Mob raum raug mob cuam tshuam rau Hypokalemia Associated With Yokukansan Kev Npaj: Kev Tshawb Fawb Txog Kev Tshawb Fawb

Lub sijhawm kawm ntawmmob raum mobthiabhypokalemiatseem unelucidated. Peb tau tshawb xyuas seb puas hloov lub raum ua haujlwm cuam tshuam rau hypokalemia thiab cov kws kho mob raumob raum mobin patients who used Yokukansan preparation. We performed a secondary analysis of retrospective observational cohort data from adult patients who started Yokukansan preparation. The study was conducted from June 2015 to May 2019 at Tokyo Women's Medical University, Medical Center East. The effect of acute kidney injury (>1ntshav creatininetheem) los yog lub raum ua haujlwm rov qab los ntawm hypokalemia (cov ntshav cov poov tshuaj<3.0 mEq/L) was investigated. The clinical predictors for acute kidney injury were determined using a multivariate Cox proportional hazard analysis. Out of 258 patients, 12 patients had both outcomes and all but one patient experienced in the order of mob raum mobthiab hypokalemia. Tsis suav nrog ib tus neeg mob, hypokalemia tshwm sim hauv 11/34 (32%) cov neeg mob tom qab mob raum mob thiab 27/223 (12%) cov neeg mob tsis muajmob raum mob(p= 0.005). Hypokalemia tshwm sim nyob rau hauv 9/25 (36%) ntawm mob raum raug mob nrog rov qab, 2/9 (22%) ntawm lub raum mob tsis zoo, thiab 27/223 (12%) ntawm tsis muajmob raum mob(p= 0.014). Cov neeg mob uas mob raum raug mob tau pom qhov pib lig ntawm hypokalemia piv nrog cov tsis muaj mob raum raug mob (p= 0.001). Hauv 258 tus neeg mob, multivariate Cox proportional hazard tsom xam pom tias cov ntshav siab systolic siab thiab txhais tau tias cov hlab ntsha siab ua rau muaj kev pheej hmoo ntawm mob raum raug mob. Cov kws kho mob yuav tsum nco ntsoov tias hypokalemia tshwm sim tom qabmob raum mobthaum Yokukansan npaj kho.

Ntsiab lus mob raum mob; ntshav siab;hypokalemia; Yokukansan; Kev ua txhaum cai

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Taw qhia

Mob raum raug mob(AKI) yog txuam nrog ntau yam mob thiab tuag nyob rau hauv ntau haiv neeg.1–3) AKI pathogenesis yog categorized li prerenal, raum, thiab postrenal.4,5) Ib tug meej.kev nkag siab ntawm AKI etiology(piv txwv li, septic shock, mob plawv tsis ua hauj lwm, electrolyte disorders, thiab tshuaj) yog ib qho tseem ceeb los txiav txim siab txog kev kho mob.kho cov tswv yim.6) 

Cov kws kho mob tau nqis peev ntau rau hauvAKI kev kho mobtshem tawm cov neeg mob ua ntej thiab txhim kho covlig txim ntawm AKI. Kev taw qhia ntawm intensivekev kho mob rau AKItuaj yeem pab kom nce ntxivlub raum potassium excretion, yog li tsav cov normalization ntawm cov ntshav hauv cov ntshav vim yog lub raum rov qab txheej txheem thiab kev tswj hwm ntawm hyperkalemia.7) Yog li, kev rov ua haujlwm ntawm lub raum yog qhov muaj feem pheej hmoo ntawm hypokalemia. Hloov pauv, hypokalemia nws tus kheej tau cuam tshuam nrog kev pheej hmoo ntawm lub raum kev ua haujlwm thiab tag nrho cov kev ua rau tuag.8,9) Tsis muaj cov ntaub ntawv hais txog cov xwm txheej ntawm cov tshuaj kho mob ntawm AKI thiab hypokalemia. Yokukansan thiab Yokukansankachimpihange (ob leeg Tsumura Co., Tokyo, Nyiv), uas suav nrog qhov sib npaug ntawm Glycyrrhiza. Yokukansan muaj xya yam khoom tsis zoo (Atractylodes lancea rhizome, Poria sclerotium, Cnidium sp. rhizome, Uncaria sp. nuv, Angelicae radix, Bupleuri radix, thiab Glycyrrhiza sp.). Yokukansankachimpihange muaj Cit rus unshiu tev thiab Pinellia sp. tuber ntxiv rau Yokukansan. Glycyrrhetinic acid, active metabolite ntawm Yokukansan npaj (Yokukansan thiab Yokukansankachimpihange), inhibits 11 -hydroxysteroid dehydrogenase hom 2,ua rau hypokalemia.10) Cov neeg mob laus feem ntau muaj kev pheej hmoo siab ntawm hypokalemia cuam tshuam nrog Yokukansan npaj thiab AKI hauv chaw kho mob.11–13) Tsis tas li ntawd, Yokukansan kev npaj ua rau pseudo-aldosteronism (hypokalemia thiab kub siab) thiab kub siab tuaj yeem yog qhov muaj peev xwm kwv yees rau AKI.14. ,15) Yokukansan kev npaj yog feem ntau siv rau hauv cov neeg laus los tiv thaiv cov tsos mob xws li Alzheimer's kab mob los ntawm kev thaiv cov kev ua ntawm glutamate paj hlwb thiab stimulating serotonin 5-HT1A receptor.16,17) Yog li ntawd, peb xaiv Kev npaj Yokukansan ua ib qho tshuaj zoo tshaj plaws uas muaj pov thawj los teb cov lus nug hauv chaw kho mob txog lub sijhawm - cov chav kawm ntawm AKI thiab hypokalemia.

Txoj kev tshawb no tsom los txheeb xyuas lub sijhawm ntawm kev txhim kho / rov qab los ntawm AKI thiab hypokalemia, kev sib raug zoo ntawm kev txhim kho / rov qab los ntawm AKI thiab hypokalemia, thiab cov kws kho mob rau AKI.

KHOOM PLIG THIAB MUAB

Kawm Tsim thiab Kev Tsim Nyog Rau Tus Neeg Mob

We further analyzed a previously described single-center retrospective observational cohort dataset collected between June 2015 and May 2019 at Tokyo Women's Medical University, Medical Center East (a 450-bed university hospital in Tokyo, Japan).13) The study population included inpatients and outpatients aged >20 xyoo uas tau pib Yokukansan npaj thaum Lub Rau Hli 2015 thiab Tsib Hlis 2019 thiab saib xyuas lawv cov qib poov tshuaj hauv cov ntshav thaum kho. Cov txheej txheem cais tawm suav nrog cov hauv paus hauv cov ntshav cov ntshav ntawm cov poov tshuaj<3.0 mEq/L, no multiple data for serum creatinine level, and baseline estimated glomerular filtration rate (eGFR) <30 mL/min/1.73 m2. This study was conducted in compliance with the Declaration of Helsinki and approved by the Institutional Review Board at Tokyo Women's Medical University (#5199).

Cov ntaub ntawv sau

Tus neeg mob cov ntaub ntawv kho mob hluav taws xob tau raug tshuaj xyuas los sau cov ntaub ntawv rau pej xeem cov yam ntxwv (poj niam txiv neej, hnub nyoog, qhov siab, lub cev qhov hnyav, thiab lub cev hnyav), kev kuaj mob thawj zaug (delirium, dementia, thiab lwm yam mob puas siab ntsws), cov ntaub ntawv kuaj mob (serum albumin, ntshav. urea nitrogen, creatinine, serum sodium, serum poov tshuaj, thiab cov tshuaj chloride), cov cim tseem ceeb (systolic ntshav siab (SBP), diastolic ntshav siab (DBP), thiab lub plawv dhia), cov ntsiab lus ntawm Yokukan san npaj ( koob tshuaj thiab ua raws- nce lub sij hawm), thiab cov tshuaj txaus siab (benzodiazepine, ramelteon, suvorexant, cholinesterase inhibitors (donepezil, rivastigmine, thiab galantamine), N-methyl-D-aspartate antagonist (memantine), raug lossis atypical antipsychotics, qhov ncauj corticosteroids, angiotenings. inhibitors, angiotensin II receptor blockers, voj diuretics, thiazide diuretics, thiab potassium-sparing diuretics). Peb xam qhov piv ntawm cov ntshav urea nitrogen rau cov ntshav creatinine los ntsuas qhov ntim raws li txoj cai.18) Kev kwv yees kwv yees, suav nrog poj niam txiv neej, hnub nyoog, thiab qib ntshav creatinine, tau siv los txiav txim siab eGFR.19) Vim peb tsis tuaj yeem tau txais cov ntaub ntawv roj ntshav. los ntawm cov ntaub ntawv kho mob hauv hluav taws xob, peb tau txiav txim siab qhov sib txawv ntawm cov ntshav sodium thiab cov tshuaj chloride ua lwm txoj hauv kev rau cov kua qaub-piv qhov cuam tshuam.20) Peb suav cov txhais tau tias cov hlab ntsha siab (MAP) siv cov kab zauv hauv qab no.

Cov txiaj ntsig Peb tau soj ntsuam ob qhov kev tshawb fawb tau tshwm sim thaum lub sij hawm Yokukansan npaj kho: AKI thiab hypokalemia (cov kua dej hauv cov poov tshuaj<3.0 mEq/L). Because data on urine volume were unavailable, we assessed AKI based on Kidney Disease Improving Global Outcomes (KDIGO) criteria, using the definition of >1.5 npaug nce los ntawm lub hauv paus hauv cov ntshav creatinine theem.21) Muaj kev txhawj xeeb tias KDIGO cov txheej txheem ntawm kev nce ntxiv ntawm cov ntshav creatinine muab cov txiaj ntsig tsis tseeb.22) Tsis tas li ntawd, KDIGO cov txheej txheem sij hawm (48 h lossis 7 d) tau tsim feem ntau. rau kev kho mob hnyav.21)

Kev Tshawb Fawb Txog Kev Tshawb Fawb Feem ntau cov ntaub ntawv faib tau raug tshaj tawm raws li qhov txhais tau tias ± tus qauv sib txawv thiab muab piv nrog Cov Tub Ntxhais Kawm T-test, qhov uas tsis yog ib txwm faib cov ntaub ntawv tau tshaj tawm raws li qhov nruab nrab thiab qhov sib txawv (IQR) thiab muab piv nrog Mann–Whitney's U-test. Categorical cov ntaub ntawv tau nthuav tawm raws li tus lej thiab feem pua, thiab heterogeneity raug ntsuas los ntawm kev ntsuas chi-square.

Lub sijhawm-rau-kev tshwm sim tshwm sim (AKI lossis hypokalemia cuam tshuam nrog Yokukansan npaj) tau txheeb xyuas raws li Ka txoj kev npaj-Meier nkhaus. Lub sijhawm ua raws li tau hais tseg yog lub sijhawm los ntawm kev qhia txog Yokukansan kev npaj mus rau kev txiav tawm ntawm Yokukansan kev npaj lossis kev loj hlob ntawm qhov tshwm sim (AKI lossis hypokalemia). Peb piv qhov nruab nrab qhov pib thiab qhov tshwm sim ntawm hypokalemia ntawm cov neeg mob uas muaj thiab tsis muaj AKI. Vim tias peb tau txiav txim siab ntxiv cov poov tshuaj tso tawm ua pov thawj ntawm lub raum kev ua haujlwm rov qab, peb tau soj ntsuam ntxiv txog kev txhim kho hypokalemia raws li AKI rov qab. Kev rov ua haujlwm ntawm lub raum tau txhais tias tsis tsawg dua li 1. Cov kev kho p qhov tseem ceeb tau teeb tsa ntawm 0.025 (0.05 muab faib los ntawm 2) piv txwv tias ob pawg kev tshuaj ntsuam xyuas tau ua. Cov tsos mob ntawm kev txaus siab rau cov neeg mob AKI thiab hypoxia lamia tau sau tseg. Tsis tas li ntawd, Kaplan-Meier nkhaus tau txheeb xyuas qhov tshwm sim ntawm hypokalemia stratified los ntawm AKI saum toj no. Qhov kev sib piv no tau siv los ntawm kev ntsuas ntsuas ntsuas. Cov hnub ntsuas yog qhov pib ntawm Yokukansan npaj rau cov neeg mob tsis muaj AKI thiab kev loj hlob ntawm AKI rau cov neeg mob AKI. Peb tau tshawb xyuas cov kws kho mob ua ntej rau AKI siv ntau qhov sib txawv Cox qhov kev ntsuas phom sij. Peb xav tias kwv yees li ntawm 12% ntawm cov neeg laus tsim AKI.24,25) Yog li, peb txoj kev tshawb fawb xav tau tsawg kawg 250 tus neeg mob los txheeb xyuas peb qhov txawv txav ntawm tus qauv kawg yog tias peb xav tias 10 tus neeg mob yuav tsum tau kuaj xyuas ib qho kev hloov pauv ywj pheej. Qhov sib txawv ntawm qhov sib txawv yog AKI kev txhim kho thaum lub sij hawm kho Yokukansan npaj. Cov kev hloov pauv ywj pheej yog cov yam ntxwv ntawm pej xeem, kev kuaj mob thawj zaug, cov ntaub ntawv kuaj mob, cov cim tseem ceeb, koob tshuaj Yokukansan, thiab cov tshuaj txaus siab. eGFR tau categorized li binary variable (< 60 or ≥ 60 mL/min/1.73 m2 ) because this cut-off value was used for diagnosing chronic kidney disease.26) The daily dose of the Yokukansan preparation was categorized as ≥7.5 or <7.5 g because a daily dose of 7.5 g of Yokukansan preparation has been used in clinical trials.27) We prescreened potential independent variables using univariate Cox proportional hazard analyses, and all independent variables with a p-value <0.10 were further evaluated in the multivariate Cox proportional hazard analysis. We confirmed each independent variable for multicollinearity. Additionally, we constructed three final models using three blood pressure components (SBP, DBP, and MAP), because the effect of each blood pressure on renal function differed.28) We used a stepwise backward selection method to construct three final models according to the Akaike information criterion. The robustness of the final models was confirmed using a stepwise forward selection method. Three final models were used to determine the hazard ratio (HR) and 95% confidence interval (95% CI). We attempted to examine the interactions of independent variables by introducing a cross-product term of respective independent variables into each final model as needed.

Txhua qhov kev txheeb xyuas kev txheeb xyuas yog ob sab thiab ua tiav siv JMP® Pro 14 (SAS Institute Inc., Cary, NC, USA). Ib p-value<0.05 was considered statistically significant unless otherwise mentioned. Figures were prepared using GraphPad Prism ver. 8.00 (GraphPad Software, San Diego, CA, U.S.A.).

TSEEM CEEB

Kawm Pej Xeem

A flow chart of the eligible populations is depicted in Fig. 1. We identified 678 patients at Tokyo Women's Medical University, Medical Center East, who were >20 xyoo thiab leej twg tau pib Yokukansan npaj thaum Lub Rau Hli 2015 txog Lub Tsib Hlis 2019. Ntawm lawv, peb tsis suav nrog 13 nrog cov qib poov tshuaj hauv paus.<3.0 mEq/L, 307 with no multiple data for serum creatinine, and 100 with a baseline eGFR <30 mL/min/1.73 m2. The remaining 258 patients were included in the main analysis.

Table 1 shows the baseline clinical characteristics of the study cohort. Approximately 60% of patients were male. The median age was younger in the AKI group than the no AKI Fig. 1. The Flow Chart of Eligible Populations We identified 678 patients between June 2015 and May 2019 at Tokyo Women's Medical University, Medical Center East, who were >20 xyoo thiab siv Yokukansan npaj (Yokukansan thiab Yokukansankachimpihange). Peb tsis suav nrog 420 tus neeg mob vim tias cov ntshav qab zib hauv qib poov tshuaj<3.0 mEq/L, no multiple data for serum creatinine level, and baseline estimated glomerular filtration rate <30 mL/min/1.73 m2 (13, 307, and 100 patients, respectively). The final study cohort included 258 patients. Of them, 35 (14%) developed acute kidney injury, and 223 (86%) of patients did not. Hypokalemia developed in 12 (34%) patients in the acute kidney injury group and 27 (12%) patients in the no acute kidney injury group. Among 12 patients with acute kidney injury and hypokalemia, 11 (92%) patients experienced subsequent hypokalemia after acute kidney injury. N, number; K, potassium; Cr, creatinine; eGFR, estimated glomerular filtration rate, AKI; acute kidney injury group (75 [68–81] vs. 80 [73–85] years old, p< 0.01). The majority of patients had hypoalbuminemia (mean serum albumin <3.0 g/dL), and 83% of the patients in both groups received a daily dose of ≥ 7.5 g Yokukansan preparation.

Kev Nyuaj Siab ntawm AKI thiab AKI Recovery ntawm Hypokalemia

Lub Kaplan-Meier nkhaus tau qhia tias qhov tshwm sim ntawm AKI yog 35 ntawm 258 (14%) cov neeg mob nrog lub sijhawm nruab nrab ntawm 10 (IQR: 5–26) hnub (Fig. 2). Lub Kaplan– Meier nkhaus rau qhov tshwm sim ntawm hypokalemia yog piav nyob rau hauv Ntxiv daim duab 1. Muaj 12 ntawm 35 (34%) cov neeg mob uas muaj ob qho tib si AKI thiab hypokalemia. Qhov nruab nrab ntawm qhov pib ntawm hypokalemia yog 35 (IQR: 18–146) hnub hauv cov neeg mob AKI, uas tau ntev dua li cov neeg mob uas tsis muaj AKI (18 d, IQR: 10–36) (p= 0.001). Table 2 qhia txog cov yam ntxwv ntawm kev txaus siab rau cov neeg mob uas muaj AKI thiab hypokalemia. Muaj 11 ntawm 12 (92%) cov neeg mob uas tau ntsib hypokalemia tom qab AKI. Lub sijhawm nruab nrab ntawm AKI mus rau kev txhim kho hypokalemia yog 30 (IQR: 13-47) hnub.

Tsis suav nrog ib tus neeg mob uas tsim hypokalemia ua ntej AKI, cov kev kho mob ntawm AKI thiab hypokalemia cuam tshuam nrog Yokukansan kev npaj tau muab sau tseg rau hauv Table 3. Qhov kev pheej hmoo ntawm hypokalemia siab dua hauv 11 ntawm 34 (32%) cov neeg mob AKI dua li ntawm 27 ntawm 223 (12). %) cov neeg mob uas tsis muaj AKI (p= 0.005). Ntawm 34 tus neeg mob uas tau ntsib AKI, 25 (74%) tau zoo. Hypokalemia tau pom nyob rau hauv 9 ntawm 25 (36%) cov neeg mob nrog AKI rov qab, 2 ntawm 9 (22%) cov neeg mob uas tsis muaj AKI rov qab, thiab 27 ntawm 223 (12%) cov neeg mob uas tsis muaj AKI (p= 0.014). Qhov nruab nrab ntawm qhov pib ntawm hypokalemia hauv cov neeg mob uas muaj thiab tsis muaj AKI rov qab tau ntev dua li cov neeg mob uas tsis muaj AKI (56 [23–149] vs. 25 [10–615] vs. 18 [10–36], p.< 0.001). However, the Kaplan–Meier curve revealed no difference in the cumulative incidence of hypokalemia (Supplementary Fig. 2, log-rank test, p= 0.303). Clinical Predictors of AKI Focusing on included 258 patients, univariate Cox proportional hazard analyses identified SBP, DBP, MAP, oral corticosteroids, angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, potassium-sparing diuretics, and a daily dose of Yokukansan preparation of ≥ 7.5 g as potential independent variables for AKI. There was no multicollinearity except for the blood pressure component. A stepwise backward selection method determined three final models (Table 4), all of which remained unchanged regardless of a stepwise forward selection method. The final model demonstrated that SBP was the clinical predictor for AKI during Yokukansan preparation treatment (Model 1, HR = 1.007, 95% CI; 1.000–1.013, p= 0.036). However, DBP was an insignificant clinical predictor for AKI (Model 2, HR = 1.008, 95% CI; 0.999–1.018, p= 0.093). Conversely, MAP was a significant predictor for AKI (Model 3, HR = 1.010, 95% CI; 1.001–1.019, p= 0.035). A daily dose of ≥7.5 g/d Yokukansan preparation was significantly associated with AKI in Model 1 (HR = 1.520, 95% CI; 1.026–2.325, p= 0.036). As shown in Table 1, the limited number of patients who used Yokukansan preparation <7.5 g/d might contribute to an alpha error (false-positive). We did not perform further analysis of the interaction between blood pressure components and the daily dose of Yokukansan preparation.