Advanced Mob raum Kab Mob Nrog Lub Neej-Thiab Hypokalemia Vim Yog Tsis Pom Zoo Gitelman Syndrome
Oct 19, 2023
Vim li cas peb yuav nkees? Peb yuav daws tau qhov teeb meem qaug zog li cas?
【 Hu rau】 Email: george.deng@wecistanche.com / WhatsApp: 008613632399501 / Wechat: 13632399501
Abstract.Peb tshaj tawm ib rooj plaub ntawm tus poj niam muaj hnub nyoog 58-xyoos uas muaj cov tsos mob ntawm oliguria, qaug zog, anorexia, cem quav, hypovolemic cov tsos mob, thiab kev kuaj kuaj pom tias mob hypokalemia (1.7 mEq/L), hyponatremia (120 mEq/L) cov ntshav siab creatinine (SCr, 6.46 mg / dL) thiab urea (352 mg / dL). Tus neeg mob yav dhau los tau kuaj pom tias muaj kab mob raum ntev (CKD), nrog SCr txog 2.58 mg / dL 1 xyoo ua ntej, thiab tau muaj nyob rau hauv tag nrho nws cov kev kuaj sim dhau los pom tias hypokalemia, uas tau kho nrog kev ntsuas kev saib xyuas thiab eplerenone txawm tias ntshav qis qis. siab thiab lub plawv ua haujlwm. Kev ntsuas kev sib koom tes tau siv los kho cov poov tshuaj tsis txaus, thim rov qab hypovolemic hyponatremia, thiab txhawb lub raum kev ua haujlwm (suav nrog 4 ntu kev lim ntshav). Tsis tas li ntawd, kev soj ntsuam ceev faj tau qhia txog qhov tsis tsim nyog tso zis siab sodium thiab potassium losses, hypocalciuria, thiab hyperreninemic hyperaldosteronism ua rau kev kuaj mob ntawm Gitelman syndrome thiab hypokalemia-koom nrog mob tubulointerstitial nephropathy. Qhov tseem ceeb, ua raws li cov lus qhia yooj yooj yim ntawm kev noj zaub mov muaj poov tshuaj thiab liberal sodium tau ua rau tus neeg mob tsis yog nyob twj ywm euvolemic, tsis muaj tsos mob, thiab nrog cov electrolytes ib txwm, tab sis kuj kom rov zoo ib feem tseem ceeb ntawm lub raum ua haujlwm thiab ruaj khov ntawm theem CKD ua ntej. . Gitelman syndrome yog ib yam kab mob tsawg uas tuaj yeem kuaj tau yooj yim thiab kho tau raws li kev ntsuas yooj yim; nws qhov kev kuaj mob ntxov yog tsim nyog kom tsis txhob muaj teeb meem txog kev ua neej.
Cistanche tuaj yeem ua raws li kev tiv thaiv kev qaug zog thiab lub zog ua kom muaj zog, thiab cov kev tshawb fawb sim tau pom tias decoction ntawm Cistanche tubulosa tuaj yeem tiv thaiv daim siab hepatocytes thiab endothelial hlwb puas hauv cov nas ua luam dej hnyav, txhawb kev qhia ntawm NOS3, thiab txhawb cov kab mob siab glycogen. synthesis, yog li exerting los tiv thaiv qaug zog. Phenylethanoid glycoside-nplua nuj Cistanche tubulosa extract tuaj yeem txo cov ntshav creatine kinase, lactate dehydrogenase, thiab lactate qib, thiab nce qib hemoglobin (HB) thiab piam thaj hauv ICR nas, thiab qhov no tuaj yeem ua lub luag haujlwm tiv thaiv kev qaug zog los ntawm kev txo qis cov leeg nqaij. thiab ncua lub lactic acid enrichment rau lub zog cia hauv nas. Compound Cistanche Tubulosa ntsiav tshuaj ua rau lub sijhawm ua luam dej hnyav, nce siab glycogen cia, thiab txo qis qib urea tom qab kev tawm dag zog hauv cov nas, qhia nws cov nyhuv tiv thaiv kev qaug zog. Lub decoction ntawm Cistanchis tuaj yeem txhim kho kev ua siab ntev thiab ua kom lub cev qaug zog hauv kev tawm dag zog nas, thiab tuaj yeem txo qhov siab ntawm cov ntshav creatine kinase tom qab kev tawm dag zog thiab ua kom lub cev nqaij daim tawv nqaij ntawm cov nas ib txwm muaj tom qab kev tawm dag zog, uas qhia tau hais tias nws muaj cov teebmeem. ntawm kev txhim kho lub cev muaj zog thiab tiv thaiv qaug zog. Cistanchis kuj tseem ua rau lub sijhawm muaj sia nyob ntawm cov nas uas muaj nitrite-poisoned thiab txhim kho lub siab ntev tiv thaiv hypoxia thiab qaug zog.
Nyem rau nkees txhua lub sijhawm
Ntsiab lus
Gitelman syndrome - hypokalemia - hypokalemia nephropathy
Taw qhia
Gitelman syndrome (GS), tseem hu ua familial hypokalemia-hypomagnesemia, yog ib qho tsis tshua muaj kab mob ntsev-poob tubulopathy. Nws yog tshwm sim los ntawm ntau qhov kev hloov pauv, feem ntau ntawm cov kev txhawj xeeb ntawm SLC12A3 gene encoding thiazide-sensitive NaCl cotransporter (NCC) nyob rau hauv lub distal convoluted tubule (DCT), thiab tau txais los ntawm autosomal recessive qauv [1]. Qhov no apical cotransporter cuam tshuam tshwj xeeb nrog NaCl reabsorption hauv thawj feem ntawm DCT [2]. Feem ntau, cov mob no suav nrog kev sib xyaw ntawm cov kab mob electrolyte uas tshwm sim los ntawm kev thauj mus los tsis zoo los ntawm NCC, piv txwv li, hypokalemia, metabolic alkalosis, hypomagnesemia, thiab hypocalciuria, uas ua raws li kev ua ntawm thiazide diuretics ntawm NCC [3]. Kev nthuav qhia kev kho mob ntawm GS sib txawv, thaum lub sij hawm ntev ntawm qhov tshwm sim ntawm tus kab mob uas tsis kho yog txhais tsis zoo.
Ntawm no, peb piav qhia txog tus neeg mob uas muaj kab mob raum ntev (CKD) ntawm qhov tsis paub txog etiology nthuav tawm nrog rau lub raum tsis ua haujlwm ntawm lub raum ua haujlwm ua ke nrog kev ua rau lub neej muaj kev phom sij thiab hyponatremia hnyav, uas, tom qab ua tib zoo soj ntsuam cov txheej txheem raug ntaus nqi rau GS, ua kom kho cov electrolyte cuam tshuam. thiab txhawb kev rov ua haujlwm ntawm lub raum.
Case report
Ib tug poj niam Dawb muaj hnub nyoog 58-xyoo-laus tau nthuav tawm rau lub tuam tsev kho mob xwm txheej ceev ntawm peb lub tsev kho mob theem nrab yws yws txog oliguria, qaug zog, thiab anorexia pib ob peb hnub dhau los, thiab cem quav nws tus kheej tau kho cov tsos mob los ntawm lactulose tsis tu ncua. Cov txiaj ntsig kev sim dhau los tau qhia CKD (serum creatinine (SCr) ntawm 1.74 mg / dL 2.5 xyoo ua ntej, 2.58 mg / dL 13 lub hlis ua ntej, 1.93 mg / dL 11 lub hlis ua ntej, 1.98 mg / dL 5 lub hlis ua ntej, thiab 5.12 mg / dL 1 lub lis piam ua ntej) nrog cov poov tshuaj thiab sodium ntawm 3.39 mEq / L thiab 132 mEq / L 2.5 xyoo ua ntej, 2.37 mEq / L thiab 132.5 mEq / L 13 lub hlis ua ntej, 2.31 mEq / L thiab 129.7 mEq / L 11 lub hlis ua ntej, 3. mEq / L thiab 127.1 mEq / L 5 lub hlis ua ntej, 1.79 mEq / L thiab 119 mEq / L 5 hnub ua ntej, feem. Tus so ntawm nws yav dhau los kev kho mob keeb kwm suav nrog dyslipidemia, hypothyroidism, thiab thalassemia zoo. Nws tau txais eplerenone 25 mg ib hnub ib zaug (od), effervescent ntsiav tshuaj ntawm potassium bicarbonate 675 mg ob zaug hauv ib hnub (kev twv), 25-hydroxycholecalciferol 400 IU od, calcium carbonate 500 mg od, epoetin alfa 5, {{49} } IU subcutaneously txhua 3 lub lis piam, folic acid 5 mg od, simvastatin 20 mg od, levothyroxine 25 ug od, thiab lactulose hauv koob loj, tshwj xeeb tshaj yog lub lim tiam dhau los. Kev tshawb nrhiav ntau ntawm tus neeg mob cov ntawv sau yav dhau los los ntawm cov ntaub ntawv hluav taws xob tsis suav nrog lwm tus kws kho mob.
Ntawm kev kuaj mob, tus neeg mob qhov kub thiab txias yog 36.1 o C, nws cov ntshav siab (BP) yog 109/60 mmHg, nws lub plawv dhia (HR) yog 60 neeg ntaus / min, thiab nws cov pa oxygen saturation (Sp02) yog 98% hauv chav cua. . Lub plawv thiab lub ntsws auscultation thiab kev kuaj mob plab tsis tau qhia txog qhov txawv txav, tab sis cov tsos mob ntawm kev txo qis hauv cov hlab ntsha (txo cov tawv nqaij turgor, txias extremities, thiab qhuav mucous membranes) tau tshwm sim. Kev kuaj lub cev ntxiv yog qhov tsis zoo.
Arterial blood gases tsom xam pH=7.225, HCO3 –=9.9 mEq/L, pCO2=24.9 mmHg, anion gap (AG)=23.1 mEq /L, chloride (Cl– )=86 mEq/L. Cov txiaj ntsig ntawm kev soj ntsuam, piav qhia hauv Table 1, pom tias nce siab SCr (6.46 mg / dL) thiab urea (352 mg / dL), hematocrit ntawm 22.6%, qis cov poov tshuaj tsawg (1.7 mEq / L) thiab sodium ntau (120 mEq / L) thiab magnesium siab (4.8 mg / dL). urinalysis yog qhov zoo rau cov protein thiab hemoglobin, thaum cov sediment pom 50-55 leukocytes thiab 51 - 80 cov qe ntshav liab rau ib qho chaw muaj zog. Lub tshuab electrocardiogram (ECG) tau qhia txog U tsis muaj zog thiab ntev QT lub sijhawm (480 ms), thaum lub raum ultrasound tsis pom muaj pov thawj ntawm kev cuam tshuam thiab lub raum loj nyob rau hauv ib txwm nrog kev poob ntawm corticomedullary sib txawv.
Raws li qhov hnyav thiab qhov ceev ntawm kev soj ntsuam thiab kev kuaj pom, tus neeg mob tau txais kev kho dej hauv cov hlab ntsha (IV) nrog 250 mL ib txwm saline (N / S) enriched nrog 27 mEq ntawm potassium chloride (KCl) hauv 2 teev ntawm chav nyob luv. ntawm peb lub tsev kho mob. Tom qab ntawd, tus neeg mob tau txais mus rau lub tuam tsev kho mob nephrology rau kev tshawb nrhiav thiab kho ntxiv. Nyob rau hnub tom ntej, tus neeg mob tau txais kev kho mob nrog IV kua dej nrog ceev faj ntxiv KCl (los ntawm 81 txog 108 mEq / hnub) thiab ceev faj kev tswj hwm bicarbonate. Tus neeg mob lub diuresis yog 700 mL hauv thawj 8 teev thiab 1,200 mL rau hnub tom qab. Hnub 2, tsis txhim kho SCr (5.6 mg / dL) thiab qib urea (316 mg / dL) ua rau kev pib ntawm hemodialysis (4 zaug hauv tag nrho) nrog cov poov tshuaj dialysate siab. Tus neeg mob kuj tau txais kev txhaj tshuaj nrog 2 units ntawm cov qe ntshav liab, thiab kev kho epoetin tau pib. Ib qho tshuaj tua kab mob nrog ciprofloxacin 200 mg kev twv kuj tau pib raws li kev coj noj coj ua ntawm cov zis zoo.
Ib 24- teev cov zis tso zis ua rau hnub 2 pom tau tias tshem tawm creatinine ntawm 485 mg / 24h, urea ntawm 7 g / 24h, protein ntawm 2.32 g / 24h, sodium ntawm 79 mEq / 24h, thiab potassium ntawm 8 mEq / 24h, sib piv rau ib feem ntawm kev tso tawm ntawm cov poov tshuaj (FeK) ntawm 42% thiab tso zis potassium-rau-creatinine piv (UK: UC) ntawm 16.49 mEq / g. Tus neeg mob tau txais kev kho hemodialysis kawg rau hnub 6; Tom qab ntawd, SCr tseem nyob nruab nrab ntawm 3 thiab 3.5 mg / dL thiab urea 80 - 100 mg / dL. Ntshav qab zib poov tshuaj mus txog qib qub (3.6 mEq / L) hnub 10; Nyob rau hnub no, tso zis poov tshuaj tso tawm yog 34 mEq / 24h, sib npaug rau FeK ntawm 27%, thiab qhia tias tsis muaj cov poov tshuaj ntxiv hauv cov zis. Tom qab ntawd, IV KCl supplementation tau hloov nrog qhov ncauj supplementation ntawm poov tshuaj gluconate nyob ntawm seb cov qib ntshav.
Hnub 3, nrog tus neeg mob BP ntawm 103/55 mmHg, plasma renin kev ua haujlwm (PRA) nyob ntawm 18.72 ng/mL/h (saib ntau yam hauv supine txoj hauj lwm: 0.2 – 1.4 ng / mL / h), thiab aldosterone ntawm 36 ng / dL (kev siv ntau yam: 1.0 - 16 ng / dL), qhia tias hnyav theem nrab hyperaldosteronism. Hnub 5, ib qho echocardiogram qhia txog qhov loj ntawm lub chamber nyob rau hauv ib txwm muaj ntau yam thiab ib txwm ua haujlwm systolic (sab laug ventricular ejection feem ntawm 60 - 65%), me me tricuspid thiab mitral valve regurgitation, me me aortic valve calcification, thiab qhov tsawg kawg nkaus ntawm pericardial kua nyob ib ncig ntawm. tom qab lub plawv phab ntsa. Nws yuav tsum raug sau tseg tias tus neeg mob yav dhau los raug xa mus rau tus kws kho plawv thiab tus kws kho mob nephrologist thiab muaj, 3 thiab 4 xyoo ua ntej, tau txais 2 PRA thiab aldosterone ntsuas, ib zaug qhia qhov qub, thiab lwm lub sijhawm qhia me ntsis nce qib; Nws kuj tau dhau los ua CT scan qhia cov qog adrenal.
Tom qab 13 hnub ntawm kev mus pw hauv tsev kho mob, tus neeg mob tau tawm hauv tsev kho mob nrog cov lus qhia kom noj cov poov tshuaj siab (ob lub txiv tsawb ib hnub) thiab kev noj zaub mov zoo liberal sodium nrog rau cov txheej txheem hauv qab no: folic acid 5 mg od, calcium carbonate 500 mg 3 zaug ib hnub. hnub (tid), potassium bicarbonate 1,350 mg bid, levothyroxine 22 ug od, simvastatin 20 mg od, alfacalcidol 1 ug od, thiab epoetin alfa 5, 000 IU subcutaneously 3 zaug ib lub lim tiam. Plaub hnub tom qab, tus neeg mob tau raug soj ntsuam hauv lub chaw kho mob nephrology nrog SCr=1.99 mg/dL thiab K+=5.5 mEq/L, ua rau muaj cov tshuaj potassium bicarbonate nres. Tus neeg mob tau mus xyuas lub tsev kho mob tom qab ~ 1, 2, thiab 5 lub hlis; Nws cov txiaj ntsig hauv kev sim tau nthuav tawm hauv Table 1. Raws li pom nyob rau hauv tib lub Rooj, los ntawm kev ua raws li cov lus qhia ntawm cov poov tshuaj thiab liberal sodium kom tsawg (80 - 90 mEq / hnub thiab 136 - 182 mEq / hnub), tus neeg mob muaj peev xwm tswj tau euvolemia. thiab cov poov tshuaj hauv cov ntshav ib txwm muaj, tsis muaj tsos mob ( kiv taub hau, cem quav, thiab lwm yam), thiab rov ua kom lub raum ua haujlwm tseem ceeb (SCr=1.5 mg/dL).
Kev sib tham
GS yog ib hom kab mob qog noj ntshav, nrog heterozygote prevalence kwv yees li ntawm ~ 1% ntawm cov neeg Dawb [4]. Loss-of-function mutations ntawm NCC thaum ntxov DCT ua rau txo Na + reabsorption, nrog rau cov dej isotonic nkim. Qhov tshwm sim hypovolemic stimulus activates renin-angiotensin-aldosterone system (secondary hyperaldosteronism). Nce Na + tus me nyuam nrog rau qib aldosterone nyob rau hauv lub distal nephron ua rau Na + reabsorption pauv rau K + (kaliuria) thiab H + (aciduria) [5]. Nce magnesiuria thiab hypocalciuria feem ntau kuj tshwm sim. Kev ua xyem xyav ntawm GS yog raws li cov hauv qab no [3]: 1) mob hypokalemia nrog rau lub raum poov tshuaj tsis tsim nyog (nce FeK thiab UK: UC); 2) metabolic alkalosis; 3) hypomagnesemia nrog rau lub raum tsis zoo magnesium nkim (nce FeMg); 4) hypocalciuria (txo FeCa); 5) fractional excretion ntawm chloride (FeCl) > 0.5%; 6) siab PRA; 7) Tsawg lossis ib txwm-tsawg BP; 8) lub raum ultrasound [3].
Txawm hais tias qee cov neeg mob uas muaj GS tuaj yeem nyob tsis muaj tsos mob, lawv feem ntau tuaj yeem nthuav tawm ntau yam tsos mob thiab cov tsos mob, suav nrog kev xav ntsev, qaug zog, cov tsos mob neuromuscular ( kiv taub hau, paresthesia, carpopedal spasms, nqaij tsis muaj zog, mob sib koom), cov tsos mob ntawm lub raum (polyuria, polydipsia, nocturia), plab hnyuv tsis txaus siab ( cem quav, mob plab), cov tsos mob ntawm cov hlab plawv (palpitations, ventricular arrhythmias), thiab kev loj hlob cuam tshuam (luv stature, loj hlob thiab / los yog pubertal qeeb) [3, 6]. Nco ntsoov, Fujimura et al. [7] pom tias ntau dua 50% ntawm cov neeg mob GS raug kuaj los ntawm kev kuaj ntshav random, txawm tias muaj ntau yam tsos mob rau lub sijhawm sib txawv.
Cov ntaub ntawv no qhia txog cov lus qhia tseem ceeb txog GS. Ua ntej, hauv peb tus neeg mob, qhov kev kuaj mob tau ncua sijhawm ntev, txawm hais tias muaj cov tsos mob tshwm sim thiab pheej mob hypokalemia thiab hyponatremia ntau xyoo. Tus neeg mob yav dhau los tau pom los ntawm cov kws kho mob ntawm ntau yam tshwj xeeb, suav nrog cov kws kho mob dav dav, kws kho plawv, thiab txawm tias tus kws kho mob nephrologist, txhua tus uas tsis quav ntsej cov lus saum toj no thiab kho hypokalemia symptomatically nrog cov tshuaj potassium ntxiv thiab pib ntawm eplerenone, tej zaum yog vim kev txhais lus yuam kev. ib txwm PRA thiab aldosterone kuaj thiab ib txwm adrenal morphology. Kev nce hauv PRA thiab aldosterone tej zaum yuav tsis raug kuaj pom txawm tias, yog tias hypovolemia tau rov qab los ib ntus ntawm lub sijhawm ntawd, tso cai rau PRA thiab aldosterone rov qab mus rau ze li qub. Qhov thib ob, qhov mob hypokalemia no tau ua rau lub raum tsis ua haujlwm tsis tu ncua, nce mus txog SCr ntawm 2.58 (sib npaug rau qhov kwv yees glomerular filtration rate (eGFR) ntawm 20 mL / min / 1.73m2, piv txwv li, CKD theem 4) twb 1 xyoo ua ntej nws mus pw hauv tsev kho mob, nrog rau tus neeg mob tau ceeb toom txog qhov muaj peev xwm xav tau pib kho lub raum hloov mus ntev. Ib qho kev raug mob raum superimposed mob raum (AKI), tejzaum nws yog vim lub ntim depletion, ntxiv rau lub raum tsis ua haujlwm thiab tsim nyog pib ntawm hemodialysis. Txawm li cas los xij, qhov kev kuaj mob tsim nyog ntawm hypokalemia-txuas nrog mob ntev interstitial nephritis thiab kev saib xyuas kom zoo ntawm lub hauv paus GS nrog kev ncaj ncees ntawm kev ntsuas hauv- thiab tawm hauv tsev kho mob tau ua rau tus neeg mob rov zoo li qib siab ntawm lub raum ua haujlwm, ncav cuag SCr ntawm 1.5 mg. /dL thiab eGFR ntawm 38 mL / min / 1.73m2.
Thaum nkag mus rau peb lub tsev kho mob, tus neeg mob tau nthuav tawm nrog hypovolemia, oliguria, mob hnyav hypokalemia, hyponatremia, hypochloremia, thiab ib feem them nyiaj metabolic acidosis nrog nce AG, taw qhia rau kev sib koom ua ke ntawm hypochloremic metabolic alkalosis, tej zaum vim yog hypovolemia. Raws li cov lus saum toj no, kev kuaj xyuas ua haujlwm ntawm AKI superimposed ntawm CKD, tsis yog kev nce qib CKD mus rau theem kawg, tau ua. Kev siv zog thaum muaj xwm txheej ceev tau raug coj mus rau kev txhim kho ntawm hypokalemia, hypovolemic hyponatremia, thiab prerenal AKI. Tsis tas li ntawd, kev sib koom ua ke tau ua kom ncav cuag qhov kev kuaj pom tseeb ntawm tus kab mob hauv qab.
Following continuous administration of isotonic solutions enriched with potassium, serum potassium levels were increasing slowly, a fact indicating the presence of chronic, severe total-body potassium deficit. In the case of our patient, an underlying salt-wasting tubular disorder, aggravated by intestinal losses due to lactulose overuse was possible. In any case, two calculations of FeK and UK: UC, both validated tools in the assessment of hypokalemia in healthy and diseased populations [3, 8], confirmed inappropriate kaliuresis despite very low serum potassium. Results of high PRA and aldosterone were compatible with hyperreninemic hyperaldosteronism. These findings, together with the high urine chloride concentration (>15 - 20 mEq / L), tso zis calcium ntawm 63 mg / 24h (< 100 mg/24h), and the absence of use of thiazide diuretics, pointed towards the diagnosis of GS as the most plausible cause of our patient's clinical presentation, according to existing diagnostic algorithms (Figure 1) [9, 10]. Our patient presented with hypermagnesemia, instead of the hypomagnesemia anticipated by the diagnostic features of GS. This finding could be explained either by reduced renal magnesium excretion in the presence of reduced renal function [11], or by overconsumption of lactulose, as this laxative can increase the intestinal absorption of Mg2+ when it is catabolized to organic acids in the large intestine [12].
Kev loj hlob ntawm CKD hauv peb tus neeg mob nrog GS tuaj yeem yog cov hauv paus chiv keeb (Daim duab 2). Mob hypokalemia per se ua rau tubulointerstitial nephritis nrog tubular vacuolization, cystic formations, thiab interstitial fibrosis hauv lub raum biopsy [13]. Cov tswv yim pom zoo muaj xws li lub raum tsis zoo angiogenesis thiab concomitant peritubular capillary poob txuas nrog cov vascular endothelial kev loj hlob tsis zoo (VEGF) qhia [14], qhov tsis txaus ntseeg ntawm cov tshuaj vasoactive (nce hauv zos endothelin-1 thiab angiotensin II, txo lub raum kallikrein thiab TSIS TAU) ua rau lub raum vasoconstriction thiab txo cov ntshav khiav thiab oxygenation hauv lub raum medulla [15, 16], thiab nce hauv zos ammoniagenesis ua rau kev ua kom muaj lwm txoj hauv kev ntxiv [17]. Tsis tas li ntawd, cov mob hypovolemia ntev ua rau cov neeg mob tuaj yeem ntsib ntau lub sijhawm ntawm prerenal AKI, tshwj xeeb tshaj yog thaum muaj cov xwm txheej nyob ib sab (xws li, lub cev qhuav dej, thiab raws plab) [18]. Thaum kawg, cov qib siab ntawm aldosterone incited los ntawm lub ntim ntim tsis txaus tuaj yeem ua rau muaj kev cuam tshuam ncaj qha rau nephrotoxic, cuam tshuam rau cov kev xav tau ntawm kev ua rau thiab pro-fibrotic cuam tshuam los ntawm kev ua kom cov mineralocorticoid receptors, raws li tau qhia yav dhau los hauv cov qauv ntawm AKI, hypertensive, thiab mob raum mob ntshav qab zib thiab mob calcineurininhibitors toxicity [19]. Qhov kev xav no tau txhawb nqa los ntawm kev soj ntsuam kev soj ntsuam ntawm lub raum kev ua haujlwm hauv cov neeg mob GS thiab Bartter syndrome, uas tau txiav txim siab tias qib ntawm hypokalemia per se tsis tuaj yeem cuam tshuam ncaj qha rau qib ntawm GFR kev puas tsuaj, thiab tej zaum aldosterone nws tus kheej ua lub luag haujlwm tseem ceeb hauv qhov kev puas tsuaj no. [20]. Txawm li cas los xij, hauv kev tshawb fawb me me ntawm 6 tus neeg mob nrog GS, qhov tsis muaj qhov cuam tshuam ntawm pro-inflammatory thiab profibrotic cuam tshuam ntawm aldosterone, tshwm sim los ntawm kev nce oxidative kev nyuaj siab thiab ua kom txoj hauv kev Rho kinase, tau sau tseg [21]. Yog li, kev tshawb fawb ntxiv tshwj xeeb hauv cov tib neeg ntawm hom no yog xav tau.
Qhov tseeb nthuav txog peb tus neeg mob yog tias nws lub raum ua haujlwm tsis tu ncua rau qee lub xyoo thiab txhim kho tau zoo nyob rau ob peb lub hlis tom qab mus pw hauv tsev kho mob. Txawm li cas los xij, hauv qee cov neeg mob uas muaj tus kab mob tubulointerstitial, vim tias qhov kev puas tsuaj tsis tuaj yeem ntawm cov mob fibrotic tubulointerstitial raug mob tsis yog qhov dav, kev tshem tawm ntawm cov kab mob pathogenetic tuaj yeem tsis tsuas yog ruaj khov tab sis kuj txhim kho lub raum ua haujlwm me ntsis [22, 23]. Nyob rau hauv cov xwm txheej zoo li no, muaj ib feem ntawm glomeruli yam tsis muaj kev puas tsuaj loj tuaj yeem ua rau muaj kev pom ntau ntxiv hauv qhov qub nephrons, uas, raws li kev xav ib txwm muaj, tuaj yeem them nyiaj, tsawg kawg ntawm ib feem, rau kev ua haujlwm poob nrog cov nephrons puas [24 , 25] ib. Rau qhov zoo tshaj plaws ntawm peb txoj kev paub, qhov no yog thawj rooj plaub ntawm tus neeg mob hypokalemia-txuas nrog mob ntev tubulointerstitial nephropathy uas ua rau lawv lub raum ua haujlwm tau zoo li ob peb lub hlis tom qab tshem tawm cov kab mob pathogenetic.
Hauv kev xaus, qhov no qhia txog qhov tseeb tias qhov tsis ua tiav ntawm kev kuaj mob zoo ntawm GS ua rau muaj kev sib raug zoo ntawm hypovolemia thiab hypokalemia tuaj yeem ua rau lub raum tsis ua haujlwm tseem ceeb uas yuav tsum tau lim ntshav. Hauv cov xwm txheej zoo li no, qhov tsis txaus ntseeg ntawm cov poov tshuaj nrog cov hypovolemia yuav tsum nco ntsoov qhia cov kws kho mob txog qhov muaj peev xwm ntawm tubular teeb meem thiab ua rau muaj feem cuam tshuam txog kev kuaj mob uas tuaj yeem yooj yim qhia qhov kev kuaj mob kom raug. Qhov no tuaj yeem ua rau lub koom haum ntawm cov kev ntsuas yooj yim los kho cov teeb meem cuam tshuam thiab qhov tseem ceeb tshaj plaws, tom qab lub sij hawm mob hnyav, kev taw qhia kom raug ntawm tus neeg mob ntawm kev noj zaub mov yooj yim uas tuaj yeem khaws cov electrolyte thiab kua dej sib npaug, daws cov tsos mob ntev, thiab ua rau kev saib xyuas, los yog kev txhim kho ntawm lub raum ua haujlwm.
Nyiaj txiag
Daim ntawv no tsis tau txais kev txhawb nqa los ntawm ib qho twg thiab sawv cev rau qhov kev siv zog ntawm tus kws sau ntawv.
Kev tsis sib haum xeeb
Tsis muaj leej twg tshaj tawm.
Cov ntaub ntawv
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