Pyuria tsis muaj Casts thiab ob lub raum loj yog qhov tshwm sim ntawm qhov mob raum mob hnyav tshwm sim los ntawm mob Pyelonephritis: Cov Ntaub Ntawv Qhia thiab Phau Ntawv Ntsuam Xyuas

Abstract:Tus neeg mob yog ib tug txiv neej muaj hnub nyoog 38- xyoo uas muaj xeev siab thiab kub taub hau rau ob peb hnub thiab nthuav tawm nrog mob nraub qaum, oliguria, thiab pyuria, qhia txog mob pyelonephritis (APN). Nws qhiamob raum raug mob(AKI) nrog ob sab ob lub raum o thiab tau siv nonsteroidaltshuaj tiv thaiv kab mob(NSAIDs). AKI-induced los ntawm APN tau lees paub los ntawm lub raum biopsy. AKI tau ua tiav kev kho mob nrog tshuaj tua kab mob. Kev tshawb nrhiav ntawm cov ntaub ntawv muaj feem xyuam rau cov lus ceeb toom ntawm histopathologically proven APN-induced hnyav AKI qhia tias tus yam ntxwv tseem ceeb yog ob sab ob lub raum o nrog pyuria yam tsis muaj casts.Oligoanuriatau nquag txuam nrogAPN-induced hnyav AKI, thiab kev siv NSAID tej zaum yuav muaj kev pheej hmoo. Kev kho tshuaj tua kab mob sai sai raws li kev kho mob cov yam ntxwv ntawm APN-induced AKI tuaj yeem txhim kho lub raum.

Ntsiab lus: mob raum raug mob,lub raum loj, nonsteroidal anti-inflammatory tshuaj, pyelonephritis, pyuria

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Taw qhia

Mob pyelonephritis(APN) yog feem ntauzej zog cov kab mob kab mob ntawm lub raum(1). APN muaj peev xwm ua rau tuag taus vim sepsis lossis septic shock, uas yuav ua raumob raum raug mob(AKI) vim mob tubular necrosis. Severe AKI [txhais tau tias Kab Mob Raum Txhim Kho Kev Txhim Kho Ntiaj Teb (KDIGO) theem 2 lossis 3 (2)] tshwm sim los ntawm APN nws tus kheej tsis tshua muaj. Cov kab mob histopathology ntawm APN yog ib qho kab mob hauv tubulointerstitial uas qhia txog kev nkag mus rau hauv lub raum interstitium thiab tubules los ntawm cov kab mob inflammatory, nrog rau tubular necrosis thiab cov kua paug tawm. Lub focal tsub zuj zuj ntawm leukocytes yuav ua rau abscess tsim ntawm qhov chaw ntawm lubpuas raum cov ntaub so ntswg(3). Kev kho mob ntxov ntawm APNs tuaj yeem zam kev tuag thiab txhim kho lub raum.

APN qhia cov cim thiab cov tsos mob ntawm ob qho tib sikab mob othiabzais zis o. Txawm li cas los xij, txog li 20% ntawm cov neeg mob tsis muaj cov tsos mob ntawm lub zais zis (4). Cov kev nthuav qhia kev kho mob thiab cov kab mob hnyav sib txawv, xws li mob me me nrog lossis tsis ua npaws mus rau septic shock (4, 5). Nws tsis zoo li tias ob lub raum yuav kis tau tib lub sijhawm. Yog li, APN-induced hnyav AKI yog qhov tsawg heev nyob rau hauvtsis muaj coexisting zistract obstruction (5), thiab tej zaum yuav nyuaj rau kev kho mob paub meej tias APN-induced AKI.

Peb ntawm no qhia txog qhov tsis tshua muaj tshwm sim ntawmAPN raug mob hnyavAKI uas tau lees paub los ntawm lub raum biopsy. Peb tau tshuaj xyuas cov ntaub ntawv Askiv muaj feem xyuam rau cov neeg mob APN-induced hnyav AKI, uas tau kho nyob rau hauv 50 xyoo dhau los thiab tshuaj xyuas cov yam ntxwv kho mob.

Case Report

Ib tug txiv neej muaj hnub nyoog {{{0}}} xyoo tau nthuav tawm rau peb lub tuam tsev nrog xeev siab thiab qab los noj mov, uas tau mob siab rau 4 hnub ua ntej nws nkag mus, thiab kub taub hau ntawm 39 degree thiab mob caj pas, uas tau mob ntev 3 hnub ua ntej nws nkag. Nws tau noj tramadol hydrochloride, acetaminophen, thiab loxoprofen sodium hydrate raws li xav tau. Ib hnub ua ntej tus neeg mob nkag mus, nws tau tshwm sim ntawm chav kho mob xwm txheej ceev hauv peb lub tsev kho mob, yws txog cov tsos mob uas tau hais los saum no. Tom qab rov qab los tsev, nws pib mob plab plab thiab sab laug sab nraub qaum thiab raug xa mus rau peb lub tsev kho mob. Nws keeb kwm yav dhau los suav nrog Kawasaki kab mob thiab cerebral infarction nrog sab laug hemiplegia uas tsis paub ua rau thaum muaj hnub nyoog 11 xyoos. Nws tus kab mob Kawasaki tau tsis muaj zog txij li lub sijhawm ntawd. Nws tau noj carbamazepine, trihexyphenidyl hydrochloride, thiab tizanidine hydrochloride rau kev tswj cov tsos mob tom qab cerebral infarction. Nws kuj tau noj 200 mg/hnub ntawm celecoxib rau qhov mob hauv nws sab laug sab laug rau 10 hnub ua ntej nkag. Txawm hais tias nws muaj cerebral infarction, tus neeg mob tsis tau kuaj pom tias muaj lub zais zis neurogenic thiab nws tsis muaj qhov cuam tshuam rau cov zis ua ntej nws nkag. Nws tsis haus cawv thiab tsis kam siv tshuaj yeeb. Cov ntshav creatinine qib ntawm 0.66 mg / dL tau sau tseg 6 xyoo dhau los. Kev kuaj lub cev ntawm kev nkag tau qhia cov hauv qab no: ceeb toom; qhov siab, 165.0 cm; lub cev hnyav, 75.0 kg; lub cev kub, 38.5 degree; ntshav siab, 127/87 mmHg; lub plawv dhia, 107 neeg ntaus / min; oxygen saturation, 99%.

Palpation ntawm nruab nrab mus rau sab laug sab hauv plab yog mob, thiab rhiab tshwm sim nyob rau hauv sab laug costovertebral lub kaum sab xis. Spastic sab laug hemiplegia tau pom. Kev kuaj zis qhia tau cov txiaj ntsig hauv qab no: pH 5.0; ntshav tsis zoo occult; 3+ protein; 1+ leukocyte esterase; zoo nitrites; 1-4 cov qe ntshav liab (RBCs)/high-power field; 30-49 cov qe ntshav dawb (WBCs)/high-power field; muaj cov kab mob; thiab tsis muaj cov kab mob pathological. Cov tshuaj urinary tau nthuav tawm cov kev tshawb pom hauv qab no: protein, 0.91 g / g creatinine; N-acetyl{11}}D-glucosaminidase, 37.1 U/L; 2-microglobulin, 1.4210 ug / L; thiab alpha 1- microglobulin, 51.0 mg/L. Kev soj ntsuam ntshav qhia cov kev tshawb pom hauv qab no: hemoglobin, 14.7 g / dL; WBC suav, 24,400/μL; platelet suav, 155, 000/μL; albumin, 2.5 g / dL; ntshav urea nitrogen, 49.3 mg / dL; creatinine, 2.67 mg / dL; hemoglobin A1c, 5.6%; Na, 128 mEq/L; thiab K, 3.5 mEq/L. Cov tshuaj tiv thaiv kab mob muaj raws li hauv qab no: C-reactive protein, 31.66 mg / dL; ib txwm ntxiv 3 thiab 4 qib; kab mob siab B thiab C serology, tsis zoo; anti-streptolysin O titer, ib txwm; anti-nuclear antibody, tsis zoo; thiab anti-DNA antibody, tsis zoo. Lub hauv siab X-ray pom lub ntsws li qub. Kev suav tomography pom ob sab ob lub raum loj tsis muaj hydronephrosis lossis cov tsos mob ntawm papillary necrosis (Daim duab 1a).

Peb tus neeg mob tau kub taub hau, mob nraub qaum, oliguria, pyuria, bacteriuria, nitrites hauv nws cov zis, leukocytosis, thiab qib siab C-reactive protein, uas qhia tias APN yog qhov kev kuaj mob tsim nyog thaum nkag; Yog li, ceftriaxone sodium (2 g txhua 24 teev) tau muab tso rau hauv txoj hlab ntshav. Txawm hais tias nws pom AKI nrog oliguria yam tsis muaj hypotension thiab nws cov fractional excretion ntawm Na yog 0.01%, hydration txaus tsis ua kom nws cov zis ntim thiab nws cov ntshav creatine tsis txo qis, txiav tawm lub raum ua ntej AKI ib leeg. Hloov chaw, nws cov ntshav creatinine tau nce los ntawm 2.67 mg / dL rau 5.22 mg / dL nyob rau hnub thib ob ntawm kev nkag. Txawm tias nwsqib creatinine hauv cov ntshavpeaked, lub raum biopsy tau ua nyob rau hnub 4 ntawm kev lees paub kom paub meej qhov ua rau AKI.

Covraum biopsyqhia tawmntiaj teb sclerosisnyob rau hauv 1 ntawm 23 glomeruli. Qee cov glomeruli tau pom me me ntawm cov cell infiltration, suav nrog polymorphonuclear leukocytes (Fig. 2a). Muaj ib qho me me mus rau nruab nrab ntawm kev sib xyaw ntawm cov cell infiltration, muaj li ntawm polymorphonuclear leukocytes, lymphocytes, thiab tsawg eosinophils, nyob rau hauv zonal cheeb tsam ntawm lub tubulointerstitium nrog patchy tubular epithelial cell flattening thiab atrophy (Fig. 2b). Pus casts tau pom nyob rau hauv cov tubules (Fig. 2b, c). Ib qho me me ntawm arteriolar hyalinosis tau pom. Tsis muaj vasculitis nyob rau hauv ib theem ntawm cov hlab ntsha. Ib qho kev tshawb fawb immunofluorescence tsis zoo rau IgG, IgA, IgM, C3, thiab C1q. Cov kev tshawb pom no tau lees paub tias AKI feem ntau tshwm sim los ntawm kev mob nephritis (AIN) vim APN.

Daim duab 2. Lub teeb microscopy ntawm lubraum biopsy qauv. A: Ib lub glomerulus nrog infiltration ntawm ib co polymorphic leukocytes (xub taub hau; periodic acid-Schiff staining; thawj magnification × 400). B: Patchy inflammatory cell infiltration, tubular atrophy, thiab tubular dilatation tau pom nyob rau hauv cheeb tsam zonal. Qee cov tubules nrog flattened epithelial hlwb muaj xws li cov kua paug pov tseg (asterisks; Hematoxylin thiab Eosin staining; thawj magnification × 200). C: Ib tug tubule nrog flattened epithelial hlwb yog obstructed nrog kua paug tsim nrogpolymorphic leukocytes(lub taub hau; Periodic acid-Schiff staining; thawj magnification × 200).

Cov ntshav tsis muaj kappa thiab lambda lub teeb saw theem, myeloperoxidase- thiab proteinase 3-anti-neutrophil cytoplasmic antibody qib, thiab tiv thaiv.glomerular hauv qab daus membrane(GBM) cov tshuaj tiv thaiv kab mob tau tshaj tawm tias nyob rau hauv qhov qub. Txawm hais tias tsis muaj kab mob loj hlob hauv cov zis thiab ntshav kab lis kev cai, tej zaum yog vim kev siv tshuaj tua kab mob yav dhau los, kev kho tshuaj tua kab mob nrog ceftriaxone sodium tau txuas ntxiv rau 14 hnub ntxiv rau daptomycin (700 mg txhua 48 teev intravenously). Tus neeg mob cov ntshav creatinine qib tau nce mus rau 1.60 mg / dL nyob rau hnub ntawm lub raum biopsy thiab maj mam txo mus rau 0.70 mg / dL nyob rau hnub 15 ntawm kev nkag. Kev soj ntsuam tom qab ultrasound tsis pom cov zis nyob hauv lub zais zis tsuas yog tom qab tso zis. Kev suav tomography pom tau tias ob lub raum yog qhov loj me uas tsis muaj papillary necrosis ntawm 2 lub hlis tom qab tso tawm (Fig. 1b).