Membranoproliferative glomerulonephritis
Cistanche tiv thaiv lub raumkab mob
Taw qhia
Lub cev tiv thaiv kab mob koom nrog ntau homlub raumkab mob, tab sis tsis muaj kev lees paub thoob ntiaj teb ntawm lo lus autoimmune raum kab mob. Qhov feem ntau ua rau lub raum tsis ua haujlwm thoob ntiaj teb niaj hnub no yog ntshav qab zib mellitus, thiab tsawg kawg rau hom ntshav qab zib hom I, lub hauv paus chiv keeb yog suav tias yog autoimmune. Covlub raumKev puas tsuaj hauv ntshav qab zib nephropathy tsis yog tshwm sim los ntawm autoimmunity, txawm li cas los xij, thiab hom ntshav qab zib hom 1 tau them rau hauv Tshooj 24 hauv qhov teeb meem no. Qhov thib ob feem ntau ua raumob ntevlub raumua tsis tiavyog glomerulonephritis, uas nyob rau hauv lem yog ib tug collective lub sij hawm siv rau ib tug ntau yam ntawm cov kab mob nrog cov feem ntau denominator ntawm histological.lub raummobemanating los ntawm glomerular tuft. Txawm hais tias txhua hom glomerulonephritis yuav tsum raug suav hais tias yog kab mob autoimmune yog qhov sib cav, tab sis kev tiv thaiv kab mob tseem ceeb hauv txhua tus. Cov txheej txheem tiv thaiv kab mob kuj koom nrog hauv cov kab mob ntawm ntau hom kab mob tubulointerstitial, tab sis ntawm no autoimmunity yog suav tias yog qhov tseem ceeb tsawg rau feem ntau ntawm cov neeg mob. Yog li ntawd, peb yuav tsom mus rau qhov kev tshuaj xyuas no rau cov kab mob glomerular
Glomerulonephritis feem ntau yog cais ua thawj thiab theem nrab. Secondary glomerulonephritis tuaj yeem pom nyob rau hauv cov kab mob inflammatory xws li vasculitis me me (saib Tshooj 20 hauv qhov teeb meem no) thiab kab mob lupus erythematosus (saib Tshooj 14 hauv qhov teeb meem no), kab mob sib kis (malaria, HIV, kab mob siab, thiab lwm yam), thiab nyob rau hauv malignancies. Kev faib tawm ntawm thawj glomerulonephritis yog qhov sib cav thiab tsis meej pem. Ib qho laj thawj tseem ceeb ntawm kev tsis meej pem yog qhov tsis sib haum xeeb ntawm kev tshawb pom histological thiab kev kho mob, ua rau muaj kev cuam tshuam loj heev ntawm cov kab mob uas tau teev tseg los ntawm cov chaw kho mob thiab cov kab mob uas txhais los ntawm histological nta. Nrog rau qhov no hauv siab, peb tau xaiv los tsom qhov kev tshuaj xyuas no thiab plaub hom kev piav qhia zoo ntawm thawj glomerulonephritis, tag nrho nrog cov ntsiab lus histological uas tau txais dav: Goodpasture's disease (GP),IgAnephritis(IGAN), membranous nephropathy (MN), thiab membranoproliferative glomerulonephritis (MPGN).
Cistanche tiv thaiv lub raumua tsis tiav
2. Feem ntau ntawm glomerulonephritis
2.1. Kev tshawb pom thiab kev kuaj mob
Cov tsos mob ntawm glomerulonephritis yog hematuria, proteinuria, tso zis tso zis, thiab txo qis glomerular pom tus nqi (GFR). Lub xub ntiag thiab qhov hnyav ntawm txhua yam ntawm cov cim qhia no sib txawv heev ntawm cov kab mob thiab ntawm tus neeg mob. Txawm li cas los xij, nws yog ib qho kev sib txawv ntawm qhov sib txawv ntawm cov cim hauv kev kho mob syndromes, ib daim ntawv teev npe ntawm 6 cov lus siv feem ntau rau glomerulonephritis syndromes tau nthuav tawm hauv Table 1. Muaj kev sib raug zoo ntawm cov kev tshawb pom histological thiab cov tsos mob, tab sis kev sib raug zoo tsis txaus. tso cai kuaj mob yam tsis muaj alub raumbiopsy. Ib qho txiaj ntsig ncaj qha ntawm lub luag haujlwm tseem ceeb ntawmlub raumbiopsies yog qhov qhia thiab contraindications rau cov txheej txheem no muaj kev cuam tshuam loj heev rau cov neeg uas tau txais kev kuaj mob ntawm glomerulonephritis. Qhov no blurs daim duab rau txhua tus neeg xav txog caj ces lossis ib puag ncig cuam tshuam rau cov kab mob glomerular.
2.2. Lub raum biopsy
Lub raumKev sau npe biopsy yog cov ntaub ntawv tseem ceeb thaum sim txheeb xyuas qhov sib txawv ntawm kev kis tus kab mob glomerular, tab sis muaj ntau qhov kev txiav txim siab los txiav txim siab. Ib rab koob biopsy yog tus txheej txheem invasive, uas yog nrog los ntawm me me, tab sis muaj peev xwm txaus ntshai los ntshav loj. Alub raumbiopsy tsuas yog tsim nyog yog tias cov ntaub ntawv tau txais tuaj yeem hloov kho kev kho mob rau tus neeg mob. Thaum cov kev kho tshiab tau qhia, qhov no cuam tshuam rau kev kuaj mob. Lub raum biopsies tsis tshua muaj nyob rau hauv cov neeg mob sab nraud, thiab cov kev pabcuam raum pathology feem ntau txwv rau cov chaw xa mus rau qib siab thiab tsev kho mob hauv tsev kawm ntawv. Socioeconomic yam tseem ceeb cuam tshuam qhov muaj feem yuav tau txais kev nkag mus rau biopsies thaum xav tau, uas txwv tsis pub muaj peev xwm kawm txog cov txiaj ntsig zoo li no ntawm qhov tshwm sim ntawm glomerulonephritis.
Cov neeg mob hnub nyoog muaj feem cuam tshuam loj rau kev txiav txim siab ua biopsy [1]. Qhov feem pua ntawm cov neeg mob uas yog cov neeg laus thaum lub sij hawm biopsy nws txawv heev ntawm cov chaw zov me nyuam thiab dhau sij hawm. Hauv kev tshawb fawb raws li kev sau npe Suav, feem pua ntawm cov neeg mob N60 xyoo uas muaj tus kab mob glomerular thawj zaug tau nce los ntawm 0 feem pua hauv xyoo 1993 txog 9 feem pua hauv 2007 [2,3]. Hauv Serbia thaum lub sijhawm xyoo 1987-2006, tsuas yog 8.5 feem pua ntawm 1626 tus neeg mob tau siab dua 60 thaum lub sijhawm biopsy [4], thaum nyob Spain 26 feem pua ntawm cov neeg laus laus dua 65 [5].
Cov urinary abnormalities tsis tu ncua (UA) muaj ntau, thiab cov kev tshawb fawb qhia tias qib qis hematuria thiab/los yog proteinuria yuav tsum muaj nyob rau hauv 2-5 feem pua ntawm cov pejxeem. Tsuas yog ib feem me me ntawm cov neeg no thaum kawg yuav nce mustheem kawglub raumkab mob, thiab biopsy feem ntau tsis qhia [6,7]. Muaj, txawm li cas los xij, muaj ntau qhov sib txawv ntawm cov teb chaws, hauv cheeb tsam Limburg hauv Netherlands 46 feem pua ntawm cov tshuaj biopsies tau ua nrog UA raws li qhov qhia [6], thaum nyob hauv Serbia [4] thiab Tuam Tshoj [3] cov ntaub ntawv sib xws yog 29 feem pua. thiab 16 feem pua. Rau lwm cov kev qhia xws li, xws li nephrotic syndrome nyob rau hauv cov tub ntxhais hluas, ib tug muaj peev xwm xav tias me me variations nyob rau hauv kev kho mob ntawm cov tsev kho mob thiab cheeb tsam. Yog li ntawd, thaum sim sib piv cov xwm txheej ntawm cov teb chaws nws yog qhov muaj kev ntseeg siab dua los sib piv qhov feem pua ntawm cov neeg mob uas muaj qee yam kev kuaj mob nrog nephrotic syndrome dua li kev sib piv ntawm cov neeg mob hauv tag nrho cov ntawv sau npe muaj qhov kev kuaj mob no.
Tsis tas li ntawd, lublub raumKev kuaj biopsies feem ntau yog kuaj tsis yog los ntawm lub teeb microscopy nkaus xwb tab sis kuj los ntawm immunofluorescence (IF) thiab electron microscopy (EM). Txawm hais tias IF yog qhov xav tau tiag tiag rau qee qhov kev kuaj mob, tsis yog txhua qhov biopsies raug kuaj xyuas hauv qee qhov [4], thaum nyob rau hauv lwm cov qauv xws li cov qauv raug suav tias tsis txaus thiab tsis suav. Nyob rau hauv ib qho zoo sib xws tej yam kev kuaj mob, xws li cov kab mob hauv qab daus nyias, tsis tuaj yeem ua yam tsis muaj EM.
Lub raumKev kuaj ntshav biopsy tsis suav tias yog qhia tau thaum kuaj pom muaj qhov tsim nyog yam tsis muaj histology. Qhov no yog rooj plaub rau mob tubular necrosis nyob rau hauv mob raum tsis ua hauj lwm, tsawg heev hloov kab mob nyob rau hauv cov me nyuam yaus nrog nephrotic syndrome, thiab ntshav qab zib.nephropathyHauv cov neeg mob ntshav qab zib mellitus thiab cov proteinuric ntevlub raumua tsis tiav. Hauv cov xwm txheej zoo li no, feem ntau cov kws kho mob nephrologists xaj ib koob tshuaj tsuas yog tias muaj cov cim qhia tsis sib xws. Txawm li cas los xij, qhov sib txawv loj muaj nyob rau ntawm qhov tseem ceeb los muab cov cim sib txawv ntawm qhov tsis sib xws.
3. Anti-GBM kab mob
3.1. Cov kev tshawb pom tseem ceeb
Goodpasture's disease, tseem hu ua anti-GBM kab mob, yog ib yam kab mob autoimmune tsawg. Cov neeg mob tsim autoantibodies tawm tsam noncollagenous domain 1 ntawm 3 saw ntawm hom IV collagen (3(IV) NC1) ua rau glomerulonephritis thiab ntsws hemorrhage [8]. Cov neeg mob muaj kev loj hlob sai mus raulub raumtsis ua hauj lwm thiab tuag yog tias tus kab mob no tsis paub thiab kho thaum ntxov.
Qhov kev nthuav qhia raug yog hais tias ntawm reno-pulmonary syndrome piv txwv li kev sib xyaw ntawmlub raumthiab pulmonary insufficiency. Txawm li cas los xij, ntau hom kev nthuav qhia tau piav qhia. Hauv qee qhov, ntau dua 50 feem pua, ntawm cov neeg mob tam sim no tsuas yoglub raumkev koom tes [9]. Feem ntau txhua tus muaj microhematuria, ntau tus muaj macrohematuria thiab sai heevlub raumkev tsis txaus yog tshwm sim. Qee lub sij hawm qhov kev loj hlob yog tawg ua rau anuria nyob rau hauv ib hnub, thaum ib tug tsawg ntawm cov neeg mob muaj ib tug protracted chav kawm uas tuslub raummuaj nuj nqi yog khaws cia rau ob peb lub hlis. Cov tsos mob tshwm sim rau cov neeg mob uas muaj mob ntsws yog hemoptysis, exertional dyspnoea, hnoos, thiab qaug zog. Cov hemorrhage tshwm sim feem ntau nyob rau hauv alveolar qhov chaw thiab tej zaum yuav ua rau cov cim tsis muaj hlau tsis txaus anemia lossis exertional dysnoea txawm tias tsis muaj hemoptysis. Muaj tsawg zaus, cov neeg mob muaj cov kab mob tshwm sim uas nyob rau hauv lub ntsws
3.2. Histology thiab pathogenesis
Lub teeb microscopy feem ntau qhia pom dav dav dav crescent tsim. Qhov feem pua ntawm glomeruli nthuav tawm crescents feem ntau tshaj 80 feem pua , thiab feem pua feem ntau cuam tshuam raulub raumua haujlwm nrog rau qhov tshwm sim tom qab kev kho mob. Qhov kev tshawb pom ntawm qhov tsis ncaj qha immunofluorescence microscopy yog linear staining ntawm IgG raws GBM, feem ntau nrog C3 deposition. Lwm cov qauv staining yog qee zaum pom, tshwj xeeb tshaj yog nyob rau hauv cov mob me me nrog khaws cialub raumua haujlwm zoo li hauv kev puas tsuaj glomeruli.
Ntau tus qauv tsiaj tau piav qhia qhia lub luag haujlwm ntawm cov kab mob ntawm cov tshuaj tiv thaiv GBM. Hauv kev sim classic, primates tsim glomerulonephritis tom qab txhaj tshuaj autoantibodies eluted los ntawm ob lub raum ntawm tus neeg mob nephrectomized raug kev txom nyem los ntawm kab mob GBM [10]. Kev sib raug zoo ntawm ib ntus ntawm kev rov qab los thiab rov tshwm sim ntawm autoantibodies kuj tau tshaj tawm. Lub titer ntawm circulating anti-GBM cov tshuaj tiv thaiv, raws li ntsuas los ntawm ELISA, tau pom tias muaj qhov tseem ceeb prognostic [11]. Cov neeg mob muaj cov tshuaj tiv thaiv kab mob polyclonal thiab txhim kho autoantibodies rau ntau qhov chaw ntawm antigen [12]. Ob lub epitopes loj tau raug txheeb xyuas [13], tab sis tsuas yog cov tshuaj tiv thaiv kab mob tiv thaiv ib qho cuam tshuam cov tshuaj lom ntawm cov tshuaj tiv thaiv [12]. Qhov no epitope yog nyob ze ntawm lub triple-helical junction. Lub epitope yog ib qho cryptotope thiab kev nkag tau rau cov tshuaj tiv thaiv GBM yog ib txwm txwv. Cov khoom cryptic tsis ntev los no tau pom tias yog vim kev sib txuas ntawm NC1 hexamer ntawm hom IV collagen [14]. Muaj pov thawj rau T-cell tivthaiv hauv kev tiv thaiv GBM kab mob. Lub autoantibody IgG subclass faib yog sib xws nrog Tcell mediated cov tshuaj tiv thaiv ntawm cov protein antigen. Ib tug mononuclear interstitial cell infiltrate yog invariably pom nyob rau hauv tib neeg los tiv thaiv GBM kab mob, muaj feem ntau ntawm CD4 ntxiv hlwb. Cov qauv tsiaj qhia txog lub luag haujlwm ntawm autoreactive T-cells thiab kev txhaj tshuaj nrog luv luv peptide, piv txwv li T-cell epitope, tuaj yeem ua rau muaj florid glomerulonephritis yam tsis muaj qhov ntsuas tau ntawm cov tshuaj tiv thaiv GBM [15].
3.3. Geoepidemiology
Tshaj tawm cov neeg mob tau tuaj ntawm New Zealand, Australia, UK, Asmeskas, Tuam Tshoj, thiab Scandinavia thiab kwv yees zaus sib txawv ntawm 0.5 mus rau 1 rooj plaub rau ib lab tus neeg nyob hauv ib xyoos. Tsis muaj qhov sib txawv loj ntawm cov neeg Esxias thiab Caucasian, raws li pom nyob rau hauv ntau lwm yam kab mob. Muaj ob lub ncov ntawm qhov tshwm sim ntawm hnub nyoog, nyob rau hauv peb thiab nyob rau hauv lub xya xyoo caum. Tus kab mob no tsis tshua muaj ua ntej puberty thiab tus txiv neej rau poj niam piv yog sib npaug [9,16,17].
Cov kev tshawb fawb caj ces tau nthuav tawm qhov sib txuas muaj zog ntawm cov kab mob antiGBM thiab HLA-DRB1 * 1501 thiab DRB1 * 1502. Cov ntawv tshaj tawm feem ntau yog los ntawm cov neeg Caucasian uas DRB1-15 antigen pom hauv 70–80 feem pua ntawm cov neeg mob, piv rau 20–30 feem pua ntawm cov tswj. Qhov kev sib txuas tsis zoo yog pom rau HLA-DR7 thiab DR1, yog li ua haujlwm tiv thaiv [16].
3.4. Environmental agents
Ntau qhov kev sim tau ua los nrhiav kev koom tes nrog kev kis kab mob tab sis tsuas yog cov ntaub ntawv qhia txog cov ntaub ntawv tau tshaj tawm. Qee cov ntawv tshaj tawm piav qhia txog kev txhim kho cov kab mob tiv thaiv GBM tom qab kev kho lithotripsy raulub raumpob zeb, tab sis lub koom haum no tsis tau lees paub hauv kev tshawb fawb loj [18]. Kev cuam tshuam rau cov tshuaj lom neeg, xws li cov kuab tshuaj organic thiab cov pa luam yeeb kuj tau hais kom muaj feem cuam tshuam [19]. Txawm li cas los xij, tsis muaj pov thawj tias ib qho ntawm cov xwm txheej no tuaj yeem ua rau muaj kab mob ib leeg, txawm hais tias nws zoo li txhua tus tuaj yeem hloov tus kab mob subacute mus rau qhov mob hnyav. Qhov txwv tsis pub lees paub yog sib xws nrog lub luag haujlwm muaj peev xwm rau molecular mimicry lossis kev txhaj tshuaj tiv thaiv tus kheej nrog cov seem ntawm cov tshuaj tiv thaiv. Muaj cov ntawv ceeb toom hais tias ib puag ncig yam xws li cov pa luam yeeb lossis lwm cov pa nqus pa tuaj yeem ua rau lub ntsws tshwm sim ntawm tus kab mob [19].
4. IgA-nephritis
4.1. Cov kev tshawb pom tseem ceeb
IgAnephritisAmeslikas piav raws li recurrent macroscopichematuria thiab mesangio proliferative glomerulonephritis nrog IgAdeposits nyob rau hauv lub mesangial cheeb tsam. Nws raug suav hais tias yog kab mob benigntshwm sim tshwj xeeb tshaj yog nyob rau hauv cov txiv neej hluas. Tom qab ntawd nws tau pom tias afeem ntawm cov neeg mob tau nce mus rau theem kawglub raumkab mob, thiabhais tias qee tus neeg mob muaj tus kab mob loj zuj zus yam tsis muaj ntu ntawmmacroscopic hematuria [20] Lwm yam kev nthuav qhia kuj taupiav xws li nephrotic syndrome (12 feem pua) thiab mob hnyavlub raumua tsis tiav
(9%) [21].
4.2. Histology thiab pathogenesis
Lub ntsiab lus txhais yog qhov tso tawm ntawm IgA hauv mesangium. IgA feem ntau nrog C3 thiab tsawg dua los ntawm IgG thiab C4. Cov qib ntawm hypercellularity txawv, tab sis feem ntau nws yog ib qho kev nce ntawm cov cell nyob rau hauv mesangial cheeb tsam nrog rau kev nce hauv mesangial matrix. Feem ntau ntawm IgA tso tawm yog ntawm IgA1 subclass thiab ntau tus neeg mob kuj tseem muaj ntau qhov sib txawv ntawm cov subclass no. Tej zaum muaj ntau yam laj thawj vim li cas IgA1 tuaj yeem khi thiab tau tso rau hauv glomeruli, vim qhov no tshwm sim raws li qhov tshwm sim thib ob hauv ntau yam mob, suav nrog daim siab cirrhosis, HIV, thiab dermatitis herpetiformis [22]. Hauv thawj IGAN(IgA nephritis)Kev tshawb nrhiav tshuaj tau qhia tias IgA1 molecules los ntawm cov neeg mob sib txawv hauv lawv cov qauv glycosylation piv rau IgA1 los ntawm cov neeg noj qab haus huv [20]. Luv O-txuas glycans hauv thaj tsam pob khawm tsis muaj qhov seem seem, uas tuaj yeem txo cov kab mob siab thiab ua rau muaj kev tsim cov IgG anti-IgA autoantibodies thiab kev tiv thaiv kab mob [23]. Nws yog qhov ua tau tias tsim cov IgG anti-IgA cov tshuaj tiv thaiv yog tsim nyog los ua kom muaj qhov mob txaus rau cov txheej txheem kab mob kom ua tau mus tas li.lub raumua tsis tiav.
4.3. Geoepidemiology
IgAnephropathyyog daim ntawv tshaj plaws ntawm thawj GN thoob ntiaj teb tab sis zoo li muaj ntau dua nyob hauv Asia piv rau Europe thiab North America [22]. Hauv kev sau npe kawm los ntawm Tuam Tshoj tau hais hauv Table 2, IGAN(IgA nephritis)tsim muaj ntau tshaj li ib nrab ntawm cov neeg mob ntawm biopsy-proven GN [3]. IGAN(IgA nephritis)muaj tsawg dua nyob rau hauv Tebchaws Europe tab sis cov duab nyob ib ncig ntawm 30 feem pua ntawm biopsies los ntawm cov neeg mob nrog thawj GN yog muaj nyob rau hauv cov ntaub ntawv tsis ntev los no [6,24]. Hauv Teb Chaws Asmeskas cov nuj nqis qis dua feem ntau yog nthuav tawm, tab sis kev tshawb fawb tsis ntev los no tau pom ib daim duab ntawm 14.2 feem pua ntawm cov tub ntxhais hluas [25]. Haiv neeg muaj feem cuam tshuam loj rau qhov muaj ntau ntawm IGAN(IgA nephritis)Hauv Teb Chaws Asmeskas, tus kab mob no tsis tshua muaj neeg Afro-Asmeskas, tab sis zoo li muaj ntau dua ntawm cov neeg Esxias thiab Caucasians [25]. Qhov no qhia tias cov caj ces tseem ceeb, tab sis lub luag haujlwm tseem ceeb rau MHC thiab IgA2 allotypes tau raug txiav tawm [26]. Ntau tsev neeg pawg ntawm IGAN(IgA nephritis)tau tshaj tawm tab sis kev tshuaj ntsuam genetic linkage tau taw qhia ntawm cov gene loci sib txawv hauv cov neeg sib txawv [23]. IGAN(IgA nephritis)Feem ntau ntawm cov txiv neej ntau dua li cov poj niam, qhov sib txawv ntawm 1.8: 1 [25] thiab 1.14: 1 [3] hauv cov ntaub ntawv sib txawv.
4.4. Environmental agents
Muaj kev sib raug zoo ntawm qhov exacerbations ntawm GN thiab kab mob, tshwj xeeb tshaj yog cov kab mob ua pa sab sauv. Qhov kev sib raug zoo no qhia tias cov kab mob ua pa tuaj yeem ua rau muaj lub luag haujlwm etiological hauv tus kab mob no, tab sis qhov no tsis muaj pov thawj. Txawm hais tias muaj ntau qhov kev sim siab, tsis muaj ib qho kab mob me me tau raug hu ua tus ua txhaum loj. Txhawm rau txo lub nra ntawm cov kab mob ua pa, tonsillectomy tau sim thiab tawm tswv yim rau [27].
Cov tshuaj tiv thaiv tsis zoo rau cov zaub mov antigens tau raug xav tias. Hauv kev txhawb nqa ntawm qhov kev xav no, nws tau pom tias muaj kev sib raug zoo ntawm tus kab mob celiac thiab IGAN(IgA nephritis)muaj [28]. Muaj cov lus ceeb toom txog kev txhim kho tom qab kev hloov pauv kev noj haus, xws li kev cais tawm ntawm gluten. Qhov ntau zaus ntawm cov txiv neej tuaj yeem piav qhia los ntawm cov caj ces lossis cov tshuaj hormonal tab sis kuj tau sib xws nrog cov kev xav tias kev ua haujlwm ua haujlwm tau ua lub luag haujlwm. Kuj tseem muaj cov lus ceeb toom txog kev koom tes ntawm cov organic solvent exposures thiab tsawg kawg yog qhov kev nce qib ntawm IGAN(IgA nephritis) [29]
5. Membranous nephropathy
5.1. Cov kev tshawb pom tseem ceeb
Feem coob ntawm cov neeg mob uas kuaj tau MN muaj nephrotic syndrome (NS). Qhov no muaj pov thawj nyob rau hauv Table 1, thiab nyob rau hauv Italian sau npe, 86 feem pua ntawm cov neeg mob MN tau txais kev kuaj mob biopsy vim yog NS [24]. MN tuaj yeem tshwm sim qee zaum thib ob rau lwm yam kab mob xws li kev kis kab mob thiab mob qog noj ntshav, thiab nws tuaj yeem tsim teeb meem rau qee yam tshuaj [30]. Idiopathic MN yog nyob ib ncig ntawm 2/3 ntawm tag nrho cov MN, tsawg kawg hauv lub ntiaj teb industrialized. Cov neeg mob feem ntau muaj qhov qublub raumKev ua haujlwm thaum lub sijhawm kuaj mob tab sis nyob rau hauv cov neeg mob nephrosis tsis tu ncua ntau zuj zus mus rau theem kawg ntawm lub raum kab mob.
5.2. Histology thiab pathogenesis
Cov yam ntxwv tseem ceeb ntawm cov kab mob pathological yog qhov tso tawm ntawm lub cev tiv thaiv kab mob ntawm cov zis ntawm lub glomerular hauv qab daim nyias nyias. Cov kev tso nyiaj no tuaj yeem pom ncaj qha los ntawm lub teeb microscopy li me me spikes thaum siv cov nyiaj stains, tab sis lawv pom tau zoo dua siv EM lossis IF. Cov
IF pom nyob rau hauv idiopathic MN yog ntxhib granular staining ntawm IgG uas txawv nws los ntawm cov membranous variant ntawm Lupus nephritis, qhov twg feem ntau yog tag nrho cov chav kawm ntawm immunoglobulin. Tus qauv tsiaj ntawm MN, hu ua Heyman nephritis, tau tsim ntau tshaj 50 xyoo dhau los [31]. Cov qauv no yog tsav los ntawm autoantibodies tsa tawm tsam tubular epithelial hlwb. Kev tshawb nrhiav ntev ntev rau cov kab mob autoantibodies hauv tib neeg MN tsis muaj txiaj ntsig, tab sis tsis ntev los no cov ntaub ntawv pov thawj tau tshaj tawm taw qhia txog qhov muaj autoantibodies qhia tawm tsam podocyte antigen hu ua phospholipase A2 receptor [32].
5.3. Geoepidemiology
Feem ntau ntawm MN thib ob rau kev kis kab mob sib txawv raws li kev sib kis ntawm tus kab mob. Hauv cov teb chaws uas muaj kab mob siab B thiab malaria yog ib yam kab mob, theem nrab MN yog qhov ua rau NS ntawm cov menyuam yaus thiab cov hluas [30]. Rau idiopathic MN tsis muaj qhov sib txawv ntawm qhov sib txawv ntawm cov teb chaws, raws li qhia hauv Table 2, MN suav nrog 12 thiab 23 feem pua ntawm cov neeg mob uas muaj GN thawj. Feem ntau ntawm cov kev hloov pauv tuaj yeem piav qhia los ntawm cov ntaub ntawv sib txawv ntawm UA thiab NS. Cov xwm txheej txhua xyoo nyob rau hauv thaj tsam ntawm 1 rau 100,000 cov neeg nyob hauv ib xyoos. Feem ntau cov ntawv ceeb toom qhia tus txiv neej ua ntej, nrog qhov sib piv ntawm 1.3: 1 [3] thiab 2.2: 1 [33].
5.4. Environmental agents
Nws paub meej tias cov tshuaj exogenous tuaj yeem ua rau MN. Ob yam tshuaj tiv thaiv kab mob kub ntsev thiab penicillamine paub zoo tias muaj feem cuam tshuam nrog MN raws li kev mob tshwm sim. Yuav ua li cas npaum li cas idiopathic MN tshwm sim los ntawm kev ua hauj lwm raug tsis paub.
6. Membranoproliferative glomerulonephritis
6.1. Cov kev tshawb pom tseem ceeb
MPGN tsis yog daim ntawv tshuaj ntsuam xyuas rau ib tus kab mob, tab sis qhov kev piav qhia ntawm tus qauv ntawm glomerular cov tshuaj tiv thaiv rau ntau yam ua rau, piv txwv li kev kis kab mob, ntxiv rau kev ua kom muaj kab mob hauv lub cev, kev hloov pauv ntawm cov khoom siv ntxiv, thiab tsim autoantibody. Nws feem ntau cuam tshuam rau cov neeg laus thiab cov menyuam yaus nrog 50 feem pua yog thawj zaug thiab ib nrab yog qhov thib ob vim muaj kab mob, cryoglobulinemia, lossis kab mob autoimmune [34]. MPGN feem ntau tshwm sim nrog cov proteinuria, hematuria, mob nephritic lossis nephrotic syndrome. MPGN cov neeg mob muaj qhov tsis zoo thiab muaj ntau yam kev nce qib mus rau theem kawglub raumua tsis tiav lawm thaum tseem yau. Feem ntau cov tsos mob ntawm MPGN yog nephrotic syndrome (35 feem pua), nephrotic syndrome (17 feem pua), los yog tag nrho hematuria [35]. Cov kev kwv yees tsis zoo rau qhov tshwm sim yog feem pua ntawm crescents, impairedlub raumkev ua haujlwm, kub siab, thiab nephrotic ntau yam proteinuria.
Kev kuaj mob yog nyob ntawm lub raum biopsies (saib hauv qab) tab sis cov yam ntxwv serological yog qib qis ntawm cov ntsiab lus ntxiv C1q, C3, thiab C4 thiab qee zaum muaj qhov cuam tshuam nephritic (C3Nef).
6.2. Histology thiab pathogenesis
Peb hom sib txawv ntawm thawj MPGN tau piav qhia los ntawm kev tshawb pom histological, MPGN I, II, thiab III. Lub teeb microscopy nta thiab kev nthuav qhia kho mob zoo ib yam ntawm peb hom MPGN. Morphological kev hloov pauv pom nyob rau hauv lub teeb microscopy feem ntau yog hypercellular glomeruli nrog kev loj hlob ntawm endothelial thiab mesangial hlwb ua rau lobular nam ntawm capillary tuft. Nyob rau hauv xyoo tas los no, kev cuam tshuam ntawm cov txheej txheem ntxiv thiab nws cov kev tswj hwm tau pom tias yog qhov tseem ceeb hauv cov kab mob pathogenesis [36]. Hom I (MPGN I) thiab III (MPGN III) yog qhov sib txawv ntawm cov kab mob immunocomplex-mediated thiab tus cwj pwm los ntawm cov qib C3 tsis tu ncua thiab hauv li 30 feem pua ntawm cov neeg mob los ntawm qhov muaj C3NeF. Lwm yam kev cuam tshuam ntawm cov txheej txheem ntxiv suav nrog qhov ua haujlwm H tsis ua haujlwm lossis qhov tsis txaus, tsis ua haujlwm C3 molecules, thiab txo qis B qib.
Hom II (MPGn II), tseem hu ua tus kab mob dense densuction nrog txoj kev tiv thaiv kab mob nrog rau ntawm C3NEF lossis los ntawm kev tsis xws luag ntawm cov tshuaj tiv thaiv cov protein, xws li Factor H. Hauv MPGN II hypocomplementemia feem ntau pom muaj C3 tsawg hauv cov kua dej, tab sis ib txwm C1q thiab C4 qib. EM tsom xam pom pom tias muaj cov khoom siv hluav taws xob-dense deposits raws glomerular qab daus daim nyias nyias, uas yog qhov kev kuaj mob rau MPGN II. IF qhia tau hais tias kev tso tawm ntawm cov protein ntxiv, suav nrog C3, properdin, thiab cov khoom siv dav hlau txuas ntxiv, thiab feem ntau tsis muaj IgG [37]. MPGN II tus yam ntxwv nce mus rau theem kawglub raumtsis ua hauj lwm thiab qhov rov tshwm sim ntawm lub raum hloov pauv kuj tseem nyob ze 100 feem pua [38]. C3NeF yog ib qho autoantibody pom nyob rau hauv 80 feem pua ntawm cov neeg mob thiab sawv cev rau qhov tseem ceeb rau autoimmune pathogenesis. C3NeF yog qhia tawm tsam C3 convertase C3bBb, ib qho ntawm cov ntsiab lus tseem ceeb ntawm kev ua kom tiav. Qhov no C3- hloov enzyme cleaves thiab activates C3 thiab muaj ib tug luv luv ib nrab-lub neej. C3NeF ncua lub neej ib nrab ntawm cov convertase thiab ua rau cov enzyme tsis tshua muaj kev cuam tshuam rau Factor H- thiab Factor I-mediated inactivation [39]. Kev nce C3 convertase kev ua ub no ua rau kev txhim kho C3b thiab C3a tiam thiab C3 noj, ua rau qis C3 thiab qib B plasma. C3NeF sawv cev rau pawg neeg heterogeneous ntawm IgG thiab IgM cov tshuaj tiv thaiv thiab qee zaum, kev ua haujlwm kuj tseem yuav ua raws li qhov tsim nyog.
MPGN III qhia tau hais tias tus qauv zoo ib yam li hauv MPGNII ntawm immunofluorescence thiab immunohistology nrog rau qhov tshwj xeeb uas tseem muaj cov tshuaj tiv thaiv kab mob subepithelial complex deposits. Ntawm electron microscopy, txawm li cas los xij, feem ntau yog qhov txawv txav ntawm GBM los ntawm qhov loj ntawm electron-dense deposits ntawm ob sab ntawm GBM tau pom thiab qhov no yog qhov txawv ntawm qhov kev tshawb pom hauv lwm hom MPGN [40]. Hom III ntawm MPGN yog tsis tshua muaj (kwv yees li 15 feem pua ntawm tag nrho MPGN) thiab nws muaj feem xyuam rau C3 thiab properdin thiab invariably kuj mus rau lub cev tsis muaj zog thiab C1q depositions feem ntau yog vim ob qho tib si (xws li kab mob siab B thiab C).
6.3. Geoepidemiology
Cov ntaub ntawv los ntawm lub raum biopsy sau npe qhia tias MPGN yog hom GN ntau tshaj plaws nyob rau sab hnub tuaj Europe, Africa, thiab thaj chaw ntawm Asia uas muaj ntau txog 30 feem pua [35]. Hauv Tebchaws Europe sab hnub poob, qhov muaj feem ntau ntawm MPGN nyob ib ncig ntawm 6 feem pua ntawm cov neeg mob biopsy-pov thawj GN [6,24] nrog qhov txo qis hauv qhov tshwm sim nyob rau kaum xyoo dhau los tej zaum yog vim muaj kev tswj xyuas zoo dua ntawm cov kab mob hauv qab. Hauv tsab ntawv tshaj tawm los ntawm Tuam Tshoj MPGN tsuas yog kwv yees li ntawm 1 feem pua ntawm thawj GN [3] thiab hauv kev tshawb fawb txog US tsis ntev los no hauv 1228 raum biopsies los ntawm cov neeg mob nrog thawj GN ib feem ntawm 1.2 feem pua ntawm cov neeg laus thiab 0.2 feem pua hauv cov neeg laus (20-39 xyoo) tau pom rau MPGN [25]. Lwm qhov kev tshawb fawb hauv Teb Chaws Asmeskas tau tshaj tawm hnub nyoog- thiab kev sib deev-hloov tus nqi rau MPGN ntawm 0.1–0.6 rau 100.000 cov neeg nyob nruab nrab ntawm 1974 thiab 2003 [21].
6.4. Environmental agents
MPGN tuaj yeem muab faib ua tej yam kev mob uas muaj lossis tsis muaj kev sib xyaw cryoglobulinemia. MPGN nrog cryoglobulinemia yuav tshwm sim ua ke nrog kab mob siab C (70-90 feem pua ntawm cov neeg mob) lossis lwm yam kab mob, xws li kab mob endocarditis lossis kab mob siab B. Nws kuj tseem cuam tshuam nrog cov kab mob vascular, piv txwv li SLE lossis hauv cov xwm txheej ntawm malignancies. MPGN tsis muaj cryoglobulinemia yog txuam nrog lwm yam kab mob, xws li endocarditis lossis abscess, kab mob ventriculo shunt, los yog kab mob kis, xws li HBV, HCV, HGV, HIV, thiab Hantavirus. Nws tuaj yeem pom ua ke nrog lwm yam kab mob xws li SLE, hypocomplementemia vasculitis, thiab malignancies. Lwm cov laj thawj feem ntau yog los ntawm noob caj noob ces thiab tau txais qhov tsis txaus.
7. Cov ntsiab lus
autoantibodies ntawm chav kawm IgG tuaj yeem pom nyob rau hauv ntau hom ntawm thawj glomerulonephritis thiab zoo li yog qhov tseem ceeb tshaj plaws rau cov kab mob pathogenesis, uas tso cai rau cov kab mob no suav tias yog keeb kwm autoimmune. Cov autoantibodies raug coj mus rau cov molecules hauv glomerular tuft, xws li GBM hauv GP thiab rau cov podocytes hauv MN, lossis rau cov khoom ntawm lub cev tiv thaiv kab mob xws li C3 convertase hauv MPGN thiab IgA hauv IgAN.(IgA nephritis). Qhov sib txawv ntawm kev kuaj mob thiab kev faib tawm cov kev tsis sib haum xeeb tsis pom kev sib piv cov kev tshawb fawb txog kab mob sib kis, tab sis zoo li muaj qhov sib txawv loj ntawm cov xwm txheej ntawm cov teb chaws, thiab dhau sij hawm, ob qho tib si caj ces thiab kab mob zoo li muaj teeb meem tab sis cov lus qhia muaj zog rau lub luag haujlwm ntawm lwm yam ib puag ncig tseem tsis muaj. .
Cov lus nqa mus tsev
• Autoantibodies yog ib qho tseem ceeb nyob rau hauv lub pathogenesis ntawm glomerulonephritis.
• Hauv MN thiab cov kab mob tiv thaiv GBM cov autoantibodies raug coj tawm tsam cov khoom hauv lub raum.
• Hauv MPGN thiab IGAN(IgA nephritis)autoantibodies raug pom tawm tsam cov khoom hauv lub cev tiv thaiv kab mob, piv txwv li ntxiv thiab Ig molecules.
• Cov kev qhia sib txawv rau kev kuaj ntshav biopsy hauv ntau lub tebchaws ua rau nws nyuaj rau kev sib piv cov txiaj ntsig los ntawm ntau lub tebchaws.
• Cov ntaub ntawv kab mob kis tau los ntawm kev tshawb fawb txog biopsy yog qhov zoo sib xws thaum muab piv rau Tebchaws Europe thiab Tuam Tshoj, tab sis txawv heev ntawm cov kev tshawb fawb hauv Teb Chaws Asmeskas.
Los ntawm: 'autoimmune raum kab mob 'los ntawmMårten Segelmark, Thomas Hellmark ⁎
---Autoimmunity Reviews 9 (2010) A366–A371 DOI:10.1016/j.autrev.2009.11.007
Cov ntaub ntawv
[1] Haas M, Spargo BH, Wit EJ, Meehan SM. Etiology thiab qhov tshwm sim ntawm mob hnyavlub rauminsufficiency nyob rau hauv cov neeg laus: alub raumKev tshawb nrhiav biopsy ntawm 259 tus neeg mob. Am J Raum Dis 2000;35(3:433–47.
[2] Wang HL, Chen SJ, Zhang LN, Zhi LM, Dong DC, Chen QR, et al. Factor VIII-hais txog kev txiav txim siab antigen hauv cov kab mob glomerular. Chin Med J (Engl) 1983; 96(2): 117–20.
[3] Zhou FD, Zhao MH, Zou WZ, Liu G, Wang H. Cov kev hloov pauv ntawm cov kab mob glomerular hauv 15 xyoo: kev soj ntsuam ntawm 3331 cov neeg mob hauv ib lub chaw suav hauv Suav. Nephrol Dial Transplant 2009; 24(3): 870–6.
[4] Naumovic R, Pavlovic S, Stojkovic D, Basta-Jovanovic G, Nesic V.Lub raumbiopsy sau npe los ntawm ib lub chaw hauv Serbia: 20 xyoo ntawm kev paub. Nephrol Dial Transplant 2009; 24 (3): 877–85.
[5] Rivera F, Lopez-Gomez JM, Perez-Garcia R. Clinicopathologic correlations ntawmlub raumpathology hauv Spain. Raum Int 2004; 66(3): 898–904.
[6] van Paassen P, van Breda Vriesman PJ, van Rie H, Tervaert JW. Cov tsos mob thiab cov tsos mob ntawm nyias hauv qab daus daim nyias nyias nephropathy: txoj kev tshawb fawb hauv cheeb tsam ntawm tus kab mob glomerular - Lub LimburgLub raumSau npe. Raum Int 2004; 66 (3): 909–13.
[7] Fuiano G, Mazza G, Comi N, Caglioti A, De Nicola L, Iodice C, et al. Tam sim no indications raulub raumbiopsy: daim ntawv nug raws li kev soj ntsuam. Am J Raum Dis 2000;35(3:448–57.
[8] Hudson B, Wieslander J, Butkowski R, Langeveld J, Wisdom B, Noelken M. Molecular zog ntawm lub globular domain ntawm collagen IV: cryptic zog ntawm Goodpasture antigen. Hauv: Shibata S, editor. Hauv qab daim nyias nyias. Elsevier; Xyoo 1985. p. 219–26 : kuv. 0 ed.
[9] Segelmark M, Hellmark T, Wieslander J. Lub prognostic tseem ceeb nyob rau hauv Goodpasture tus kab mob ntawm tshwj xeeb, titer, thiab affinity ntawm anti-glomerular-hauv qab daus membrane antibodies. Nephron Clin Pract 2003; 94(3):c59–68.
[10] Lerner RA, Glassock RJ, Dixon FJ. Lub luag hauj lwm ntawm anti-glomerular hauv qab daus daim nyias nyias cov tshuaj tiv thaiv nyob rau hauv lub pathogenesis ntawm tib neeg glomerulonephritis. J Exp Med 1967; 126: 989–1004.
[11] Yang R, Hellmark T, Zhao J, Cui Z, Segelmark M, Zhao MH, et al. Qib ntawm epitope tshwj xeeb autoantibodies cuam tshuam nroglub raumkev puas tsuaj hauv cov kab mob tiv thaiv GBM. Nephrol Dial Transplant 2009; 24(6): 1838–44.
[12] Hellmark T, Segelmark M, Unger C, Burkhardt H, Saus J, Wieslander J. Kev txheeb xyuas qhov chaw kho mob muaj feem xyuam rau thaj tsam ntawm collagen IV hauv Goodpasture kab mob. Raum Int 1999; 55(3): 936–44.
[13] Hudson BG, Tryggvason K, Sundaramoorthy M, Neilson EG. Alport's syndrome, Goodpasture's syndrome, thiab hom IV collagen. N Engl J Med 2003; 348(25): 2543–56.
[14] Borza DB, Bondar O, Colon S, Todd P, Sado Y, Neilson EG, et al. Goodpasture autoantibodies unmask cryptic epitopes los ntawm kev xaiv dissociating autoantigen complexes tsis muaj cov txheej txheem ntxiv: tshiab mechanisms rau lub cev tsis muaj zog thiab autoimmune pathogenesis. J Biol Chem 2005; 280(29): 27147–54.
[15] Bolton WK, Chen L, Hellmark T, Wieslander J, Fox JW. Epitope kis thiab autoimmune glomerulonephritis nyob rau hauv nas induced los ntawm T cell epitope ntawm Goodpasture's antigen. J Am Soc Nephrol 2005; 16(9): 2657–66.
[16] Salama AD, Levy JB, Lightstone L, Pusey CD. Goodpasture tus kab mob. Lancet 2001; 358(9285): 917–20.
[17] Cui Z, Zhao MH, Xin G, Wang HY. Cov yam ntxwv thiab kev kwv yees ntawm Suav cov neeg mob uas muaj cov kab mob tiv thaiv glomerular hauv qab daus daim nyias nyias. Nephron Clin Pract 2005; 99(2): c49–55.
[18] Westman KW, Ericsson UB, Hoier-Madsen M, Wieslander J, Lindstedt E, Bygren PG, et al. Feem ntau ntawm autoantibodies txuam nrog glomerulonephritis, tsis cuam tshuam tom qab extracorporeal shock yoj lithotripsy raulub raumcalculi, nyob rau hauv peb lub xyoos tom qab. Scand J Urol Nephrol 1997; 31(5): 463–7.
[19] Donaghy M, Rees AJ. Kev haus luam yeeb thiab lub ntsws hemorrhage hauv glomerulonephritis tshwm sim los ntawm autoantibodies mus rau glomerular hauv qab daim nyias nyias. Lancet 1983; 2:1390–3.
[20] Tumlin JA, Madaio MP, Hennigar R. Idiopathic IgA nephropathy: pathogenesis, histopathology, thiab cov kev kho mob. Clin J Am Soc Nephrol 2007;2(5):1054–61.
[21] Kanwar YS, Farquhar MG. Detachment ntawm endothelium thiab epithelium los ntawm glomerular hauv qab daim nyias nyias uas tsim los ntawm lub raum perfusion nrog neuraminidase. Lab Invest 1980; 42:375–84.
[22] Galla JH. IgA nephropathy. Raum Int 1995; 47(2): 377–87.
[23] Narita I, Gejyo F. Pathogenetic qhov tseem ceeb ntawm aberrant glycosylation ntawm IgA1 hauv IgA nephropathy. Clin Exp Nephrol 2008; 12(5): 332–8.
[24] Gesualdo L, Di Palma AM, Morrone LF, Strippoli GF, Schena FP. Cov kev paub Italian ntawm lub teb chaws sau npe ntawmlub raumbiopsies. Raum Int 2004; 66(3): 890–4.
[25] Nair R, Walker PD. Puas yog IgA nephropathy yog qhov tseem ceeb tshaj plaws glomerupathies ntawm cov hluas hauv Tebchaws Meskas? Raum Int 2006; 69(8): 1455–8.
[26] Galla JH. Molecular genetics hauv IgA nephropathy. Nephron 2001; 88(2:107–12.
[27] Komatsu H, Fujimoto S, Hara S, Sato Y, Yamada K, Kitamura K. Cov nyhuv ntawm tonsillectomy ntxiv rau steroid pulse therapy on clinical remission of IgA nephropathy: a controlled study. Clin J Am Soc Nephrol 2008; 3(5): 1301–7.
[28] Smerud HK, Fellstrom B, Hallgren R, Osagie S, Venge P, Kristjansson G. Gluten rhiab heev rau cov neeg mob IgA nephropathy. Nephrol Dial Transplant 2009; 24(8): 2476–81.
[29] Jacob S, Hery M, Protois JC, Rossert J, Stengel B. Cov nyhuv ntawm cov organic hnyav raug rau kev mob raum mob ntev: txoj kev tshawb fawb GN-PROGRESS. J Am Soc Nephrol 2007; 18(1:274–81.
[30] Ponticelli C. Membranous nephropathy. J Nephrol 2007; 20(3:268–87.
[31] Heymann W, Hackel DB, Harwood S, Wilson SG, Hunter JL. Kev tsim cov kab mob nephrotic nyob rau hauv nas los ntawm Freund's adjuvants thiab nas raum suspensions. Proc Soc Exp Biol Med 1959; 100(4): 660–4.
[32] Beck Jr LH, Bonegio RG, Lambeau G, Beck DM, Powell DW, Cummins TD, et al. M-hom phospholipase A2 receptor raws li lub hom phiaj antigen hauv idiopathic membranous nephropathy. N Engl J Med 2009;361(1:11–21.
[33] Choi EJ, Jeong HJ, Han DS, Lee JS, Choi KH, Kang SW, et al. Kev txheeb xyuas ntawm 4,514 kis ntawmlub raumbiopsy hauv Kauslim. Yonsei Med J 2001; 42(2): 247–54.
[34] Schena FP, Alpers CE.Membranoproliferative Glomerulonephritis thiab cryoglobulinemic glomerulonephritis. Comprehensive Clinical Nephrology. Edinburgh: Mosby; Xyoo 2007.
[35] Razukeviciene L, Bumblyte IA, Kuzminskis V, Laurinavicius A. Membranoproliferative glomerulonephritis tseem yog tus nquag glomerulonephritis hauv Lithuania. Clin Nephrol 2006; 65(2:87–90.
[36] Pickering MC, Ua HT. Kev txhais lus mini-saib xyuas series ntawm kev ua kom tiav H:lub raumCov kab mob cuam tshuam nrog qhov ua tiav H: kev pom tshiab los ntawm tib neeg thiab tsiaj txhu. Clin Exp Immunol 2008; 151(2): 210–30.
[37] Walker NP. Dense deposit disease: kev pom tshiab. Curr Opin Nephrol Hypertens 2007; 16(3): 204–12.
[38] Joshi K, Nada R, Minz M, Sakhuja V. Recurrent glomerulopathy nyob rau hauv lublub raumallograft. Transplant Proc 2007;39(3:734–6.
[39] Berger SP, Daha MR. Ntxiv rau qhov raug mob glomerular. Semin Immunopathol 2007; 29(4): 375–84.
[40] Strife CF, McEnery PT, McAdams AJ, West CD. Membranoproliferative glomerulonephritis nrog kev cuam tshuam ntawm glomerular qab daus daim nyias nyias. Clin Nephrol 1977; 7(2): 65–72.
