Haemostasis in Chronic Kidney Disease (CKD) is complex, with patients experiencing both thrombotic and haemorrhagic risks. Current therapies, such as dialysis and blood transfusions, often rely on clinical judgment, which may not fully address these haemostatic abnormalities. This systematic review and meta-analysis aimed to determine whether Thromboelastography (TEG) offers a better ability to assess coagulation abnormalities in CKD compared to standard coagulation tests like activated partial thromboplastin time (aPTT), and prothrombin time (PT). A search across five databases identified 10 studies comparing TEG parameters in CKD patients versus healthy controls. TEG detected hypercoagulability in CKD, with significant reductions in Kinetics Time (P = 0.04), increases in Alpha angles (P = 0.02), and elevated Maximum Amplitude values (P = 0.0006). However, Reaction Time (P = 0.43) and Lysis 30 (P = 0.28) showed no significant differences. Standard coagulation tests, including aPTT and PT, also showed no significant differences between groups (P = 0.30 and P = 1.00), suggesting their limitations in detecting the complex haemostatic changes in CKD. Platelet counts were lower in CKD patients (P = 0.0009) but remained within normal ranges. Elevated fibrinogen levels (P = 0.003), linked to chronic inflammation, indicated a prothrombotic profile. Despite high heterogeneity in some parameters due to variability in CKD stages and treatment types, TEG demonstrates a more detailed assessment of haemostatic changes in CKD, suggesting its potential as a predictive tool for managing coagulation abnormalities.

Background Racial disparities exist in prostate cancer incidence and mortality. Radical prostatectomy, a common treatment for prostate cancer, has been associated with increased complications in African American men compared to other racial groups. An anastomotic urinary leak is associated with prolonged hospitalization rates, increased rates of ileus, and a longer time to regain continence. This analysis aims to evaluate differences in urinary anastomotic leak (UAL) rates between racial groups and potential predictive factors for this disparity. Methodology The American College of Surgeons National Surgical Quality Improvement Program database (2019-2020) was utilized to compare rates of UAL in African American versus White patients. Preoperative variables examined included patient demographics, comorbid conditions, and surgical preparation. Other variables assessed included medical complications (such as pulmonary embolism), postoperative diagnosis, and surgical complications. Results A total of 11,010 radical prostatectomy patients were analyzed after applying selection criteria. African American men were more likely to be younger, current smokers, and on dialysis. African American men were also more likely to have had prior pelvic radiotherapy, diabetes mellitus, dyspnea, and hypertension controlled with medications. The odds of having a UAL in African American men after radical prostatectomy were 51% higher than in Whites (odds ratio = 1.51, 95% confidence interval = 1.02-2.17, p = 0.032). Prior pelvic surgery, chemotherapy within 90 days, mean operative time, and readmission rates were all associated with UAL in African American men postoperatively. Conclusions There is a significant disparity in the rate of UAL in African American versus White men and multiple factors may influence this difference.

Anemia is a frequent, yet increasingly recognized, comorbidity in diabetes mellitus (DM), with prevalence often driven by multifactorial mechanisms. Hematinic deficiencies, common in this population, may arise from associated comorbidities or medications, such as metformin, as well as other drugs commonly employed for DM-related conditions. Among contributing factors, diabetic kidney disease (DKD) plays a pivotal role, with anemia developing more frequently and being more pronounced in earlier stages, than in CKD of other causes. This enhanced susceptibility stems primarily from the combined impact of impaired renal oxygen sensing and deficient erythropoietin (EPO) production linked to tubulointerstitial fibrosis. Additional mechanisms comprise glomerular dysfunction, shortened erythrocyte lifespan, uremia-induced bone marrow suppression, and increased bleeding risk. DM is also recognized as a chronic low-grade inflammatory condition, with its inflammatory burden driving iron maldistribution, suppression of erythropoiesis, and resistance to EPO. The diagnostic approach of anemia in DM mirrors that in the general population. Addressing modifiable causes such as hematinic deficiencies, and other chronic conditions, such as DKD and bone marrow disorders, is paramount. In total, the underlying pathophysiology of anemia in DM primarily reflects a state of absolute or relative EPO deficiency and/or diminished bone marrow responsiveness, effectively corresponding to 'anemia of chronic disease. Early initiation of EPO therapy, even in DM patients without overt DKD, may mitigate disease progression and improve outcomes. Future research should focus on diabetes-specific strategies integrating optimal EPO use, potentially implementing targeted management of renal and inflammatory contributors to anemia.

 Chronic kidney disease (CKD) is a progressive, irreversible, and incurable condition characterized by high morbidity and mortality, affecting approximately one-tenth of the global population. Rise of urea-derived cyanate levels in CKD patients, severalfold higher in comparison to those found in healthy individuals, leads to an increased rate of carbamylation of lysine residues of proteins and peptides. This posttranslational modification plays an important role in the progression of kidney failure but also in the onset of CKD-related complications, including previously reported coagulopathies. In this study, we have explored the impact of carbamylation on the functionality of von Willebrand factor (vWF), a pivotal player in hemostasis, and its implications for platelet adhesion.

 We have explored carbamylated vWF's interactions with its partner proteins via ELISA. Mass spectrometry was employed to identify modified lysine residues. Blood platelets isolated from healthy donors were carbamylated, and their activation, binding to endothelium and thromboxane release were evaluated using flow cytometry, adhesion assays and ELISA, respectively.

 Using mass spectrometry we detected the vWF's lysine residue smost susceptible to carbamylation. This modification has in turn affected vWF's interactions with its key binding partners: decreased binding to collagen types I/III but increased the affinity to factor FVIII, while its binding to fibrinogen remained unchanged. Carbamylation of vWF impeded vWF-blood platelet binding, but carbamylation of platelets led to their increased thrombin-dependent activation as observed by enhanced phosphatidylserine exposure, improved their binding to vascular endothelium, at the same time decreasing the production of the prothrombotic mediator, thromboxane A2.

 Our findings highlight the multifaceted impact of carbamylation on vWF and platelets, disturbing the delicate balance of coagulation cascade. These alterations could contribute to the complex hemostatic imbalance in ESKD, underscoring the need for further research to fully understand these mechanisms and their clinical implications.

Kidney function parameters including estimated glomerular filtration rate (eGFR) and urine albumin excretion are commonly used to diagnose chronic kidney disease (CKD). However, these parameters are relatively insensitive, limiting their utility for screening and early detection of kidney disease. Studies have suggested that urinary proteomic profiles differ by eGFR stage, offering potential insights into kidney disease pathogenesis alongside opportunities to increase the sensitivity of current testing strategies. In this study, we characterized and compared the urinary proteome across different eGFR stages in a Black African cohort from rural Mpumalanga Province, South Africa. We stratified 81 urine samples by eGFR stage (mL/min/1.73 m2): Stage G1 (eGFR ≥ 90; n = 36), Stage G2 (eGFR 60-89; n = 35), and Stage G3-G5 (eGFR < 60; n = 10). Urine proteomic analysis was performed using an Evosep One liquid chromatography system coupled to a Sciex 5600 TripleTOF in data-independent acquisition mode. Nonparametric multivariate analysis and receiver operating characteristic (ROC) curves were used to assess the performance of differentially abundant proteins (DAPs). Pathway analysis was performed on DAPs. Creatinine-based eGFR was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. In this study, thirty-eight urinary proteins were differentially abundant for eGFR Stages 3-5 when compared to Stages G1 (AUC = 0.95; CI: 0.86-1) and G2 (AUC = 0.84; CI: 0.64-0.98). Notably, only six urinary proteins (Cystatin M (CST6), glutathione hydrolase 6 (GGT6), sushi domain containing 2 (SUSD2), insulin-like growth factor binding protein 6 (IGFBP6), heat shock protein 90 beta family member 1 (HSP90B1), and mannosidase alpha class 1A member 1 (MAN1A1)) were differentially abundant when comparing Stage G1 and Stage G2 with a modest AUC = 0.81 (CI: 0.67-0.92). Pathway analysis indicated that DAPs were associated with haemostasis and fibrin clot formation. In a rural cohort from South Africa, the urinary proteome differed by eGFR stage, and we identified six differentially abundant proteins which, in combination, could help to differentiate earlier eGFR stages with higher predictive accuracy than the currently available tests.

Although post-procedural bleedings are infrequent in patients with cirrhosis, they are associated with significant morbidity and mortality. Therefore, predicting and preventing such bleedings is important. Established predictors of post-procedural bleeding include high-bleeding risk procedure, severe cirrhosis and high body mass index; prognostic value of anemia, acute kidney injury and bacterial infection is more uncertain. While prothrombin time and international normalized ratio do not predict post-procedural bleeding, some evidence suggests that platelet count, whole blood thrombin generation assay and viscoelastic tests may be helpful in this context. Prevention of postprocedural bleeding involves careful management of antithrombotic drugs during the periprocedural period. Patients with cirrhosis present unique challenges due to altered pharmacokinetics and pharmacodynamics of antithrombotic drugs, but there is a lack of dedicated studies specifically focused on this patient population. Guidelines for periprocedural management of antithrombotic drugs developed for patients without liver disease are thus applied to those with cirrhosis. Some technical aspects may decrease the risk of post-procedural bleeding, namely ultrasoundguidance, opting for transjugular route rather than percutaneous route, and the level of expertise of the operator. The effectiveness of platelet transfusions or thrombopoietin-receptor agonists remains uncertain. Transfusion of fresh-frozen plasma, of fibrinogen, and administration of tranexamic acid are not recommended for reducing post-procedural bleeding in patients with cirrhosis. In conclusion, prediction of post-procedural requires a global approach taking into account the patients characteristics, the risk of the procedure, and the platelet count. There is little data to support prophylactic correction of hemostasis, and dedicated studies are needed.

Bleeding and thrombotic occlusion are complications of Central venous catheters. When selecting a catheter lock solution, factors such as bleeding, thrombotic occlusion, infection, and cost-effectiveness must be considered.

The study included 35 patients who used heparin as a locking solution and 35 patients who used 0.9% saline, retrospectively. In our center, after injecting the solution equal to the catheter lumen volume from the syringe, approximately 1 cc of locking solution is left in the syringe, the catheter is locked and the syringe is removed from the catheter after locking. Intergroup complications were observed.

No significant difference was observed between the groups concerning the catheter insertion site (p = 0.143 and 0.143). Additionally, no significant differences were found between the groups in terms of thrombosis and bleeding complications (p = 0.314 and 0.239, respectively).

Our study concluded that heparin locking is not superior to normal saline locking in terms of catheter dysfunction. We aimed to emphasize that the technique of catheter locking is more important than the type of lock solution used.

The Kernohan-Woltman phenomenon, a rare and often misunderstood neurological condition, is recognized as a false localizing neurological sign. This phenomenon is characterized by a motor deficit ipsilateral to the site of the neurological lesion and occurs due to the mass effect of supratentorial lesions causing a shift of midline structures and subsequent transtentorial herniation, leading to compression of the contralateral corticospinal (pyramidal) fibers within the cerebellum, ipsilateral to the lesion. This case describes a patient with human immunodeficiency virus-1 and chronic kidney disease who presented to the emergency department with uremic syndrome and a hypertensive crisis. She experienced sudden neurological deterioration, manifesting as prostration, anisocoria, and left hemiparesis, in the context of an acute subdural hematoma of the left cerebral hemisphere, which is a rare complication of hypertensive crisis. The fact that the hemiparesis was on the same side as the hematoma indicates a rare neurological sign, known as the Kernohan-Woltman phenomenon. This case is particularly noteworthy due to the rare coexistence of these conditions and the atypical presentation of neurological symptoms in the context of supratentorial lesions. The case emphasizes the importance of recognizing this phenomenon in patients with mass-effect lesions, especially in the setting of critical illness, as early identification can influence clinical decision-making and management strategies. Given the rarity of this phenomenon, this report contributes to the literature by providing insight into its clinical presentation and diagnostic challenges, highlighting its relevance in neurocritical care.

A reduction in platelet count in critically ill patients is a marker of severity of the clinical condition. However, whether this association holds true in acute kidney injury (AKI) is unknown. We analyzed the association between platelet reduction in patients with AKI and major adverse kidney events (MAKE).

In this retrospective cohort, we included AKI patients at the Hospital Civil of Guadalajara, in Jalisco, Mexico. Patients were divided according to whether their platelet count fell >21% during the first 10 days. Our objectives were to analyze the associations between a platelet reduction >21% and MAKE at 10 days (MAKE10) or at 30-90 days (MAKE30-90) and death.

From 2017 to 2023, 400 AKI patients were included, 134 of whom had a > 21% reduction in platelet count. The mean age was 54 years, 60% were male, and 44% had sepsis. The mean baseline platelet count was 194 x 103 cells/µL, and 65% of the KDIGO3 patients met these criteria. Those who underwent hemodialysis (HD) had lower platelet counts. After multiple adjustments, a platelet reduction >21% was associated with MAKE10 (OR 4.2, CI 2.1-8.5) but not with MAKE30-90. The mortality risk increased 3-fold (OR 2.9, CI 1.1-7.7, p = 0.02) with a greater decrease in the platelets (<90 x 103 cells/µL). As the platelets decreased, the incidence of MAKE was more likely to increase. These associations lost significance when accounting for starting HD.

In our retrospective cohort of patients with AKI, a > 21% reduction in platelet count was associated with MAKE. Our results are useful for generating hypotheses and motivating us to continue studying this association with a more robust design.

As per current guidelines, acute coronary syndrome (ACS) patients who undergo percutaneous coronary intervention (PCI) should be started on dual antiplatelet therapy (DAPT) for a period of 12 months.

To assess the efficacy and safety of brief DAPT (up to 3 months) succeeded by ticagrelor monotherapy compared with a 12-month DAPT in ACS patients following PCI.

We systematically searched Cochrane, Embase, and PubMed to find relevant randomized clinical trials. Examined outcomes included the incidence of major adverse cerebrovascular and cardiovascular events (MACCE), bleeding events, and the composite incidence of net adverse clinical events (NACE).

Our primary analysis included 21,927 ACS patients from six RCTs. Our pooled results indicate that following PCI in individuals with ACS, brief DAPT followed by ticagrelor did not increase the risk of MACCE (OR 0.92, 95% CI 0.79-1.07) but significantly reduced the risk of minor or major bleeding (OR 0.52, 95% CI 0.44-0.62) and NACE (OR 0.71, 95% CI 0.59-0.86) compared with a long-term DAPT within a follow-up of 12 months.

Brief DAPT followed by ticagrelor monotherapy is superior to a 12-month DAPT in offering a net clinical advantage in ACS patients following PCI.

Individuals with chronic kidney disease (CKD) are at increased risk of thrombotic events and bleeding. Acetylsalicylic acid (ASA), an effective antiplatelet agent, is one of the most frequently used medications for both primary and secondary prevention of cardiovascular disease (CVD). However, it can also contribute to bleeding events due to its inherent antiplatelet effect. The objective of this study was to determine the characteristics of CKD patients at increased risk of bleeding under ASA therapy.

This retrospective analysis included patients with non-dialysis-dependent CKD who were treated with ASA for primary prevention of CVD for at least 3 consecutive months and did not receive anti-coagulants or anti-platelets. Data were collected from electronic medical records from January 2014 to December 2018. CKD diagnosis was based on an estimated glomerular filtration rate of <60 mL/min/1.73 m2. CKD patients who experienced major bleeding events during ASA therapy (bleeding group) versus all others (control group) were compared. Additional outcomes included first documented nonfatal cardiovascular event and all-cause mortality.

Of the 900 adult CKD patients included in this analysis, 82 (9.1%) had a major bleeding event during 31.6 ± 25.9 months of follow-up. The most common bleeding site was gastrointestinal (52 cases, 63.4% of major bleeding events). Patients who had a major bleeding event were older (76.5 ± 10 vs. 74 ± 10.3 years, p = 0.038). On multivariate analysis, age was the most important predictor of major bleeding event (odds ratio: 1.029, 95% confidence interval: 1.004-1.056).

Given its controversial efficacy in primary prevention of CVD in CKD patients, characterizing those at increased risk of bleeding under ASA therapy is important in the era of tailored medicine. Age, CKD stage, and cardiovascular risk are key factors to consider regarding the safety and effectiveness of ASA for CKD patients.

Chronic kidney disease (CKD) and kidney failure with replacement therapy (KFRT) are prevalent in patients with atrial fibrillation (AF).

The purpose of this study was to analyze procedural and long-term outcomes in AF patients with underlying CKD and KFRT after left atrial appendage occlusion (LAAO) device implantation.

Data were extracted from the National Cardiovascular Data Registry LAAO Registry from January 2017 to December 2019 and linked to Centers for Medicare & Medicaid Services billing claims. Patients were stratified into 3 groups: no CKD, CKD, and KFRT. Multivariate analyses were used to assess the associations of CKD and KFRT with procedural and long-term outcomes, respectively.

A total of 59,190 patients were enrolled in our study. CKD and KFRT were found to be independently associated with any complication from the procedure (odds ratio [OR] 1.149, 95% confidence interval [CI] 1.058-1.;247 and OR 2.163, 95% CI 1.763-2.652) and in-hospital death (OR 1.603, 95% CI 1.054-2.437; and OR 5.488, 95% CI 2.686-11.213). At 1 year, CKD and KFRT were associated with a higher risk of any major adverse event (hazard ratio [HR] 1.402, 95% CI 1.333-1.474; and HR 2.506, 95% CI 2.236-2.809) and death (HR 1.662, 95% CI 1.553-1.779; and HR 3.422, 95% CI 2.989-3.919), but no difference in the competing risk of stroke (HR 0.972, 95% CI 0.819-1.152; and HR 0.794, 95% CI 0.434-1.451).

CKD and KFRT were associated with higher rates of procedural complications and 1-year adverse events and death, but no difference in the 1-year rate of stroke.

Dissecting trends and contributing risk factors for intracranial hemorrhage (ICH) in patients treated for acute pulmonary embolism (PE) may allow for a better patient selection for existing and emerging treatment options.

The German nationwide inpatient sample was screened for patients admitted due to PE 2005-2020. Hospitalizations were stratified for the occurrence of ICH; risk factors for ICH and temporal trends were investigated.

Overall, 816,653 hospitalizations due to acute PE in the period 2005-2020 were analyzed in the study. ICH was reported in 2516 (0.3 %) hospitalizations, and time trend analysis revealed a fluctuating but overall, largely unchanged annual incidence. There was an increase of ICH with age. Patients with ICH had a higher comorbidity burden (Charlson-Comorbidity-Index [CCI], 5.0 [4.0-7.0] vs. 4.0 [2.0-5.0]; P < 0.001), and higher CCI was associated with an OR of 1.26 (95%CI 1.24-1.27) for ICH. Further independent risk factors for ICH were age ≥ 70 years (OR 1.23 [1.12-1.34]), severe (versus low-risk) PE (OR 3.09 [2.84-3.35]), surgery (OR 1.59 [1.47-1.72]), acute kidney injury (OR 3.60 [3.09-4.18]), and ischemic stroke (OR 14.64 [12.61-17.00]). The identified risk factors for ICH varied among different reperfusion treatment groups. As expected, ICH had a substantial impact on case-fatality of PE (OR 6.16 [5.64-6.72]; P < 0.001).

Incidence of ICH in patients hospitalized for acute PE in Germany was overall low and depended on the patients' comorbidity burden. Identifying patients at risk for ICH allows tailored patient selection for the different reperfusion treatments and might prevent ICH.

Heyde syndrome, marked by aortic stenosis, gastrointestinal bleeding from angiodysplasia, and acquired von Willebrand syndrome, is often underreported. Shear stress from a narrowed aortic valve degrades von Willebrand factor multimers, leading to angiodysplasia formation and von Willebrand factor deficiency. This case report aims to raise clinician awareness of Heyde syndrome, its complexity, and the need for a multidisciplinary approach. We present a 75-year-old man with aortic stenosis, gastrointestinal bleeding from angiodysplasia, and acquired von Willebrand syndrome type 2A. The patient was successfully treated with argon plasma coagulation and blood transfusions. He declined further treatment for aortic stenosis but was in good overall health with improved laboratory results during follow-up. Additionally, we provide a comprehensive review of the molecular mechanisms involved in the development of this syndrome, discuss current diagnostic and treatment approaches, and offer future perspectives for further research on this topic.

Minimally invasive bariatric surgeries provide effective weight loss with fewer complications. However, postoperative bleeding remains a significant concern due to its potential for serious morbidity and mortality. This study aimed to identify factors predicting postoperative bleeding following laparoscopic and robotic sleeve gastrectomy (SG) and Roux-en-Y gastric bypass (RYGB).

We analyzed patients who underwent SG and RYGB using the MBSAQIP database from 2015 to 2021. Four multivariate logistic regression analyses were conducted to investigate the relationship between postoperative bleeding and 24 independent factors for laparoscopic SG (lapSG), robotic SG (rSG), laparoscopic RYGB (lapRYGB), and robotic RYGB (rRYGB).

We analyzed 659,294 lapSG, 53,548 rSG, 267,171 lapRYGB, and 22,492 rRYGB patients. In lapSG, the most significant factors included anticoagulation (OR 3.76; 95% CI 3.13-4.51), renal insufficiency (OR 2.06; 95% CI 1.37-3.09), history of DVT (OR 1.87; 95% CI 1.23-2.85), history of PE (OR 1.69; 95% CI 1.04-2.76, and BMI ≤ 40 (OR 1.22; 95% CI 1.09-1.38). In the rSG group, anticoagulation (OR 4.95; 95% CI 2.83-8.66), COPD (OR 2.80; 95% CI 1.29-6.05), and hyperlipidemia (OR 1.90; 95% CI 1.29-6.05) were significant factors. In lapRYGB, the most significant factors included anticoagulation (OR 3.68; 95% CI 3.11-4.35), renal insufficiency (OR 1.60; 95% CI 1.04-2.44), history of DVT (OR 1.70; 95% CI 1.09-2.07), cardiac stent (OR 1.51; 95% CI 1.09-2.07), and BMI ≤ 40 (OR 1.16; 95% CI 1.03-1.29). For rRYGB, anticoagulation (OR 4.69; 95% CI 2.86-7.70), history of PE (OR 4.28; 95% CI 1.53-12.00), and cardiac stent (OR 2.15; 95% CI 0.06-4.34) were significant.

Preoperative anticoagulation, renal insufficiency, history of DVT and PE, a cardiac stent, and BMI ≤ 40 are associated with an increased risk of postoperative bleeding. The predictive factors were consistent across laparoscopic and robotic approaches in SG and RYGB procedures.

Individuals with kidney failure have a compromised haemostatic system making them susceptible to both thrombosis and bleeding.

Assessment of primary haemostasis in patients treated with either haemodialysis (HD) or haemodiafiltration (HDF) was performed through the measurement of several coagulation-based tests, both pre- and post-dialysis.

41 renal failure patients and 40 controls were recruited. Platelet aggregometry, Factor XIII (FXIII), Fibrinogen, Von Willebrand Factor (VWF) and Soluble P-Selectin (sP-Sel) levels were measured.

Maximum platelet aggregation was diminished in renal patients irrespective of aspirin intake. Post-dialysis, platelet function was exacerbated. Pre-dialysis FXIII levels were similar to the healthy cohort and became elevated post-dialysis. This elevation could not be explained by the relative decrease of water by dialysis. Fibrinogen levels were already elevated pre-dialysis and further increased post-dialysis. This elevation was associated with the relative decrease of water by dialysis. VWF levels in males were similar to the healthy cohort and became elevated post-dialysis. This elevation was associated with dialysis-related water loss. VWF antigen and activity in female patients were already elevated pre-dialysis and further increased post-dialysis with the exception of VWF activity in HDF treated female patients. sP-Sel levels were lower than those of the healthy cohort and became similar to the healthy cohort post-dialysis. This elevation could not be explained by the relative decrease of water by dialysis.

Whilst platelet aggregometry was diminished, we noted elevated clotting factors such as fibrinogen, FXIII and VWF with no significant differences between HD and HDF-treated patients.

The nuanced landscape of anticoagulation therapy in patients with chronic kidney disease (CKD) presents a formidable challenge, intricately balancing the dual hazards of hemorrhage and thrombosis. These patients find themselves in a precarious position, teetering on the edge of these risks due to compromised platelet functionality and systemic disturbances within their coagulation frameworks. The management of such patients necessitates a meticulous approach to dosing adjustments and vigilant monitoring to navigate the perilous waters of anticoagulant therapy. This is especially critical considering the altered pharmacokinetics in CKD, where the clearance of drugs is significantly impeded, heightening the risk of accumulation and adverse effects. In the evolving narrative of anticoagulation therapy, the introduction of direct oral anticoagulants (DOACs) has heralded a new era, offering a glimmer of hope for those navigating the complexities of CKD. These agents, with their promise of easier management and a reduced need for monitoring, have begun to reshape the contours of care, particularly for patients not yet on dialysis. However, this is not without its caveats. The application of DOACs in the context of advanced CKD remains a largely uncharted territory, necessitating a cautious exploration to unearth their true potential and limitations. Moreover, the advent of innovative strategies such as left atrial appendage occlusion (LAAO) underscores the dynamic nature of anticoagulation therapy, potentially offering a tailored solution for those at the intersection of CKD and elevated stroke risk. Yet the journey toward integrating such advancements into standard practice is laden with unanswered questions, demanding rigorous investigation to illuminate their efficacy and safety across the spectrum of kidney disease. In summary, the management of anticoagulation in CKD is a delicate dance, requiring a harmonious blend of precision, caution, and innovation. As we venture further into this complex domain, we must build upon our current understanding, embracing both emerging therapies and the need for ongoing research. Only then can we hope to offer our patients a path that navigates the narrow strait between bleeding and clotting, toward safer and more effective care.

Internationally, peritoneal dialysis (PD) is increasingly being commenced within 2 weeks of catheter insertion. Studies are warranted to evaluate outcomes of this strategy.

This study examines outcomes of early-start PD (ESPD) and conventional-start PD (CSPD), commencing at ≤14 days and >14 days after catheter insertion, respectively. All adults with kidney failure within a large metropolitan PD unit initiating PD through a new catheter, inserted using laparoscopic or modified Seldinger technique, between August 2019 and August 2022, were included in this retrospective observational study. Demographic data and episodes of infectious and mechanical complications were collected using electronic medical records. Analysis was conducted using analysis of variance and Chi-square testing. A P-value < 0.05 was significant with Bonferroni correction performed where relevant. Kaplan-Meier and competing risks analyses were performed for time to PD-related peritonitis and transfer to hemodialysis.

A total of 297 patients (70% male, mean age 58.7 years) were included, with 130 (43.8%) patients undertaking ESPD. Most patients had laparoscopically inserted catheters (65.3%) and 65 patients (22.0%) received prior hemodialysis. When compared to CSPD, ESPD was associated with a higher number of pericatheter leaks (6.9% vs. 0.6%, P = 0.003), with otherwise similar complication episodes and no significant difference with respect to time to PD-related peritonitis or transfer to hemodialysis. Catheter insertion technique or prior hemodialysis treatment did not significantly influence outcomes.

ESPD is associated with increased pericatheter leaks when compared to CSPD, with an otherwise similar complication profile.

Chronic kidney disease (CKD) has an estimated prevalence of 6% in Nepal, which has resulted in a huge public health and socioeconomic burden for the country. People with different stages of CKD come to the Emergency Department (ED) with various clinical features and complications, which if detected and managed early can result in a decreased need for renal replacement therapy and thus decreased medical cost.

The authors conducted a cross-sectional analysis taking nonprobability convenience sampling in the ED of a tertiary-level hospital of Nepal, after getting approval from the Institutional Review Committee and obtaining informed consent from the patient. Kruskal-Wallis test and χ 2 test of homogeneity were conducted to determine if there were differences in the continuous variables and categorical variables of three stages of CKD. Pairwise comparisons with a Bonferroni correction was done for both variables.

Among 291 patients of CKD, 25 were in stage 3, 15 in stage 4, and 251 in stage 5. Significant differences between groups were found in continuous variables of SBP, pulse, temp, TLC, platelet, sodium, potassium, urea, and creatinine. Similarly, a significant difference was found for the categorical variables of hyperkalemia, hyponatremia, thrombocytopenia, leukocytosis, and high creatinine levels.

Patients with CKD commonly present to the ED due to electrolyte imbalances, uremia, shortness of breath, and high SBP. Hyperkalemia, thrombocytopenia are more frequently observed in stage 5 CKD, whereas the incidence of hypertension significantly increase from stage 4 onwards. Hyponatremia, on the other hand, is more prevalent in stage 3 than in the later stages.

Traumatic brain injury (TBI) is the leading cause of death among trauma patients. Identifying preoperative factors that predict postoperative outcomes in such patients can guide surgical decision-making. The aim of this study was to develop a predictive model using preoperative variables that predicts 30-day mortality and morbidity in patients undergoing neurosurgery following TBI. The American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP) database was queried between 2005 and 2017 for patients aged 18 years or older who underwent TBI-specific surgery. The primary outcome was 30-day mortality, and the secondary outcome was a composite morbidity score. Significant variables on univariate analysis with Chi-squared test were used to compute multivariable logistic regression models for both outcomes, and Hosmer-Lemeshow test was used. A total of 1634 patients met the inclusion criteria. Most patients were elderly aged >60 years (74.48%), male (63.59%), of White race (73.62%), and non-Hispanic ethnicity (82.44%). The overall 30-day mortality rate was 20.3%. Using multivariate logistic regression, 11 preoperative variables were significantly associated with 30-day mortality, including (aOR, 95% CI) age 70-79 years (3.38, 2.03-5.62) and age >80 years (7.70, 4.74-12.51), ventilator dependency (6.04, 4.21-8.67), receiving dialysis (4.97, 2.43-10.18), disseminated cancer (4.42, 1.50-13.0), and coma >24 hours (3.30, 1.40-7.80), among others. Similarly, 12 preoperative variables were found to be significantly associated with 30-day morbidity, including acute renal failure (7.10, 1.91-26.32), return to OR (3.82, 2.77-5.27), sepsis (3.27, 1.11-9.66), prior operation within 30 days (2.55, 1.06-4.95), and insulin-dependent diabetes (1.60, 1.06-2.40), among others. After constructing receiver operating characteristic curve, the model for mortality had an area under the curve (AUC) of 0.843, whereas composite morbidity had an AUC of 0.716. This model can aid in clinical decision-making for triaging patients based on prognosis in cases of mass casualty events.

Background/Objectives: Chronic kidney disease (CKD) is identified as a risk factor for the occurrence of ischemic stroke. There is substantial evidence that CKD is linked to a worse prognosis and higher mortality rates in stroke patients. This study aimed to evaluate the characteristics and factors affecting favorable outcomes and mortality in patients treated using mechanical thrombectomy (MT) for ischemic stroke, with particular emphasis on patients suffering from CKD. Methods: The retrospective study included an analysis of data from 723 patients (139; 19.4% had CKD) with ischemic stroke treated with MT between March 2019 and July 2022. Results: Patients with CKD were significantly older (median age 76.5 vs. 65.65, p < 0.001) and more often female (59.7% vs. 42.6%, p < 0.001). CKD decreased the likelihood of achieving a favorable outcome (0-2 points in modified Rankin scale; OR: 0.56, CI95%: 0.38-0.81) and increased mortality (OR: 2.59, CI95%: 1.74-3.84) on the 90th day after stroke. In addition, CKD was associated with intracranial hemorrhage (ICH) in patients who underwent posterior circulation MT (13.85% vs. 50%, p = 0.022). In patients with CKD, inter alia, higher levels of C-reactive protein (OR: 0.94, CI95%: 0.92-0.99) reduced the chance of a favorable outcome. In addition, the occurrence of ICH in patients with CKD increased mortality on the 90th day after stroke (OR: 4.18, CI95%: 1.56-11.21), which was almost twice as high as in patients without CKD (OR: 2.29, CI95%: 1.54-3.40). Conclusions: Patients suffering from CKD had a lower probability of achieving a favorable outcome and had increased mortality following MT for ischemic stroke. It is crucial to understand the variations between patients with unimpaired and impaired renal function, as this could aid in predicting the outcomes of this method.

We sought to compare outcomes of patients receiving dialysis after cardiothoracic surgery on the basis of dialysis modality (intermittent hemodialysis [HD] vs peritoneal dialysis [PD]).

This was a retrospective analysis.

In total, 590 patients with kidney failure receiving intermittent HD or PD undergoing coronary artery bypass graft and/or valvular cardiac surgery at Cleveland Clinic were included.

The patients received PD versus HD (intermittent or continuous).

Our primary outcomes were in-hospital and 30-day mortality. Secondary outcomes were length of stay, days in the intensive care unit, the number of intraoperative blood transfusions, postsurgical pericardial effusion, and sternal wound infection, and a composite of the following 4 in-hospital events: death, cardiac arrest, effusion, and sternal wound infection.

We used χ2, Fisher exact, Wilcoxon rank sum, and t tests, Kaplan-Meier survival, and plots for analysis.

Among the 590 patients undergoing cardiac surgery, 62 (11%) were receiving PD, and 528 (89%) were receiving intermittent HD. Notably, 30-day Kaplan-Meier survival was 95.7% (95% CI: 93.9-97.5) for HD and 98.2% (95% CI: 94.7-100) for PD (P = 0.30). In total, 75 patients receiving HD (14.2%) and 1 patient receiving PD (1.6%) had a composite of 4 in-hospital events (death, cardiac arrest, effusion, and sternal wound infection) (P = 0.005). Out of 62 patients receiving PD, 16 (26%) were converted to HD.

Retrospective analyses are prone to residual confounding. We lacked details about nutritional data. Intensive care unit length of stay was used as a surrogate for volume status control. Patients have been followed in a single health care system. The HD cohort outnumbered the PD cohort significantly.

When compared with PD, HD does not appear to improve outcomes of patients with kidney failure undergoing cardiothoracic surgery. Patients receiving PD had a lower incidence of a composite outcome of 4 in-hospital events (death, cardiac arrest, pericardial effusion, and sternal wound infections).

Sevelamer is a phosphate-binding resin implicated in gastrointestinal (GI) injury. This study aimed to investigate the role of sevelamer in GI injury among chronic kidney disease (CKD) patients.

The study included 17 CKD patients (cases) with and 18 CKD patients (comparisons) without sevelamer crystals in specimens. All cases were on sevelamer. Six comparison patients were also taking sevelamer, but crystals were absent in tissue sections. The comparison group was thus subclassified into patients who were and were not taking sevelamer. The frequency of underlying disorders was similar between two groups, including hypertension (cases = 82%; comparisons = 78%) and diabetes mellitus (cases = 53%, comparisons = 50%). The most common presentation was GI bleeding (cases = 41%, comparisons = 33%). Predominant histological patterns were also similar, with ulcers (cases = 42%; comparisons = 39%) and acute ischaemia (cases = 35%; comparisons = 28%) being predominant in both cohorts. Of note, sevelamer was present with amyloidosis and cytomegalovirus in one study case each. Two study patients who continued sevelamer had follow-up biopsies; one showed persistent ulceration and the other appeared normal. Crystals were absent in both.

GI injury in CKD patients in both groups had similar features regardless of presence of sevelamer, suggesting that it adheres to tissue rather than causes injury. The study highlights other histologically identifiable causes of intestinal injury, as well as injuries unassociated with sevelamer in patients undergoing therapy. Therefore, physicians should be cautious in attributing GI injuries to sevelamer to avoid overlooking other causes and unnecessary treatment discontinuation.

Bleeding risk evaluation of thrombocytopenic patients admitted in ICU has been poorly investigated.

A prospective observational study conducted in an 18-bed medical ICU. Consecutive patients with thrombocytopenia (<150 Giga/L) and no bleeding at admission were included.

Over one year, 91 patients were included, mainly men (63%), with an age of 61 [46-68] years and a SOFA score of 6 [3-8]. Twenty-three patients (25%) had an hemorrhagic event during ICU stay, mainly digestive (n = 9; 39%) and urological (n = 6; 26%). The time between ICU admission and bleeding was 8 [2-19] days. Almost half of bleeding events required vasopressor infusion and a hemostatic procedure. At admission, two variables were significantly different between the Bleeding and No-Bleeding groups: plasma urea level was significantly higher in the Bleeding group (9 [5.1; 13] vs. 13 [8.9; 31] mmol/L; p < 0.001) and the presence of skin purpura was associated with a 3-fold higher risk for bleeding during ICU stay (HR: 3.4 [1.3-8.3]; p < 0.05). In contrast, admission platelet count was not significantly different between the 2 groups (90 [32; 128] vs 62 [36; 103] G/L; p = 0.26).

Plasma urea levels and the presence of skin purpura are helpful in identifying thrombocytopenic patients at high-risk of bleeding during ICU stay.

Little is known about the risk factors of bleeding after colonoscopic polypectomy in patients with end-stage renal disease (ESRD). This study investigated the incidence and risk factors of post-polypectomy bleeding (PPB), including immediate and delayed bleeding, in patients with ESRD.

Ninety-two patients with ESRD who underwent colonoscopic polypectomy between September 2005 and June 2020 at a single tertiary referral center were included. The patients' medical records were retrospectively reviewed. Patient- and polyp-related factors associated with immediate PPB (IPPB) were analyzed using logistic regression analysis. Additionally, the optimal cutoff polyp size related to a significant increase in the risk of IPPB was determined by performing receiver operating characteristic (ROC) analysis and calculating the area under the ROC curve (AUC).

In total, 286 polyps were removed. IPPB occurred in 24 (26.1%) patients and 46 (16.1%) polyps and delayed PPB occurred in 2 (2.2%) patients. According to multivariate analysis, the polyp size (> 7 mm), old age (> 70), and endoscopic mucosal resection (EMR) as the polypectomy method (EMR versus non-EMR) were found to be independent risk factors for IPPB. According to the Youden index method, the optimal cutoff polyp size to identify high-risk polyps for IPPB was 7 mm (AUC = 0.755; sensitivity, 76.1%; specificity, 69.6%).

Colonoscopic polypectomy should be performed with caution in patients with ESRD, especially in those with the following risk factors: advanced age (> 70 years), polyp size > 7 mm, and EMR as the polypectomy method.

To evaluate aspirin's cardiovascular (CV) protective effect in chronic kidney disease (CKD) patients.

We searched PubMed, Embase, Cochrane Library, and Web of Science (up to December 2022) for randomized controlled trials (RCTs) and observational studies comparing aspirin with placebo in CKD patients for the prevention of CV disease (CVD). Efficacy outcomes included CVD, heart failure, myocardial infarction, stroke, CV and all-cause mortality; safety outcomes included major bleeding, minor bleeding, and renal events.

Six RCTs and 6 observational studies, including 35,640 participants, met the inclusion criteria and reported relevant CV outcomes, with a mean follow-up of 46.83 months. The pooled data showed aspirin had no significant preventive effect on CVD events (RR=1.03; 95% CI, 0.84-1.27). However, CV mortality was significantly reduced in the aspirin group (RR=0.74; 95% CI, 0.58-0.95). Furthermore, aspirin use did not increase the risk of major bleeding and renal events but significantly increased minor bleeding events (RR=2.11; 95% CI, 1.30-3.44). Renal events were significantly increased after sensitivity analysis (RR=1.10; 95% CI, 1.04-1.16).

Aspirin did not prevent CV events, with a significantly increased risk of minor bleeding and renal events. Besides, aspirin use had no statistically significant reduction in the risk of all-cause mortality but had a statistically significant reduction in the risk of CV mortality.

Fondaparinux is a synthetic anticoagulant that inhibits thrombosis by suppressing factor Xa. The efficacy of fondaparinux for orthopedic surgeries has been revealed by several foreign studies; however, relevant evidence in Chinese patients is lacking. This study intended to investigate the occurrence rate and risk factors of in-hospital venous thromboembolism (VTE), major bleeding, and death in patients receiving fondaparinux after orthopedic surgery or trauma surgery.

Totally, 1258 patients who received fondaparinux after orthopedic surgery or trauma surgery were retrospectively enrolled. Meanwhile, in-hospital VTE, major bleeding, and death were obtained for assessment. Besides, adverse events were recorded.

The occurrence rates of in-hospital VTE, major bleeding, and death were 2.5%, 21.8%, and 0.0%, respectively. The multivariate logistic regression analysis revealed that only age (> 60 years vs. ≤ 60 years) (odd ratios (OR) = 3.380, P = 0.013) was independently correlated with increased risk of in-hospital VTE. Additionally, osteoarthritis diagnosis (OR = 3.826, P < 0.001), femoral head necrosis diagnosis (OR = 1.809, P = 0.034), hip replacement (vs. internal fracture fixation) (OR = 2.199, P = 0.007), knee replacement (vs. internal fracture fixation) (OR = 2.781, P = 0.002), and serum creatinine (abnormal vs. normal) (OR = 1.677, P = 0.012) were independently linked to a higher risk of in-hospital major bleeding. Moreover, the common adverse events included pain (56.6%), wound bleeding (23.0%), increased drainage (5.2%), etc. CONCLUSION: Fondaparinux realizes low occurrence rates of in-hospital VTE and major bleeding with tolerable adverse events in patients receiving orthopedic surgery or trauma surgery.

End stage renal disease (ESRD) is associated with platelet dysfunction but also thromboembolic complications. The specific role of increased blood urea nitrogen (BUN) on coagulation is unclear. We aimed to characterize thromboelastography (TEG) parameters from males and females with ESRD and normal kidney function and evaluate if exogenous urea in vitro reproduced those TEG differences.

We collected blood samples from 20 living kidney donors and 20 kidney recipients. TEG was performed without and with two increasing urea concentrations in vitro. TEG parameters were compared between recipients and donors.

Blood from kidney recipients showed baseline increased maximum amplitude (MA) and shortened time to maximum amplitude (TMA) compared to donors. These differences were not confirmed in females. In all patients, BUN was inversely correlated with TMA (r = -0.342; p = 0.031). In males, BUN and creatinine concentrations showed a direct correlation with MA (0.583; p = 0.007) and an inverse correlation with TMA (r = -0.520; p = 0.019). Urea in vitro decreased R-time (p = 0.005) and increased LY30 (p = 0.009) in donors but not recipients.

ESRD is associated with increased MA and decreased TMA on TEG. No change in MA was observed with increasing urea concentrations in vitro. Gender-specific variability in TEG parameters were observed.

Chronic subdural hematoma (cSDH) is one of the most common types of intracranial hemorrhages, particularly in the elderly. Despite extensive research regarding cSDH diagnosis and treatment, there is conflicting data on predictors of postoperative mortality (POM). We conducted a large retrospective review of patients who underwent a cSDH evacuation at a single urban institution between 2015 and 2022. Data were collected from the electronic medical record on prior comorbidities, anticoagulation use, mental status on presentation, preoperative labs, and preoperative/postoperative imaging parameters. Univariate and multivariate analyses were conducted to analyze predictors of mortality. Mortality during admission for this cohort was 6.1%. Univariate analysis showed the mortality rate was higher in those presenting with a history of dialysis. In addition, those who presented with altered mental status, were intubated, and lower GCS scores had higher rates of POM. Usage of Coumadin was correlated with higher rates of POM. Examination of preoperative labs showed that patients who presented with anemia or thrombocytopenia had higher POM. Imaging data showed that cSDH volume and greatest dimension were correlated with higher rates of POM. Finally, patients that were not extubated postoperatively had higher rates of POM. Multivariate analysis showed that only altered mental status and being not being extubated postoperatively were correlated with a higher risk of mortality. In summation, we demonstrated that altered mental status and failure to extubate were independent predictors or mortality in cSDH evacuation. Interestingly, patient age was not a significant predictor of mortality.

Kidney disease is a major global health concern, affecting millions of people. Nephrologists have shown interest in platelets because of coagulation disorders caused by renal diseases. With a better understanding of platelets, it has been found that these anucleate and abundant blood cells not only play a role in hemostasis, but also have important functions in inflammation and immunity. Platelets are not only affected by kidney disease, but may also contribute to kidney disease progression by mediating inflammation and immune effects. This review summarizes the current evidence regarding platelet abnormalities in renal disease, and the multiple effects of platelets on kidney disease progression. The relationship between platelets and kidney disease is still being explored, and further research can provide mechanistic insights into the relationship between thrombosis, bleeding, and inflammation related to kidney disease, and elucidate targeted therapies for patients with kidney disease.

The aim of this study was to determine the comparative effectiveness and safety of direct oral anticoagulants (DOACs) and warfarin in adults with atrial fibrillation (AF) by level of kidney function.

We pooled findings from five retrospective cohorts (2011-18) across Australia and Canada of adults with; a new dispensation for a DOAC or warfarin, an AF diagnosis, and a measure of baseline estimated glomerular filtration rate (eGFR). The outcomes of interest, within 1 year from the cohort entry date, were: (1) the composite of all-cause death, first hospitalization for ischaemic stroke, or transient ischaemic attack (effectiveness), and (2) first hospitalization for major bleeding defined as an intracranial, upper or lower gastrointestinal, or other bleeding (safety). Cox models were used to examine the association of a DOAC vs. warfarin with outcomes, after 1:1 matching via a propensity score. Kidney function was categorized as eGFR ≥60, 45-59, 30-44, and <30 mL/min/1.73 m2. A total of 74 542 patients were included in the matched analysis. DOAC initiation was associated with greater or similar effectiveness compared with warfarin initiation across all eGFR categories [pooled HRs (95% CIs) for eGFR categories: 0.74(0.69-0.79), 0.76(0.54-1.07), 0.68(0.61-0.75) and 0.86(0.76-0.98)], respectively. DOAC initiation was associated with lower or similar risk of major bleeding than warfarin initiation [pooled HRs (95% CIs): 0.75(0.65-0.86), 0.81(0.65-1.01), 0.82(0.66-1.02), and 0.71(0.52-0.99), respectively). Associations between DOAC initiation, compared with warfarin initiation, and study outcomes were not modified by eGFR category.

DOAC use, compared with warfarin use, was associated with a lower or similar risk of all-cause death, ischaemic stroke, and transient ischaemic attack and also a lower or similar risk of major bleeding across all levels of kidney function.

Hemodialysis patients are prone to gastrointestinal bleeding, and Mallory-Weiss syndrome (MWS) is one of the causes. Mallory-Weiss syndrome is often induced by severe vomiting, manifests as upper gastrointestinal bleeding, and is self-limited with a good prognosis. However, mild vomiting in hemodialysis patients can lead to the occurrence of MWS, and the mild early symptoms are easy to misdiagnose, leading to the aggravation of the disease.

In this paper, we report four hemodialysis patients with MWS. All patients displayed symptoms of upper gastrointestinal bleeding. The diagnosis of MWS was confirmed by gastroscopy. One patient had a history of severe vomiting; however, the other three reported histories of mild vomiting. Three patients received the conservative hemostasis treatment, and the gastrointestinal bleeding stopped. One patient underwent the gastroscopic and interventional hemostasis treatments. The conditions of three of the patients improved. Unfortunately, one of the patients died due to the cardia insufficiency.

We think that the mild symptoms of MWS are easily covered up by other symptoms. This may lead to delays in diagnosis and treatment. For patients with severe symptoms, gastroscopic hemostasis is still the first choice, and interventional hemostasis can also be considered. For patients with mild symptoms, drug hemostasis is the first consideration.

Neurologic complications are a major contributor to death and disability in patients with renal disease. Oxidative stress, endothelial dysfunction, accelerated arteriosclerosis, and uremic inflammatory milieu affect both the central and peripheral nervous systems. This article reviews the unique contributions of renal impairment to neurologic disorders and their common clinical manifestations as the prevalence of renal disease increases in a globally aging population.

Advances in the understanding of the pathophysiologic interplay between the kidneys and brain, also referred to as the kidney-brain axis, have led to more widespread recognition of associated changes in neurovascular dynamics, central nervous system acidification, and uremia-associated endothelial dysfunction and inflammation in the central and peripheral nervous systems. Acute kidney injury increases mortality in acute brain injury to nearly 5 times that seen in matched controls. Renal impairment and its associated increased risks of intracerebral hemorrhage and accelerated cognitive decline are developing fields. Dialysis-associated neurovascular injury is increasingly recognized in both continuous and intermittent forms of renal replacement therapy, and treatment strategies for its prevention are evolving.

This article summarizes the effects of renal impairment on the central and peripheral nervous systems with special considerations in acute kidney injury, patients requiring dialysis, and conditions that affect both the renal and nervous systems.

Anticoagulant-associated intracranial hemorrhage has a high mortality rate, and many factors can cause intracranial hemorrhage. Until now, systematic reviews and assessments of the certainty of the evidence have not been published.

We conducted a systematic review to identify risk factors for anticoagulant-associated intracranial hemorrhage. The protocol for this systematic review was prospectively registered with PROSPERO (CRD42022316750). All English studies that met the inclusion criteria published before January 2022 were obtained from PubMed, EMBASE, Web of Science, and Cochrane Library. Two researchers independently screened articles, extracted data, and evaluated the quality and evidence of the included studies. Risk factors for intracranial hemorrhage were used as the outcome index of this review. Random or fixed-effect models were used in statistical methods. I2 statistics were used to evaluate heterogeneity.

Of 7322 citations, we included 20 studies in our analysis. For intracranial hemorrhage, moderate-certainty evidence showed a probable association with race, Glasgow Coma Scale, stroke, leukoaraiosis, cerebrovascular disease, tumor, atrial fibrillation, previous bleeding, international normalized ratio, serum albumin, prothrombin time, diastolic blood pressure, and anticoagulant. Low-certainty evidence may be associated with age, cerebral microbleeds, smoking, alcohol intake, platelet count, and antiplatelet drug. In addition, we found very low-certainty evidence that there may be little to no association between the risk of intracranial hemorrhage and hypertension and creatinine clearance. Leukoaraiosis, cerebral microbleeds, cerebrovascular disease, and international normalized ratio are not included in most risk assessment models.

This study informs risk prediction for anticoagulant-associated intracranial hemorrhage and informs guidelines for intracranial hemorrhage prevention and future research.

This study aimed to evaluate the prevalence, causes, medical interventions, and mortality outcome of acute gastrointestinal bleeding (AGIB) among COVID-19 patients hospitalized during the delta pandemic in Vietnam.

The medical records of COVID-19 patients hospitalized in a tertiary hospital in Vietnam from July to October 2021 were retrospectively collected. Data regarding age, sex, comorbidities, COVID-19 severity, onset time of AGIB, therapeutic interventions for AGIB, and mortality outcome were analyzed.

Of 1567 COVID-19 inpatients, 56 (3.6%) had AGIB. The independent risk factors for AGIB in COVID-19 inpatients included age (OR = 1.03, 95% CI: 1.01-1.04, p = .003), male sex (OR = 1.86, 95% CI: 1.06-3.26, p = .03), chronic liver disease (OR = 6.21, 95% CI: 2.97-13.00, p < .001), and chronic kidney disease (OR = 2.17, 95% CI: 1.01-4.65, p = .047). Among 34 AGIB patients undergoing endoscopy, upper AGIB was determined in 24 (70.6%) patients. Peptic ulcer disease and hemorrhagic erosive gastritis were the most common causes (64.7%, 22/34). The therapeutic interventions for AGIB included blood transfusion (76.8%, 43/56), endoscopic hemostasis (23.5%, 8/34), and surgery (1.8%, 1/56). The mortality rate in the AGIB group was significantly higher than that in the non-AGIB group (46.4% vs. 27.7%, OR = 2.26, 95% CI: 1.32-3.87, p = .002). However, the majority (76.9%) of deaths in COVID-19 inpatients with AGIB were not bleeding-related.

Age, male sex, chronic liver disease, and chronic kidney disease are risk factors for AGIB among COVID-19 inpatients. Peptic ulcer disease is the most common cause. COVID-19 inpatients with AGIB have a higher risk of mortality, but a large percentage of deaths are not bleeding-related.

While angioectasia is an important cause of acute hematochezia, relevant clinical features remain unclear. This study aims to reveal risk factors, clinical outcomes, and the effectiveness of therapeutic endoscopy for patients with acute hematochezia due to angioectasia.

This retrospective cohort study was conducted at 49 Japanese hospitals between January 2010 and December 2019, enrolling patients hospitalized for acute hematochezia (CODE BLUE-J study). Baseline factors and clinical outcomes for angioectasia were analyzed.

Among 10,342 patients with acute hematochezia, 129 patients (1.2%) were diagnosed with angioectasia by colonoscopy. The following factors were significantly associated with angioectasia: chronic kidney disease, liver disease, female, body mass index < 25, and anticoagulant use. Patients with angioectasia were at a significant increased risk of blood transfusions compared to those without angioectasia (odds ratio [OR] 2.61; 95% confidence interval [CI] 1.69-4.02). Among patients with angioectasia, 36 patients (28%) experienced rebleeding during 1-year follow-up. The 1-year cumulative rebleeding rates were 37.0% in the endoscopic clipping group, 14.3% in the coagulation group, and 32.8% in the conservative management group. Compared to conservative management, coagulation therapy significantly reduced rebleeding risk (P = 0.038), while clipping did not (P = 0.81). Multivariate analysis showed coagulation therapy was an independent factor for reducing rebleeding risk (hazard ratio [HR] 0.40; 95% CI 0.16-0.96).

Our data showed patients with angioectasia had a greater comorbidity burden and needed more blood transfusions in comparison with those without angioectasia. To reduce rebleeding risk, coagulation therapy can be superior for controlling hematochezia secondary to angioectasia.