Background: Cirrhotic patients with septic shock have variable responses to albumin infusion depending on the infection site. While albumin improves outcomes in spontaneous bacterial peritonitis (SBP), it offers no benefit in non-SBP infections and increases the risk of pulmonary edema, particularly in cirrhotic patients with pneumonia. We hypothesized cirrhotic patients with septic shock due to pneumonia would exhibit higher pulmonary vascular permeability index (PVPI) values. Using Pulse index Continuous Cardiac Output (PiCCO) monitoring, we examined the impact of infection site on PVPI and extravascular lung water index (EVLWI). Methods: We conducted a retrospective cohort study of 147 cirrhotic patients with septic shock. All patients underwent PiCCO monitoring. Measurements including PVPI, EVLWI, disease severity scores, and laboratory biomarkers on the first and second day of ICU admission were analyzed. Results: Pneumonia was the most common infection and was associated with significantly elevated PVPI and EVLWI values on both day 1 and day 2 compared to the non-pneumonia group. By contrast, patients with SBP had significantly lower PVPI and EVLWI values than those with non-SBP infections. Within the pneumonia subgroup, 28-day non-survivors had higher PVPI and EVLWI values than survivors. PVPI on day 2 was the strongest predictor of 28-day mortality (AUROC 0.83) among the PiCCO parameters. A PVPI on day 2 > 2.65 identified a high-risk phenotype, with a higher 28-day mortality (77.1% vs 18.9%, p < 0.001). PVPI on day 2 remained an independent predictor of 28-day mortality after adjustment for disease severity. Additionally, PaO2/FiO2 ratio on day 2 was an independent factor associated with day-2 PVPI ≤ 2.65. Conclusions: In cirrhotic patients with septic shock, non-SBP infections, mostly from pneumonia, were associated with elevated PVPI and EVLWI values. PVPI-based risk stratification may help optimize resuscitation strategies for patients at risk of pulmonary edema while reducing heterogeneity in future clinical trials.

Key PointsThe combined effect of sodium-glucose cotransporter-2 inhibitors (SGLT2is) and KA-AA-supplemented low-protein diets has rarely been studied.This cohort included 1729 type 2 diabetes mellitus patients with eGFR <= 30 ml/min per 1.73 m2 who newly received KA-AA supplemented low protein diet (sLPD), with or without SGLT2is.The combination of SGLT2is and KA-AA sLPD is linked to lower all-cause and cardiovascular disease mortality than KA-AA sLPD alone.BackgroundThe combination of a supplemented low protein diet (sLPD) with ketoacid analogs and amino acids (KA-AA)-which has been shown to be safe for patients with diabetic kidney disease in some previous studies-and the antidiabetic sodium-glucose cotransporter-2 inhibitors (SGLT2is)-known for their cardiovascular and kidney-protective effects-may represent a treatment strategy for patients with advanced diabetic kidney disease. However, this combination has rarely been investigated in previous studies.MethodsThis retrospective cohort study included a total of 1729 adult patients with type 2 diabetes mellitus with an eGFR <= 30 ml/min per 1.73 m2 and newly received sLPD treatment. We then divided the patients into two groups on the basis of whether they received a combination of KA-AA and SGLT2is (combination group) or KA-AA alone (KA-AA group). Inverse probability of treatment weighting was performed to balance baseline characteristics.ResultsAt the 3-year follow-up, compared with the KA-AA group, the combination group exhibited significantly lower risks of all-cause death (16% versus 27%; hazard ratio [HR], 0.73; 95% confidence interval [CI], 0.61 to 0.87), composite of all-cause death and ESKD (54% versus 63%; subdistribution HR, 0.84; 95% CI, 0.75 to 0.93), and cardiovascular death (7% versus 12%; subdistribution HR, 0.68; 95% CI, 0.52 to 0.89). The risk of new-onset ESKD requiring dialysis and heart failure-related hospitalization did not significantly differ.ConclusionsThese findings suggest that the addition of SGLT2is to KA-AA sLPD is associated with lower all-cause and cardiovascular mortality.

The high density of urban population and development has been posing extensive challenges for adaptation strategies of climate change. However, the impacts of urban density and its direct effect - energy usage - upon the thermal environment have remained inadequately explored, resulting in insufficient evidence-based reasoning towards the development of climate adaptation strategies in urban areas.This study connects the data of urban microclimate, neighborhood electricity usage, urban density for such exploration. It was empowered by the analytical mapping of GIS (geographical information system) data. It also applied statistical tests to confirm the connections in question.This study examines: (1) The electricity usage data at community level is applicable to reflect the practical (de facto) urban land use, especially considering the complex nature of urban development associated with climate change. (2) The detailed process of GIS layering analytical mapping and multivariate statistics to formulate a connective approach for temporal-spatial analysis.It is statistically established in this study, a human biometeorological indicator of the connections between microclimate and practical land use. In winter the effect of energy usage with the mPET (Modified Physiologically Equivalent Temperature) is negatively correlated (p

Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited cause of end-stage kidney disease (ESKD) worldwide. Guidelines for the diagnosis and management of ADPKD in Taiwan remains unavailable. In this consensus statement, we summarize updated information on clinical features of international and domestic patients with ADPKD, followed by suggestions for optimal diagnosis and care in Taiwan. Specifically, counselling for at-risk minors and reproductive issues can be important, including ethical dilemmas surrounding prenatal diagnosis and pre-implantation genetic diagnosis. Studies reveal that ADPKD typically remains asymptomatic until the fourth decade of life, with symptoms resulting from cystic expansion with visceral compression, or rupture. The diagnosis can be made based on a detailed family history, followed by imaging studies (ultrasound, computed tomography, or magnetic resonance imaging). Genetic testing is reserved for atypical cases mostly. Common tools for prognosis prediction include total kidney volume, Mayo classification and PROPKD/genetic score. Screening and management of complications such as hypertension, proteinuria, urological infections, intracranial aneurysms, are also crucial for improving outcome. We suggest that the optimal management strategies of patients with ADPKD include general medical care, dietary recommendations and ADPKD-specific treatments. Key points include rigorous blood pressure control, dietary sodium restriction and Tolvaptan use, whereas the evidence for somatostatin analogues and mammalian target of rapamycin (mTOR) inhibitors remains limited. In summary, we outline an individualized care plan emphasizing careful monitoring of disease progression and highlight the need for shared decision-making among these patients.

Backgrounds and Aims: Patients with cirrhosis are susceptible to sepsis and septic shock. Cirrhotic patients also have increased capillary permeability and are prone to developing volume overload. Patients with septic shock may have an enhanced pulmonary vascular permeability index (PVPI) and extravascular lung water index (EVLWI), both of which are associated with an unfavorable prognosis. It is plausible that pre-existing hyperpermeability may deteriorate when cirrhotic patients develop septic shock. However, it remains unknown whether PVPI and EVLWI can predict the prognosis of cirrhotic patients with septic shock. Pulse Indicator Continuous Cardiac Output (PiCCO) is an established tool to measure PVPI and EVLWI. Therefore, we conducted this retrospective study to investigate the prognostic significance of PVPI and EVLWI in cirrhotic patients with septic shock using PiCCO monitoring. Methods: We included 83 patients with liver cirrhosis and septic shock. EVLW indexed to actual body weight (aEVLWI), EVLW indexed to predicted body weight (pEVLWI), PVPI, disease severity scores, and other biomarkers were analyzed. We collected the PiCCO data on the first 2 days. Results: The overall 28-day mortality was 43.4%. The values of PVPI, aEVLWI, and pEVLWI on day 2 (PVPID2, aEVLWID2, EVLWID2) were significantly higher in non-survivors. The discriminating power of PVPID2 and EVLWID2 to predict 28-day mortality was tested using the area under a ROC curve. The areas under ROC curves (mean ± SEM) were 0.713 ± 0.061 and 0.650 ± 0.063 for PVPID2 and pEVLWID2. In the multivariate analysis, PVPID2, bilirubin, and lactate were independent factors which predicted 28-day mortality. Conclusions: Higher levels of PVPID2 and pEVLWID2 are associated with higher 28-day mortality rates in cirrhotic patients with septic shock. PVPI and pEVLWI may be useful to guide fluid management in this clinical setting.

Acute kidney injury is a common and complex complication that has high morality and the risk for chronic kidney disease among survivors. The accuracy of current AKI biomarkers can be affected by water retention and diuretics. Therefore, we aimed to identify a urinary non-recovery marker of acute kidney injury in patients with acute decompensated heart failure. We used the isobaric tag for relative and absolute quantification technology to find a relevant marker protein that could divide patients into control, acute kidney injury with recovery, and acute kidney injury without recovery groups. An enzyme-linked immunosorbent assay of the endothelial cell protein C receptor (EPCR) was used to verify the results. We found that the EPCR was a usable marker for non-recovery renal failure in our setting with the area under the receiver operating characteristics 0.776 ± 0.065; 95%CI: 0.648–0.905, (p < 0.001). Further validation is needed to explore this possibility in different situations.

Background / Aims: Effects of anti-hepatitis C virus (HCV) therapeutic regimens and mixed cryoglobulinemia on long-term renal function of HCV-infected patients with viral clearance have not been determined. Methods/Materials: A prospective 10-year cohort study of 1212 HCV-infected patients (interferon-based therapy, n = 615; direct-acting antiviral (DAA) therapy, n = 434) was conducted. Results: At baseline, age, body mass index (BMI), hemoglobin (Hb) and uric acid (UA) levels, and fibrosis-4 score were associated with estimated glomerular filtration rates (eGFRs) in HCV-infected patients. At 24 weeks posttherapy, age, BMI, and Hb and UA levels were associated with eGFRs in patients with a sustained virological response (SVR) (n = 930). Compared with those at baseline, the eGFRs were lower in SVR patients at 24 weeks posttherapy, regardless of the therapeutic regimen. The eGFRs reverted to baseline levels in interferon-treated SVR patients up to 10 years posttherapy but remained decreased in DAA-treated SVR patients up to 4 years posttherapy. Longitudinally, repeated measures analyses with generalized estimating equations showed that the interactions between DAA-based therapy and mixed cryoglobulinemia (OR: 3.291) and Hb levels (1.778) were positively, while DAA-based therapy (0.442), age (0.956), UA levels (0.698), homeostasis model assessment-insulin resistance index (0.961) and complement 4 levels (0.9395) were negatively associated with the eGFR. Among DAA-treated SVR patients, the baseline eGFR (OR: 1.014; 95%CI OR: 1.004-1.023) and high-sensitivity C-reactive protein (HR: 1.082; 95%CI HR: 1.018-1.15) were associated with eGFR reduction at 24 weeks and 4 years posttherapy, respectively. Conclusions: Hepatic fibrosis was an HCV-related factor for renal function. Longitudinally, DAA therapy was negatively, while the interaction between DAA therapy and mixed cryoglobulinemia was positively associated with renal function in SVR patients; deteriorated renal function was recovered in interferon-treated SVR patients. Particularly in DAA-treated SVR patients, baseline renal function and systemic inflammation were associated with short- and long-term reductions in renal function, respectively. (c) 2024 The Author(s). Published by Elsevier Ltd on behalf of King Saud Bin Abdulaziz University for Health Sciences. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/ 4.0/).

AIMS:PPAR-gamma shows promise in inhibiting malignancy cell progression. However, pioglitazone, the sole current PPAR-gamma agonist, was reported to have risks of bladder cancer in previous clinical researches. This study is aimed to assess the influence of pioglitazone on the development of tumors. METHODS:By using Taiwan's National Health Insurance Research Database, this nested case-control study identified incident type2 diabetes initiating metformin treatment between 2000 and 2014, and then categorized into two groups based on whether they developed malignancies after enrollment or not. The index date was defined as the date of malignancy diagnosis in the cancer group or a matched date in the non-cancer group. We analyzed the exposure to pioglitazone preceding the index date. RESULTS:47,931 patients in the cancer group and 47,931 patients in the matched non-cancer group were included. The non-cancer group exhibited a significantly higher rate of pioglitazone prescription before the index date for overall malignancies (odds ratios for pioglitazone use were 0.91, 0.92, 0.94, and 0.93 in the first, second, third, and fourth years before the index date). For breast cancer and prostate cancer, pioglitazone was frequently prescribed in the non-cancer group, whereas for pancreatic cancer, pioglitazone use was more common in the cancer group. CONCLUSIONS:PPAR-gamma agonists may be associated with reduced risks of overall malignancies, particularly for breast and prostate cancers. However, it may be linked to an elevated risk of pancreatic cancer.

BACKGROUND AND AIMS:Different from other high cardiovascular (CV) risks populations, the evidence supporting the CV protective effect of LDL-C reduction with statins in chronic kidney disease (CKD) patients is comparatively scarce. This study is aimed to investigate the role of maintaining lower LDL-C level in advanced CKD patients. METHODS:By using Chang Gung Research Database, on the basis of Taiwan's largest healthcare group, a total of 5367 adult patients newly-diagnosed with stage 4 CKD and receiving statin were extracted and further categorized into three groups based on their LDL-C levels: <70 mg/dL, 70-100 mg/dL, and ≥100 mg/dL. The main outcome is major adverse cardiac and cerebrovascular events (MACCEs), a composite of cardiovascular death, myocardial infarction, and stroke. The inverse probability of treatment weighting was performed to achieve balance of baseline characteristics. RESULTS:At 5-year follow-up, the LDL-C < 70 mg/dL group exhibited significantly lower risks of MACCEs (14.3 % vs. 18.7 %, hazard ratio [HR]: 0.77, 95 % CI: 0.69-0.86), cardiovascular death (7.1 % vs. 9.7 %, subdistribution HR [SHR]: 0.75, 95 % CI: 0.65-0.88), ischemic stroke (4.1 % vs. 5.4 %, [SHR]: 0.65, 95 % CI: 0.54-0.79), and new-onset end-stage renal disease requiring chronic dialysis (25.6 % vs. 29.4 %, SHR: 0.87, 95 % CI: 0.80-0.91) compared to LDL-C > 100 mg/dL group. In contrast, the group with LDL-C levels between 70 and 100 did not significantly differ from the group with LDL-C > 100 mg/dL in study outcomes. CONCLUSIONS:Maintaining LDL-C lower than 70 mg/dL may be beneficial for cardiovascular protection in advanced CKD patients and a lower LDL-C treatment target may be required as CKD progression.

This study explores the extended renal effects of endocrine-disrupting chemicals (EDCs) exposure, a linkage already established with adverse health outcomes, notably chronic kidney disease. To delve deeper, the Chang Gung Community Research Center conducted a longitudinal study with 887 participants. Among them, 120 individuals were scrutinized based on EDC scores, analyzing 17 urinary EDCs and renal function. Findings revealed elevated mono-(2-ethylhexyl) phthalate (MEHP) and bisphenol A levels in higher EDC exposure cases. MEHP notably correlated with increased urinary albumin-to-creatinine ratio (UACR), predicting a > 15% decline in estimated glomerular filtration rate. Higher MEHP levels also hinted at declining renal function. UACR escalation linked significantly with specific EDCs: MEHP, methylparaben, nonylphenol, and 4-tert-octylphenol. This research underscores enduring renal hazards tied to environmental EDC exposure, particularly MEHP, emphasizing the urgent call for robust preventive public health strategies.

ImportanceThe interplay among baseline kidney function, severity of acute kidney disease (AKD), and post-AKD kidney function has significant associations with patient outcomes. However, a comprehensive understanding of how these factors are collectively associated with mortality, major adverse cardiac events (MACEs), and end-stage kidney disease (ESKD) in patients with dialysis-requiring acute kidney injury (AKI-D) is yet to be fully explored.ObjectiveTo investigate the associations of baseline kidney function, AKD severity, and post-AKD kidney function with mortality, MACEs, and ESKD in patients with AKI-D.Design, Setting, and ParticipantsThis nationwide, population-based cohort study of patients with AKI-D was conducted between January 1, 2015, and December 31, 2018, using data from various health care settings included in the Taiwan nationwide population-based cohort database. Data analysis was conducted from April 28, 2022, to June 30, 2023.ExposureExposure to severe AKI and baseline and post-AKD kidney function.Main Outcomes and MeasuresThe primary outcomes were all-cause mortality and incident MACEs, and secondary outcomes were risks of permanent dialysis and readmission.ResultsA total of 6703 of 22 232 patients (mean [SD] age, 68.0 [14.7] years; 3846 [57.4%] male) with AKI-D with post-AKD kidney function follow-up and AKD stage data were enrolled. During a mean (SD) 1.2 (0.9) years of follow-up, the all-cause mortality rate was 28.3% (n = 1899), while the incidence rates of MACEs and ESKD were 11.1% (n = 746) and 16.7% (n = 1119), respectively. After adjusting for known covariates, both post-AKD kidney function and baseline kidney function, but not AKD severity, were independently associated with all-cause mortality, MACEs, ESKD, and readmission. Moreover, worse post-AKD kidney function correlated with progressive and significant increases in the risk of adverse outcomes.Conclusions and RelevanceIn this cohort study of patients with AKI-D, more than one-quarter of patients died after 1.2 years of follow-up. Baseline and post-AKD kidney functions serve as important factors associated with the long-term prognosis of patients with AKI-D. Therefore, concerted efforts to understand the transition from post-AKD to chronic kidney disease are crucial.

The phenotype of cryoglobulinemia in hepatitis B virus (HBV) carriers remains elusive. A 7-year prospective cohort of 648 hepatitis B e antigen (HBeAg)-negative Taiwanese HBV carriers [males: 344 (53

BACKGROUND:Acute kidney injury (AKI) is associated with increased in-hospital and short-term hypoglycemia risk. However, the impact of non-recovery of renal function before discharge on hypoglycemia risk in AKI survivors after discharge have not been well studied. We aim to analyze the association between non-recovery of AKI and hypoglycemia, hyperglycemia crisis risk, to identify additional risk factors for hypoglycemia, and to examine the impact of AKI non-recovery on HbA1c variability. METHODS:This multi-institutional retrospective cohort study based on Chang Gung Research Database included type 2 diabetes patients with first admission for AKI. Participants were categorized into renal recovery or non-recovery groups. Hypoglycemia, hyperglycemia crisis, new insulin use, re-AKI admission, all-cause mortality and HbA1c variability within 2 years after discharge were assessed. IPTW was used for covariate balance. RESULTS:A total of 16,796 participants were enrolled. AKI non-recovery was associated with increased higher hypoglycemia risk (HR: 1.19; 95% CI: 1.11-1.28), increased new insulin prescriptions (HR: 1.21; 95% CI: 1.14-1.27), and lower mean HbA1c levels compared to the recovery group. Subgroup analysis showed higher hypoglycemia risk in the non-recovery group with post-AKI anemia/hypoalbuminemia status (HR: 1.39; 95% CI: 1.23-1.55). De novo CKD development in AKI non-recovery group was a protective factor for hyperglycemia crisis (HR: 0.77; 95% CI: 0.69-0.87). CONCLUSION:Non-recovery AKI is associated with an increased risk of hypoglycemia, regardless of whether de novo CKD develops, and is linked to lower mean A1c level within two-years post-discharge. Identifying high-risk individuals for post-AKI hypoglycemia is vital for optimal patient care.

Introduction:Extracorporeal membrane oxygenation(ECMO) is widely used; however, studies on the long-termoutcomes of ECMO are scarce. We investigated the long-term clinical outcomes of acute kidney disease (AKD) inpatients receiving ECMO.Methods:Electronic data(2009-2018) were retrospectively collected from a multi-center database. Patients were divided into two groups (AKDand non-AKD) according to their AKD status 8-90 days afterthe initiation of ECMO. Inverse probability of treatmentweighting was used to balance baseline covariates betweenthe two groups. The primary outcomes were major adversekidney events (MAKEs) and major adverse cardiovascularevents (MACEs), and the secondary outcomes were all-causereadmission, sepsis-related readmission, infection-relatedreadmission, and dementia.Results:Totally, 395 patientswere eligible for analysis; of them, 160 patients (40.5%)developed AKD. The AKD group had a higher risk of MAKEs(hazard ratio [HR]: 2.06; 95% confidence interval [CI]:1.68-2.53) than did the non-AKD group. Subgroup analysisrevealed that the observed unfavorable effect of AKD on therisk of MAKEs was more pronounced in patients receivingvenovenous ECMO than in those receiving venoarterialECMO (HR: 5.69 vs. 1.85, respectively;pfor interaction =0.004). AKD group had a higher risk of MACE during theinitial 3-year post-ECMO in comparison to those without (HR:1.68; 95% CI: 1.22-2.30). Moreover, the risks of all-cause,sepsis-related, and infection-related readmissions were highin AKD survivors.Conclusions:AKD is associated with anincreased risk of long-term MAKEs and initial 3-year MACE inECMO recipients. In addition, AKD is associated with in-creased risks of all-cause, infection-related, and sepsis-related readmissions.(c) 2024 The Author(s).Published by S. Karger AG, Basel

Listeria monocytogenes causes listeriosis, a serious foodborne illness with a high mortality rate, especially in vulnerable populations. It accounts for 19% of foodborne deaths, with invasive cases having a mortality rate of up to 44%, leading to conditions like meningitis, bacteremia, and meningoencephalitis. However, the prognostic factors remain unclear. This study examines the hospital outcomes of invasive listeriosis and identifies risk factors for in-hospital and one-year mortality. We analyzed the electronic medical records of 118 hospitalized patients with non-perinatal, culture-proven invasive listeriosis collected over a 21-year period. The in-hospital mortality rate was 36.4%, with only 33.1% surviving one year and 22.0% surviving two years. The key findings indicate that a quick Sequential Organ Failure Assessment (qSOFA) score of ≥2 (OR 106.59, p < 0.001), respiratory failure (OR 7.58, p = 0.031), and shorter ampicillin duration (OR 0.53, p = 0.012) independently predicted poorer in-hospital outcomes. Additionally, a qSOFA score of ≥2 (OR 8.46, p < 0.001) and shorter ampicillin duration (OR 0.65, p < 0.001) were linked to higher one-year mortality. This study is the first to identify a qSOFA score of ≥2 as a significant marker for high-risk invasive listeriosis patients, with poorer outcomes linked to a qSOFA score of ≥2, respiratory failure, and shorter ampicillin use.

ABSTRACT Background Immune checkpoint inhibitors (ICIs) have been associated with acute kidney injury (AKI). However, the occurrence rate of ICI-related AKI has not been systematically examined. Additionally, exposure to proton pump inhibitors (PPIs) and non-steroidal anti-inflammatory drugs (NSAIDs) were considered as risk factors for AKI, but with inconclusive results in ICI-related AKI. Our aim was to analyse the occurrence rate of all-cause AKI and ICI-related AKI and the occurrence rates of severe AKI and dialysis-requiring AKI, and to determine whether exposure to PPIs and NSAIDs poses a risk for all-cause and ICI-related AKI. Methods This study population was adult ICI recipients. A systematic review was conducted by searching MEDLINE, Embase and PubMed through October 2023. We included prospective trials and observational studies that reported any of the following outcomes: the occurrence rate of all-cause or ICI-related AKI, the relationship between PPI or NSAID exposure and AKI development or the mortality rate in the AKI or non-AKI group. Proportional meta-analysis and pairwise meta-analysis were performed. The evidence certainty was assessed using the Grading of Recommendations Assessment, Development and Evaluation framework. Results A total of 120 studies comprising 46 417 patients were included. The occurrence rates of all-cause AKI were 7.4% (14.6% from retrospective studies and 1.2% from prospective clinical trials). The occurrence rate of ICI-related AKI was 3.2%. The use of PPIs was associated with an odds ratio (OR) of 1.77 [95% confidence interval (CI) 1.43–2.18] for all-cause AKI and an OR of 2.42 (95% CI 1.96–2.97) for ICI-related AKI. The use of NSAIDs was associated with an OR of 1.77 (95% CI 1.10–2.83) for all-cause AKI and an OR of 2.57 (95% CI 1.68–3.93) for ICI-related AKI. Conclusions Our analysis revealed that approximately 1 in 13 adult ICI recipients may experience all-cause AKI, while 1 in 33 adult ICI recipients may experience ICI-related AKI. Exposure to PPIs and NSAIDs was associated with an increased OR risk for AKI in the current meta-analysis.

Background: Listeriosis is caused by the facultative anaerobic bacterium Listeria monocytogenes. Infection from Listeriacontaminated food or water is the main etiology. If Listeria travels outside the intestines, it can cause invasive listeriosis, such as sepsis, meningitis, and meningoencephalitis. Invasive illness is especially dangerous for pregnant women and their newborns, elderly people, and people with compromised immune systems or medical conditions such as end-stage kidney disease (ESKD) patients receiving long-term dialysis. Purpose: Describe the manifestations and hospital outcomes of invasive listeriosis and identify the risk factors for in-hospital and one-year mortality in ESKD patients receiving long-term dialysis. Patients and Methods: This retrospective observational study examined hospitalized patient records at a Taiwanese tertiary medical center from August 1, 2000, to August 31, 2021. ESKD patients on chronic dialysis were identified with invasive listeriosis by blood culture and discharge diagnosis. Over 21 years, we accurately recorded 26 cases. Results: ESKD patients on chronic dialysis with invasive listeriosis have a poor prognosis. Only 53.8% of chronic dialysis patients with invasive listeriosis survived their first hospital episode. 42.3% of hospitalized ESKD patients with invasive listeriosis survived one year later. In univariate analysis, shock, tachypnea (RR > 22), respiratory failure, qSOFA score > 2, and lower initial platelet count were linked to greater in-hospital mortality rates. Conclusion: ESKD patients with invasive listeriosis have a grave prognosis. Our research reveals that an early blood sample for a bacterial culture may identify invasive listeriosis in chronic dialysis patients with fever, nausea or vomiting, confusion, and respiratory distress. This study is the first to identify a lower platelet count and qSOFA score > 2 as markers of high-risk invasive listeriosis in ESKD patients.