Ntu Ⅱ:Biomarkers Ntawm Kab Mob Raum Mob Mob thiab Mob Raum
Mar 13, 2022
Hu rau: Audrey Hu Whatsapp / hp: 0086 13880143964 Email:audrey.hu@wecistanche.com
Cov kev nce qib hauv kev txheeb xyuas cov ntshav qab zib thiab cov zis biomarkers uas sawv cev rau tubular noj qab haus huv tau tshawb xyuas dav hauv AKI thiab tuaj yeem ntxiv cov ntshav creatinine los txhim kho kev tswj tus neeg mob. Biomarkers tuaj yeem ua kom tiav thiab muab cov ntsiab lus siv rau kev nce hauv cov ntshav creatinine thiab txhim kho kev tswj xyuas cov kab mob raum hauv ntau qhov chaw (Daim duab 4).
Kev tshawb pom ntxov ntawm subclinical AKI tom qab phais plawv.—Kev phais plawv yog ib qho ua rau ischemic AKI hauv cov neeg mob hauv tsev kho mob thiab muaj feem cuam tshuam nrog kev mob hnyav thiab kev tuag. Txawm li cas los xij, cov ntshav creatinine nce lig hauv chav kawm kab mob ntawm 48-72 teev tom qab kev phais thiab txwv tsis pub muaj peev xwm tshawb pom ntxov thiab cuam tshuam ntawm cov xwm txheej ntawm AKI. Qhov tsis muaj txiaj ntsig ntawm kev sim kho cov neeg mob tom qab paub txog kev raug mob raum raws li cov ntshav creatinine tau muab piv rau kev pib kho mob myocardial infarction lossis mob stroke 48 teev tom qab pib ntawm ischemia. Preclinical qauv tau pom cov kev hloov pauv thoob ntiaj teb hauv lub raum noob qhia thaum lub sijhawm raug mob ischemic thaum ntxov (79, 80), suav nrog kev tsim cov proteins uas txij li tau txheeb pom tias yog biomarkers ntawm AKI (81). The use of these biomarkers can augment the clinical ability to detect cases of kidney injury, improve risk stratification, and provide insight into therapeutic targets (82). Biomarkers ntawm lub raum raug mob, suav nrog IL-18, NGAL, thiab KIM-1, ntsuas hauv 6 teev tom qab kev phais plawv, tau ua pov thawj los kwv yees qhov kev pheej hmoo ntawm AKI zoo ua ntej nce hauv cov ntshav creatinine. Piv txwv li, qhov siab tshaj plaws quintiles ntawm cov ntshav IL-18 nyob rau hauv 6 teev tom qab kev phais tau cuam tshuam nrog xya npaug ntawm kev pheej hmoo ntawm AKI hauv cov neeg laus thiab cov menyuam yaus, piv rau cov quintiles qis tshaj (83, 84). Ib yam li ntawd, cov quintiles siab tshaj plaws ntawm plasma NGAL thiab urinary KIM-1 tau cuam tshuam nrog kev pheej hmoo ntawm kev tsim AKI, piv nrog thawj quintile (hloov OR 5.0, 95 feem pua CI: 1.6–15.3; kho OR 4.8, 95 feem pua CI : 1.6–14.6, ntsig) (40, 83).
cistanche tshuaj ntsuab kho mob raum mob
Although serum creatinine returns to normal levels in many of these cases of AKI, the
burden on the kidneys may not be completely benign. For example, preclinical studies have
demonstrated the development and persistence of inflammation, renal fibrosis, abnormal
kidney gene expression profiles, and functional deficits after ischemic kidney injury, despite a
return of serum creatinine concentrations to normal values (85, 86). Accordingly, these
biomarkers of tubular injury were also associated with the severity and progression of AKI in
the postcardiac surgery setting. The highest quintile of urinary IL-18 predicted those who
progressed from early AKI (Acute Kidney Injury Network [AKIN] Stage 1) to more severe
stages of AKI (AKIN Stage 2 or 3) (adjusted OR 3.00, 95% CI: 1.25–7.25) and was
associated with duration of AKI >7 hnub (hloov OR 2.90, 95 feem pua CI: 1.80–4.68) (87, 88). Ib yam li ntawd, cov neeg uas muaj quintile siab tshaj plaws ntawm plasma NGAL muaj ze li yim npaug ntawm qhov yuav ua rau muaj kev vam meej AKI (LOSSIS 7.72, 95 feem pua CI: 2.65–22.49) piv nrog cov hauv thawj ob quintiles. Qhov siab tshaj plaws quintile ntawm urinary KIM-1 kuj tseem cuam tshuam nrog lub sijhawm ntev ntawm AKI (hloov OR 2.3, 95 feem pua CI: 1.51–3.53) (88). L-FABP tau txuam nrog lub sijhawm ntawm AKI, thiab ob qho tib si plaub thiab thib tsib quintiles tau txuam nrog lub sijhawm ntev ntawm AKI (hloov OR 1.77, 95 feem pua CI: 1.17–2.67; kho OR 1.92, 95 feem pua CI: 1.26–2.93 ib., (88).
Tsis tas li ntawd, cov biomarkers ntawm tubular raug mob tau txawm pom lub peev xwm los qhia txog kev tuag mus ntev tom qab kev phais plawv. Txawm tias nyob rau hauv cov neeg mob uas tsis muaj AKI, qhov siab tshaj plaws tertile ntawm IL-18 yog txuam nrog muaj kev pheej hmoo ntawm kev tuag nyob rau hauv nruab nrab lub sij hawm tom qab ntawm 3.0 xyoo [interquartile range (IQR) 2.2 txog 3.6] piv nrog thawj tertile [kho qhov phom sij piv (HR) 1.23, 95 feem pua CI: 1.02–1.48]. Cov nyhuv no tau nthuav dav hauv cov kev kawm nrog perioperative AKI (hloov HR 3.16, 95 feem pua CI: 1.53–6.53) (89). Ib yam li ntawd, qhov siab tshaj plaws tertile ntawm perioperative urinary KIM-1 tau txuam nrog kev tuag ntau ntxiv (hloov HR 1.83, 95 feem pua CI: 1.44–2.33) hauv cov neeg uas tsis tau tsim AKI nrog rau cov neeg tsim AKI (hloov HR 2.01, 95% CI: 1.31–3.1) (89). Cov kev tshawb pom no yuav yog qhov tseem ceeb tshwj xeeb vim tias kev koom tes ntawm troponin nrog kev tuag, nrog rau nws cov ntaub so ntswg tshwj xeeb, yog ib qho tseem ceeb ntawm nws kev koom ua ke rau hauv kev kuaj mob ntawm myocardial infarction (90). Txawm li cas los xij, muab qhov ntev latency ntawm ib ntu ntawm lub raum raug mob thiab kev tuag, piv rau myocardial infarction, nws yuav nyuaj rau kev txiav txim siab causality. Txawm li cas los xij, cov ntaub ntawv no qhia tias kev rov qab los ntawm cov ntshav creatinine tsis tuaj yeem ntes cov kev raug mob seem thiab fibrosis hauv lub raum uas ua rau muaj kev mob hnyav ntxiv thiab kev tuag. Cov ntaub ntawv pov thawj tsis ntev los no tau pom tias ua rau lub raum siab biomarkers ntawm tubular kev puas tsuaj, suav nrog 1M, PIIINP, thiab NGAL, yog qhov muaj kev pheej hmoo ywj pheej rau ob qho tib si CVD thiab kev tuag nyob rau lub sijhawm nruab nrab ntawm 12.4 xyoo ntawm cov neeg laus uas muaj lub hauv paus raum kev ua haujlwm hauv ib lub raum. case-cohort study of the Health, Aging, and Body Composition (ABC) Study (91).
Cistanche tiv thaiv lub raum raug mob
Distinguishing etiologies ntawm AKI nyob rau hauv cardiorenal thiab hepatorenal syndromes.—Kev raug mob raum hauv qhov chaw ntawm cardiorenal thiab hepatorenal syndromes (CRS, HRS) tej zaum yuav muaj ntau hom kab mob hauv qab. Ob lub plawv tsis ua haujlwm thiab cirrhosis tuaj yeem txo lub raum perfusion los ntawm kev txo qis rau pem hauv ntej thiab nce venous congestion, predisposing cov neeg mob rau lub raum raug mob ntawm prerenal physiology thiab intrinsic tubular raug mob. Ntau hom kev sib txawv thiab kev kho mob tuaj yeem ua rau nyuaj ntxiv rau kev txhais cov ntsiab lus ntawm kev nce ntshav creatinine concentrations. Biomarkers ntawm tubular raug mob tau pom muaj txiaj ntsig hauv kev paub qhov txawv ntawm cov txheej txheem pathological.
Piv txwv li, nyob rau hauv qhov chaw ntawm CRS, aggressive diuresis yog lub hauv paus ntawm kev kho mob kom txo tau congestion thiab restore plawv hemodynamics tab sis kuj yog txuam nrog nce nyob rau hauv cov ntshav creatinine, ib tug tshwm sim hu ua mob raum ua hauj lwm nyob rau hauv cov ntaub ntawv cardiology thiab feem ntau suav hais tias yog AKI. (92, 93). Vim qhov pom tias lub raum puas tsuaj, uas xav tias cuam tshuam nrog cov xwm txheej tsis zoo (94, 95), diuresis thiab kev kho mob ntxiv feem ntau raug tso tseg (96). Txawm li cas los xij, kev nce hauv cov ntshav creatinine yuav tsis tas yuav cuam tshuam nrog kev puas tsuaj rau lub raum thiab cov txiaj ntsig tsis zoo. Piv txwv li, hauv kev tshawb fawb yav tom ntej ntawm cov neeg mob uas mob plawv tsis ua hauj lwm, cov neeg uas tsim AKI tom qab kev kho diuretic tsis muaj qhov nce ntxiv hauv cov zis NGAL (97). Tsis tas li ntawd, ib qho kev tshawb fawb tsis ntev los no ntawm Kev Tshawb Fawb Lub Raum Optimization Strategies Hauv Kev Mob Lub Plawv Tsis Zoo (ROSE-AHF) kev sim tshuaj siv biomarkers ntawm tubular kev noj qab haus huv ntawm 283 tus neeg koom nrog kev mob hnyav diuresis tau pom tias kev ua rau lub raum tsis zoo tsis cuam tshuam nrog kev nce hauv biomarkers ntawm lub raum raug mob. , suav nrog NGAL thiab KIM-1, lossis nrog cov txiaj ntsig tsis zoo (98). Cov txiaj ntsig tau pom tias qhov nce hauv creatinine tuaj yeem cuam tshuam qhov kev hloov pauv hloov pauv hauv kev nkag mus thiab qhia tias qhov nce hauv creatinine tuaj yeem tsis lav tshem tawm cov txiaj ntsig kho.
Ib yam li ntawd, biomarkers muaj peev xwm los pab nqaim qhov kev kuaj mob sib txawv hauv qhov teeb meem ntawm cirrhosis ntawm ob qho tib si etiologies ntawm HRS thiab mob tubular necrosis. Kev muaj peev xwm ua kom qhov sib txawv ntawm hepatorenal physiology thiab kev raug mob ntawm lub cev yog qhov tseem ceeb vim tias kev kho mob sib txawv heev. HRS tuaj yeem thim rov qab nrog kev kho lub raum perfusion los ntawm kev kho mob vasoconstrictor ntxiv rau kev kho cov hlab ntsha albumin thiab hloov lub siab tom qab. Hauv qhov sib piv, cov neeg mob uas raug mob hauv lub cev yuav tsum tau kho nrog kev lim ntshav thiab txiav txim siab rau kev hloov pauv hauv lub raum ua ke (99-102). Txawm li cas los xij, tam sim no qhov chaw kho mob los kuaj HRS feem ntau yog raws li cov ntshav creatinine. Biomarkers ntawm tubular kev noj qab haus huv tuaj yeem paub qhov txawv ntawm AKI thiab ua kom muaj kev kuaj mob sai dua thiab kev kho mob tsim nyog. Hauv kev tshawb fawb ntawm cov neeg mob cirrhosis uas tsim AKI, urinary theem ntawm NGAL, IL-18, thiab L-FABP tau nce siab hauv cov neeg mob uas tau txais kev kho mob rau cov neeg mob qog nqaij hlav hauv lub cev tab sis tsis yog nyob rau hauv cov neeg uas muaj HRS lossis prerenal etiologies (103). Tsis tas li ntawd, cov qib biomarker siab tshaj plaws tau pom nyob rau hauv cov neeg mob uas raug mob tubular raug mob, ua raws li HRS thiab prerenal azotemia, raws li, concordant nrog lub physiology ntawm qhov kev raug mob tubular (100, 104). Kev sib xyaw ua ke ntawm ntau lub biomarkers, suav nrog NGAL, L-FABP, thiab IL-18, kuj tau raug soj ntsuam hauv kev kuaj mob hom AKI hauv cov neeg mob cirrhosis, nrog rau qhov zoo li yuav raug kuaj mob mob tubular raug mob nce zuj zus mus. nrog tus naj npawb ntawm biomarkers uas tau tshaj qhov pom kev txiav txim siab zoo. Piv txwv li, cov neeg mob ntshav siab uas muaj tsawg kawg yog ib qho biomarker siab tshaj qhov txiav tawm yog tsib zaug uas yuav muaj qhov raug mob ntawm tubular thiab cov neeg uas muaj tag nrho cov cim zoo yog 13 zaug uas yuav muaj qhov mob hnyav (105).
Delineating prognosis ntawm AKI nyob rau hauv tuag pub raum hloov pauv.—Ischemia-reperfusion raug mob-kho kho AKI feem ntau pom nyob rau hauv cov neeg mob lub raum tuag, uas tom qab ntawd muaj ntau dua pov tseg. Muab qhov tseem ceeb ntawm lub raum tsis txaus rau kev hloov pauv, kev cawm txhua lub raum yog qhov tseem ceeb. Txawm li cas los xij, ntshav creatinine yuav tsis raug ntes raum raug mob thiab muab cov ntaub ntawv hais txog kev ua haujlwm tom qab hloov pauv. Qhov tseeb, kev tshuaj xyuas ntawm cov kab mob biopsy tau pom tias ntau dua 20 feem pua ntawm cov neeg mob biopsy-pov thawj mob mob tubular raug mob tsis tau raws li Kab Mob Raum: Txhim Kho Ntiaj Teb Cov txiaj ntsig (KDIGO) cov ntshav creatinine-based AKI txhais (106). Biomarkers ntawm tubular raug mob tuaj yeem muab kev pom rau qhov zoo ntawm cov neeg pub rau lub raum tuag. Piv txwv li, kev tshawb fawb ntawm cov neeg mob lub raum tuag tau pom tias cov ntshav creatinine tsis muaj qhov tseeb rau kev kuaj mob tus kab mob qog nqaij hlav, thaum cov qib NGAL urinary outperformed qhov kev kuaj mob ntawm mob tubular raug mob (107). Tsis tas li ntawd, cov biomarkers ntawm tubular noj qab haus huv yuav muab cov ntaub ntawv prognostic. Kev tshawb fawb loj ntawm cov neeg pub dawb ntawm lub raum raug mob tau pom tias nce zis ntau ntxiv ntawm NGAL, KIM-1, IL-18, thiab L-FABP tau cuam tshuam nrog cov neeg pub dawb AKI tab sis tsis nrog ncua kev ua haujlwm graft (107) . Qhov zoo siab, txoj kev tshawb fawb tau tshaj tawm tias qib siab dua ntawm lub raum kev raug mob biomarkers tau cuam tshuam nrog ntau dua 6-hli eGFRs hauv cov neeg tau txais kev ua haujlwm qeeb. Kev tiv thaiv ntawm lub raum hauv lub raum raug mob los ntawm AKI ntseeg tau tias yog vim yog ischemic preconditioning, uas cuam tshuam nrog kev tswj hwm ntawm cov neeg kho mob tiv thaiv ischemic. Raws li qhov kev tshawb pom no, kev kho mob ischemic preconditioning tau pom tias muab ob qho tib si mob hnyav thiab ncua kev tiv thaiv lub raum ischemia-reperfusion raug mob hauv cov qauv nas ntawm txoj kev taw qhia sib txawv (108).
Tsis tas li ntawd, YKL {{0}}, biomarker ntawm kev hloov kho tom qab lub raum raug mob, tau pom tias yog cytoprotective hauv kev teeb tsa ntawm lub raum hloov pauv. Cov neeg mob raum tuag uas muaj qhov siab tshaj plaws YKL-40 qib siab dua eGFRs ntawm 6 lub hlis piv nrog cov neeg mob uas cov neeg pub dawb tau qis tshaj YKL-40 qib, tom qab hloov kho rau cov neeg pub dawb thiab cov neeg tau txais txiaj ntsig, nrog rau qib ntawm mob raum. Ntxiv mus, cov neeg tau txais kev pabcuam siab tshaj plaws YKL-40 qib kuj tseem muaj 50 feem pua tsawg ntawm kev ua txhaum cai tsis ua haujlwm (hloov HR 0.50, 95 feem pua CI: 0.27–0.94) (109) .
Kev kho mob ntawm CKD: CISTANCHE
Mob raum mob
In CKD, the timing and nature of the insult may be more difficult to estimate, as an accrual of kidney insults and injury over many years leads to the development of this condition. Thus, the early search for biomarkers of CKD lagged behind the research of AKI. However, because AKI and CKD share similar underlying mechanisms of functional and structural injury and exist on the same pathophysiologic continuum, biomarkers of AKI have also been applied to CKD. The biomarkers have been especially promising in identifying susceptibility to and predicting the development of incident CKD; however, they have not been as robust in predicting CKD progression after adjustment for serum creatinine, and studies in different settings may be biased based on the etiology of underlying CKD and enrollment criteria. In participants without CKD at baseline, the "renal filtration reserve" (4, 5) is able to compensate for filtration deficits and, in effect, absorbs the insult (Figure 4). Biomarkers of tubular injury are critical to providing information about kidney tubular injury in these situations in which serum creatinine does not change appreciably. Accordingly, these biomarkers of tubular injury have been shown to be especially promising in prognosticating the development of incident CKD. For example, in a nested-case control study of 686 participants from the Multi-Ethnic Study of Atherosclerosis (MESA), in which cases were defined as those with a baseline eGFR >60 ml/min who subsequently developed CKD Stage 3 and/or had a rapid drop in kidney function over the five-year study period, higher levels of KIM-1 were associated with increased odds of developing CKD stage 3 or a rapid decline in eGFR (adjusted OR 1.15, 95% CI: 1.02–1.29). Similarly, at study entry, those in the highest decile of KIM-1 had a twofold increased risk of this same endpoint compared with the lower 90%. This ability to predict the development and progression of CKD was independent of the presence of albuminuria (110). Similarly, when investigated in a cohort of 149 persons with chronic congestive heart failure during 5 years of follow-up, urinary KIM-1 levels were strongly associated with the progression of CKD, defined as a >25 feem pua poob hauv eGFR los ntawm lub hauv paus (111).
Txawm li cas los xij, thaum lub raum pom kev poob qis, txhua qhov kev thuam rau lub raum yuav sib haum nrog qhov txo qis hauv glomerular pom thiab, yog li, ntshav creatinine tuaj yeem muab cov ntaub ntawv ntau npaum li tubular raug mob biomarkers. Piv txwv li, kev tshawb fawb tsis ntev los no ntawm cov neeg koom nrog Chronic Renal Insufficiency Cohort (CRIC) nrog cov hauv paus ntsiab lus CKD tau pom tias cov zis KIM-1, NGAL, thiab L-FABP tau cuam tshuam nrog CKD kev nce qib hauv kev tshuaj ntsuam tsis kho; Txawm li cas los xij, ib zaug tswj hwm cov ntshav creatinine-based eGFR thiab tso zis albumin / creatinine piv, ob lub cim ntawm lub raum ua haujlwm, cov biomarkers no tsis muaj kev cuam tshuam nrog CKD. Tsis tas li ntawd, tsis muaj ib qho ntawm cov biomarkers txhim kho kev pheej hmoo ntawm cov qauv kev kho mob rau CKD kev loj hlob, qhia tias tubular raug mob biomarkers tej zaum yuav muaj kev siv tsawg rau cov neeg mob uas tau txo qis rau lub raum cia (112). Cov kev tshawb fawb ntxiv ntawm cov tib neeg nrog CKD kuj tau pom tias cov cim kev raug mob ntawm tubular tsis ntxiv rau qhov kev pheej hmoo ntawm kev kis tus kab mob tom qab suav rau cov cim cim ntawm lub raum ua haujlwm (113-115).
Kev kho mob ntawm CKD: cistanche extract
Mob ntshav qab zib nephropathy.—Ntshav qab zib yog ib qho kev pheej hmoo tseem ceeb thiab ua rau CKD thiab ESRD. Txawm li cas los xij, 20-30 feem pua ntawm cov neeg mob ntshav qab zib tau poob rau lub raum ua haujlwm sai txawm tias thaum kho kom zoo nrog angiotensin-hloov enzyme inhibitors lossis angiotensin II receptor blockers. Kev mob raum hauv cov ntshav qab zib mellitus yog ntau yam thiab tej zaum yuav raug tsav los ntawm kev mob tsis tu ncua, kev raug mob hauv lub cev, lossis kev kho tsis zoo, ntawm lwm txoj hauv kev (116, 117), thiab biomarkers yuav pab kom pom qhov tseem ceeb hauv qab etiologies (Daim duab 5). Hais txog cov lus nug tseem ceeb no nrog biomarkers ntawm tubular noj qab haus huv tuaj yeem txhim kho kev pheej hmoo stratification thiab pab kom muaj txiaj ntsig zoo ntawm kev mob ntshav qab zib raum.
Piv txwv li, biomarkers ntawm tubular raug mob tau pom tias muaj feem cuam tshuam nrog rau cov kab mob raum hauv cov neeg mob ntshav qab zib, qhia txog kev raug mob hauv tubular. Plasma KIM-1 tau ntsuas nyob rau hauv cov ntsiab lus los ntawm Kev Ua Kom Tswj Xyuas Kab Mob Ntshav Qab Zib (ACCORD) thiab US Veterans Administration Nephropathy hauv Diabetes (VA-NEPHRON-D) cohorts. Hauv pawg ACCORD, cov neeg uas tau mus tsim qhov xwm txheej CKD muaj cov theem pib siab dua KIM-1. Ib yam li ntawd, hauv txoj kev tshawb fawb VA-NEPHRON-D, cov neeg uas tau mus rau kev txhim kho CKD tau nce qib hauv qab (118). Hauv ob qho ntawm cov kev tshawb fawb no, cov neeg uas muaj quartile siab tshaj plaws ntawm KIM-1 concentrations yuav muaj feem cuam tshuam rau lub raum tsis zoo, piv nrog rau cov qis qis tshaj ntawm KIM-1 concentrations (119, 120).
Hauv ob pawg no, plasma TNFR1 thiab TNFR2 kuj tau pom tias muaj siab dua ntawm cov neeg mob ntshav qab zib hauv lub raum, piv nrog cov neeg muaj kab mob thaum ntxov ntawm lub hauv paus, thiab qib siab ntawm ob lub cytokine receptors tau kwv yees eGFR poob, txawm tias tom qab hloov kho. rau lub hauv paus eGFR thiab albuminuria (118). Cov biomarkers no tau cuam tshuam rau hauv txoj kev inflammatory uas sawv cev tsis tu ncua endothelial o, paub txog etiology ntawm kab mob raum mob ntshav qab zib (121). Raws li qhov kev xav no, TNF txoj hauv kev tau txuas nrog rau cov kab mob raum mob ntshav qab zib: Cov kev tshawb fawb ntawm Genome-wide koom haum tau pom tias cov ntawv teev lus sib cuam tshuam nrog GFR pawg nyob ib ncig ntawm TNF-, uas ncaj qha ua rau podocytes los nthuav tawm cov kab mob inflammatory ntawm TNFRs (122). Tsis tas li ntawd, ntau qhov kev tshawb fawb tau pom tias plasma TNFR1 thiab TNFR2 cuam tshuam nrog cov xwm txheej mob ntshav qab zib raum thiab ESRD hauv cov neeg mob ntshav qab zib (59, 60, 123, 124). Qhov zoo siab, TNFR1 thiab TNFR2 tuaj yeem sawv cev rau txoj hauv kev sib txawv, tab sis cov nuances tseem tab tom raug qhia (125).
Tsis tas li ntawd, urinary MCP-1 kuj tau pom tias tau nce siab hauv cov neeg mob ntshav qab zib nephropathy, thiab cov qib no cuam tshuam nrog albuminuria hauv tib neeg thiab hauv kev sim ntshav qab zib nephropathy (126-129). Hauv kev soj ntsuam yav tom ntej ntawm cov neeg mob uas muaj ntshav qab zib nephropathy, urinary MCP-1 qib tau cuam tshuam nrog macroalbuminuria thiab cuam tshuam nrog tus nqi tom ntej ntawm eGFR poob qis dua li qhov nruab nrab kev soj ntsuam ntawm rau xyoo. Cov kev tshawb pom no qhia tias MCP-1 cuam tshuam nrog cov kab mob tom qab thiab muaj peev xwm sawv cev rau txoj kev kho mob tsis zoo (130).
HIV-koom nrog mob raum mob.—Cov tib neeg muaj tus kab mob HIV muaj kev pheej hmoo loj heev ntawm cov kab mob raum, vim tias tus kab mob no paub tias yog tus tswv tsev thiab ua rau lub raum puas hlwb, txawm tias nyob hauv cov neeg uas muaj kab mob viremia (131). Tsis tas li ntawd, cov neeg muaj tus kab mob HIV muaj ntau yam kab mob metabolic thiab vascular comorbidities thiab kev kho mob cuam tshuam txog kev pheej hmoo uas ua rau muaj kab mob raum. Serum creatinine tsis tuaj yeem paub qhov txawv ntawm ntau lub peev xwm etiologies ntawm cov kab mob raum, uas cuam tshuam rau kev tswj xyuas kev kho mob. Biomarkers ntawm tubular tsis ua hauj lwm thiab raug mob tau tshwj xeeb tshaj yog cog lus nyob rau hauv qhov teeb meem no nyob rau hauv kev soj ntsuam kev raug mob thaum ntxov tshwm sim los ntawm tus kab mob. Piv txwv li, 1M qib ntawm cov poj niam uas muaj tus kab mob HIV tau cuam tshuam nrog ob lub raum kev ua haujlwm poob qis thiab kev tuag (132). Piv nrog rau cov uas muaj qib qis tshaj 1M, cov uas muaj qib siab tshaj plaws tau muaj kev pheej hmoo ntawm kev tsim CKD (hloov OR 2.1, 95 feem pua CI: 1.3–3.4) thiab 2.7-fold pheej hmoo ntawm 10 feem pua txo hauv eGFR. Qhov kev sib raug zoo no hauv CKD txoj kev loj hlob thiab kev loj hlob yog cais los ntawm 1.6-fold hloov kev pheej hmoo ntawm kev tuag, uas suav nrog lub raum ua haujlwm hauv lub raum nrog rau kev muaj albuminuria (132). Tsis tas li ntawd, cov zis IL-18 tau cuam tshuam nrog rau lub raum ua haujlwm tsis zoo nyob rau lub sijhawm hauv ib pawg ntawm Women's Interagency HIV Study. IL-18 tau siab dua nyob rau hauv cov poj niam uas muaj tus kab mob HIV piv rau cov uas tsis muaj tus kab mob no, nrog rau kev cuam tshuam nrog HIV RNA ntau dua thiab qis dua CD4, qhov feem pua ntawm cov kab mob siab C, thiab txo qis HDL cholesterol ( 133, 134 ib.). Cov kev tshawb pom zoo sib xws nrog IL-18 kuj tau tshaj tawm hauv kev tshawb nrhiav ntu ntu ntawm 1,144 tus txiv neej ntawm Multicenter AIDS Cohort Study (MACS), uas pom qhov nce siab ntawm IL-18, KIM-1, PIIINP, thiab albumin / creatinine piv rau cov txiv neej muaj kab mob HIV, piv nrog cov txiv neej tsis muaj kab mob (135).
Cov biomarkers no tseem tuaj yeem txheeb xyuas lub raum puas los ntawm tenofovir disoproxil fumarate (TDF), siv dav, thawj kab tshuaj tua kab mob uas paub tias ua rau mob raum ntawm cov kab mob sib kis (136, 137). Cov kev tshawb fawb hla ntu tau ua pov thawj tias kev nthuav dav TDF tshwm sim hauv cov txiv neej muaj kab mob HIV rau npe hauv MACS yog nws tus kheej cuam tshuam nrog kev nce siab hauv cov zis 1M, IL-18, KIM-1, thiab PIIINP, tab sis tsis yog nrog albuminuria. , ua raws li qhov kev xav tias TDF yog qhov sib thooj tubular toxin (138, 139). Cov tubular raug mob biomarkers tuaj yeem txheeb xyuas qhov raug mob subclinical ua ntej qhov pib ntawm overt, irreversible kab mob thiab paub qhov txawv raum raug mob los ntawm kev siv TDF. Kev ua haujlwm tsis tu ncua yog tshawb xyuas lub peev xwm ntawm cov qauv biomarker thiab kos npe kom paub txog ntau yam kev sib txawv ntawm lub raum raug mob ntawm cov neeg muaj kab mob HIV.
Cistanche siv tau rau cov kab mob raum
TSEEM CEEB
Kev siv biomarkers hauv nephrology tau txais txiaj ntsig zoo heev; Txawm li cas los xij, tseem muaj kev ua tiav ua ntej lawv tuaj yeem hla qhov pib ntawm daim ntawv thov kho mob. Raws li ntau yam biomarkers ntawm lub raum kev noj qab haus huv tau pom tias muaj kev sib koom ua ke nrog cov txiaj ntsig tsis zoo hauv ntau qhov chaw kho mob, lawv tau pib ua rau lub teeb pom kev ntawm cov kab mob lom neeg tshwj xeeb uas kho kev raug mob thiab kho. Kev kawm biomarkers hauv cov qauv kho mob kuj tseem qhia txog cov kev txwv ntawm cov qauv tsiaj uas tsis simulate qhov nyuaj ntawm kev sib tshooj, xws li ntshav qab zib, kub siab, thiab kev laus. Cov kev tshawb fawb yav tom ntej yuav xav tau los tsim cov qauv tsiaj uas tuaj yeem ntes tau qhov nyuaj no. Qhov kev nkag siab tob dua no tuaj yeem ua rau kev txheeb xyuas thiab kev ua tus kheej ntawm cov qhov rais kho tau zoo thiab cov hom phiaj uas tuaj yeem txwv qhov kev raug mob, txhawb kev kho, thiab tiv thaiv fibrosis yam tsis muaj kev cuam tshuam rau kev tiv thaiv tus tswv tsev tsim nyog.
Cov biomarkers no tuaj yeem siv los ua cov cuab yeej hauv kev sim tshuaj ntsuam xyuas kev kho tshiab (Daim duab 6). Biomarkers ntawm tubular raug mob tuaj yeem siv rau hauv kev sim tshuaj txhawm rau txhawm rau txhim kho cov pej xeem rau qhov tseeb ntawm qhov kev raug mob ntawm lub cev tiv thaiv hemodynamic raug mob (raws li kev kuaj mob biomarkers), xaiv rau cov neeg koom nrog kev pheej hmoo siab rau cov txiaj ntsig cuam tshuam (raws li kev tshawb fawb biomarkers), thiab txheeb xyuas cov neeg uas yuav yog Muaj feem ntau yuav teb rau ib qho kev cuam tshuam (raws li kev kwv yees biomarkers). Cov metrics rhiab dua thiab tshwj xeeb rau kev tso npe nkag mus sim no tuaj yeem ua rau muaj zog ntawm cov ntaub ntawv, txo cov qauv xav tau, thiab txo cov nqi mus sib hais. Hauv kev simulated kev sim tshuaj ntsuam xyuas siv cov tshuaj ntsuam xyuas biomarkers rau npe rau cov neeg mob uas muaj kev pheej hmoo siab rau AKI tom qab kev phais plawv hauv TRIBE-AKI pawg, cov neeg tshawb xyuas pom tau tias cov nqi sim yuav raug txo los ntawm 29 feem pua rau 64 feem pua, nrog rau kev sib pauv yuav tsum tau. ib pab pawg soj ntsuam loj dua ntawm cov neeg koom thiab txwv tsis pub muaj peev xwm (140). Tsis tas li ntawd, thaum IL-18 thiab NGAL tau siv los ua qhov tshwm sim rau kev simulated sim ntawm kev siv statins thaum lub sijhawm ua haujlwm, AKI txhais los ntawm kev nce siab hauv biomarkers tuaj yeem pom qhov sib txawv tseem ceeb ntawm qhov tshwm sim thiab cov teebmeem ntawm cov tshuaj statins, thaum AKI txhais los ntawm cov ntshav creatinine tsis tuaj yeem (141). Cov kev tshawb pom no nug seb qhov kev sim ua tsis tiav yav dhau los hauv nephrology yog kab tias siv lub hom phiaj tsis raug lossis cov qauv tsim tsis zoo.
Tsis tas li ntawd, cov biomarkers no tuaj yeem siv los ua kev nyab xeeb biomarkers rau kev saib xyuas cov tshuaj lom lossis kev puas tsuaj hauv kev sim tshuaj. Qhov tseeb, FDA, nrog rau nws cov European thiab Nyij Pooj cov koom tes, tau sib koom ua ke pom zoo ib lub vaj huam sib luag ntawm cov zis biomarkers ntawm lub raum raug mob uas suav nrog KIM-1, albumin, tag nrho cov protein, cystatin C, clusterin, trefoil factor 3, thiab 1M. rau siv nyob rau hauv preclinical qauv ntawm nephrotoxicity (142-144).
Zoo ib yam li cov kev kwv yees biomarkers uas tau ua tiav cov kev kho mob hauv oncology, xws li nrog kev siv Herceptin hauv tib neeg epidermal growth factor receptor 2 (HER2)-zoo mob qog noj ntshav mis, cov phiaj xwm kev cuam tshuam tuaj yeem ua lub luag haujlwm tseem ceeb hauv kev kho mob raum. kab mob. Piv txwv li, ib qho tshuaj ua rau txoj kev apoptosis ntawm nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome complex tej zaum yuav siv tau rau cov neeg mob uas txoj kev AKI no ua haujlwm. Ib qho biomarker, xws li tso zis IL-18, uas tau tso tawm thaum ua haujlwm ntawm NLRP3 inflammasome txoj hauv kev tuaj yeem yog qhov kev kwv yees biomarker los xaiv cov neeg mob rau kev tso npe hauv kev sim tshuaj. Tsis tas li ntawd, cov tib neeg uas muaj ntshav qab zib nephropathy uas tau tsav los ntawm qib siab ntawm TNFR1 thiab TNFR2 tuaj yeem qhia tau tias cov tshuaj tiv thaiv kab mob tuaj yeem rov kho dua los kho cov mob no.
Txhawm rau ua tiav cov hom phiaj no, yuav tsum muaj kev ua haujlwm ntxiv ntxiv rau phenotype cov kab mob hauv lub raum nrog biomarkers ntawm tubular raug mob thiab lwm yam ntaub ntawv lom. Txhawm rau txhawm rau txhawm rau txhawm rau txhawm rau ua kom muaj ntau yam kev tshwm sim thiab siv lawv tso siab rau kev sim tshuaj ntsuam xyuas, cov tswv yim tshiab uas tso siab rau lub vaj huam sib luag ntawm ntau cov biomarkers tshiab yuav yog qhov tsim nyog, tej zaum yog cov qhab nia biomarker sib xyaw. Kev tshawb fawb tsis tu ncua tab tom ua haujlwm rau kev sib cav nrog qhov nyuaj no los ntawm kev siv cov txheej txheem xws li metabolomics profiling (145) thiab los ntawm kev tshawb xyuas cov microRNAs, uas tau pom tias muaj kev hloov pauv hauv ntau yam kab mob raum (146). Tsis tas li ntawd, kev siv zog loj tab tom ua kom paub meej thiab taug qab txoj hauv kev ntawm cov kab mob raum. Lub koom haum National Institute of Diabetes thiab Digestive and Kidney Diseases (NIDDK)-nyiaj pab rau raum Precision Medicine Project (147) aims kom tau txais lub raum biopsies ntawm AKI thiab CKD thiab tsim ib lub raum cov ntaub so ntswg atlas los txhais cov kab mob subgroups nrog noob caj noob ces, transcriptomics, thiab coj plasma. thiab cov zis biomarkers. Qhov muaj ntawm cov ntaub so ntswg-raws li atlantes yuav tso cai rau kev sib piv ntawm biomarkers rau tus qauv kub tiag tiag ntawm lub raum biopsies thiab nrhiav pom cov biomarkers tshiab. Cov kev tshawb fawb yav tom ntej no tuaj yeem tshem tawm cov txiaj ntsig zoo ntawm biomarkers, uas tuaj yeem tshwm sim tsis zoo vim yog kev sib piv nrog cov qauv tsis zoo ntawm cov ntshav creatinine. Zoo ib yam li thaj tsam ntawm oncology, molecular phenotyping los ntawm cov peev txheej no tuaj yeem ua rau kev kho tus kheej rau cov neeg mob raum raws li cov kab mob sib txawv. Nrog rau cov kev txhim kho no, cov txheej txheem tshiab txheeb cais yuav xav tau los ntsuas qhov tseeb ntawm biomarkers hauv kev kwv yees kev pheej hmoo, tshwj xeeb tshaj yog vim cov cim no tau muab piv rau cov qauv kub tsis zoo ntawm cov ntshav creatinine. Tsis tas li ntawd, nrog rau ntau tus biomarkers uas tam sim no muaj, biomarkers yuav tsum tau muab tso ua ke rau hauv cov qhab nia sib xyaw txhawm rau txhim kho lub peev xwm kwv yees thiab txhim kho qhov ua tau zoo ntawm kev siv rau hauv kev kho mob (148-150).
Kev kho mob raum: Cistanche
Cov lus xaus
Hauv kev xaus, ntau qhov kev cog lus biomarkers ntawm lub raum kev noj qab haus huv uas koom nrog hauv cov txheej txheem pathophysiologic ntawm lub raum kev puas tsuaj tau pom tias muaj peev xwm txhim kho kev kho mob raum kab mob. Cov biomarkers no tau pom tias muaj peev xwm txheeb xyuas kev puas tsuaj thaum ntxov, ua kom raug mob, thiab kwv yees kev kis kab mob, qhov hnyav, thiab kev tuag mus ntev. Kev ua haujlwm yav tom ntej tab tom ua haujlwm los ua tus yam ntxwv ntawm txoj hauv kev lom neeg uas txhawb nqa lub raum kho thiab ua kom muaj sia nyob mus ntev, uas tuaj yeem qhia txog kev txhim kho cov kev kho tshiab hauv thaj tsam nephrology.
THOV NYEEM NO PARTⅢ
