Tomasz Hryszko

Background: Although international guidelines recommend that patients be trained in emergency self‐disconnection procedures from the dialysis machine, little is known about patients' knowledge and procedural accuracy regarding this practice. Objective: This study aimed to evaluate the knowledge of people receiving haemodialysis and their ability to correctly identify the steps required to disconnect themselves from the dialysis machine in an emergency, safely. Methods: This international multicentre descriptive study was conducted between September 2025 and January 2026 in 10 dialysis centres across six countries: Türkiye, Denmark, Greece, Portugal, Poland and Peru. Adult patients receiving maintenance haemodialysis for at least 3 months were eligible to participate. Data were collected using a participant information form and a self‐disconnection checklist consisting of two sections evaluating preparation knowledge and procedural steps. Descriptive statistics were used to summarise the data. Results: Of the 626 people receiving haemodialysis included in the study, 125 (20.0%) had received training on self‐disconnection from the dialysis machine (Türkiye, Peru, Greece, and Denmark). Overall, 22.4% of patients reported knowing how to disconnect themselves from the dialysis machine in an emergency. According to the checklist evaluation, 40.3% of patients correctly identified the first stage of the procedure, and 38.3% correctly identified the second stage. Conclusion: A substantial gap exists between perceived knowledge and actual procedural competence regarding emergency self‐disconnection among people receiving haemodialysis. These findings highlight the need for structured education, simulation‐based training and standardised protocols to improve disaster preparedness and patient safety in dialysis units. ClinicalTrials.gov: NCT07412834.

Reliable vascular access is essential for hemodialysis. While arteriovenous fistulas are preferred for long-term use, tunneled hemodialysis catheters (TDCs

TNF-related apoptosis-inducing ligand (TRAIL), a protein involved in apoptosis, and receptor-interacting serine/threonine protein kinase-3 (RIPK3), implicated in necroptosis, are known to change during organ damage and have been studied as prognostic markers in sepsis; however, cell death mechanisms also play a role in other critical illnesses. This study aimed to assess the utility of TRAIL and RIPK3 in predicting mortality and acute kidney injury (AKI) among unselected intensive care unit (ICU) patients. We performed a single-center prospective cohort study including 142 consecutive ICU admissions, collecting blood samples for TRAIL and RIPK3 measurement within 24 h of admission. The primary endpoints were in-hospital mortality and incident AKI during the ICU stay, with additional analysis of mortality over a two-year follow-up. Neither TRAIL nor RIPK3 levels at admission were significantly associated with in-hospital mortality, long-term mortality, or AKI incidence. However, higher RIPK3 levels correlated with shorter time to AKI occurrence. These results suggest that despite earlier evidence supporting their prognostic value in sepsis, TRAIL and RIPK3 did not reliably predict outcomes in a heterogeneous ICU population, underscoring the complexity of critical illness and the need for multiparametric biomarker strategies to improve risk stratification.

Sirtuin 1 (SIRT1) is implicated in oxidative stress, inflammation, and fibrosis—processes central to chronic kidney disease (CKD) and cardiovascular complications. Increased serum levels of SIRT1 have been reported in dialysis patients, and its role in peritoneal fibrosis, a leading cause of peritoneal dialysis failure, is well established. This study evaluated serum SIRT1 levels in 165 participants: peritoneally dialyzed patients (CAPD), conservatively treated CKD patients (CT), and healthy controls. Serum SIRT1 was measured by ELISA and analyzed alongside clinical factors. SIRT1 concentrations were markedly elevated in CAPD patients compared to both CT patients and controls. In CAPD patients, SIRT1 levels were not influenced by age, sex, dialysis adequacy, residual renal function, or comorbidities, but were higher in those with impaired left ventricular relaxation. Pharmacotherapy affected SIRT1 levels. Multivariate analysis identified phosphate and cholesterol as independent predictors of SIRT1. Our study suggests that serum SIRT1 levels may reflect diverse pathophysiological processes in CKD patients, including those on peritoneal dialysis. Elevated SIRT1 may indicate compensatory mechanisms related to renal dysfunction and cardiovascular stress. Future research on larger, pharmacologically homogeneous groups is warranted to clarify SIRT1’s role in peritoneal fibrosis and its potential as a biomarker of cardiovascular and renal complications in CKD.

Elevated concentrations of FGF23 are commonly observed in patients with impaired kidney function. It has been hypothesized that acute kidney injury (AKI), in contrast to chronic kidney disease (CKD), may be associated with increased FGF23 cleavage, resulting in a decreased ratio of intact to C-terminal FGF23 (iFGF23:cFGF23). However, data on the diagnostic utility of this ratio in differentiating AKI from CKD remain limited. A single-center cohort study involving 173 patients admitted to the Nephrology Department with abnormal serum creatinine levels between March 2018 and July 2021 was conducted. Blood samples were collected within 24 h of admission to measure FGF23 concentrations using both intact and C-terminal ELISAs. The iFGF23:cFGF23 ratio was calculated and analyzed across diagnostic groups. Generalized estimating equations with doubly robust adjustment were used to account for the relevant clinical and biochemical covariates. In unadjusted analyses, patients with AKI had significantly higher cFGF23 concentrations (p = 0.021) and a lower iFGF23:cFGF23 ratio (p = 0.017) compared to patients with stable CKD. No significant difference in iFGF23 levels was observed. However, after multivariable adjustment for age, serum creatinine, markers of mineral metabolism (calcium, phosphate, and parathormone) and inflammation (CRP), the observed differences were no longer statistically significant (p > 0.5 for all), and the interaction terms revealed no consistent modifiers of the exposure effect. The ROC analysis demonstrated modest discriminatory ability of the iFGF23:cFGF23 ratio, with an AUC of 0.60. After robust adjustment for key confounders, the iFGF23:cFGF23 ratio does not serve as a reliable independent marker for differentiating AKI from CKD. These results were supported by the ROC analysis, reflecting limited clinical utility for this ratio as a standalone biomarker. Our findings suggest that the observed differences in FGF23 metabolism are primarily driven by underlying disturbances in mineral metabolism and inflammation rather than the acute or chronic nature of the kidney injury itself.

Heart failure with preserved ejection fraction (HFpEF) poses a significant clinical challenge due to its increasing incidence, diagnostic complexities and pathophysiological heterogeneity. This study offers valuable insights into the role of urinary biomarkers in patients with HFpEF. Our research focused on profiling alterations in urinary biomarkers, encompassing albumin, indicators of tubular injury, oxidative stress markers, and proteomic changes in individuals with this condition. These findings may provide a potential tool for addressing the diagnostic challenges associated with HFpEF, particularly given the absence of specific cutoff points in the diagnosis of this disease. Furthermore, we explored the potential pathophysiological relationships of these biomarkers, which, in a broader context, facilitate a deeper understanding of this complex disease and may identify potential pharmacotherapeutic targets. We also examined the prognostic value of the identified biomarkers, which could serve as useful instruments for predicting disease risk and forecasting clinical outcomes. Additionally, we emphasized the existing knowledge surrounding potential biomarkers, suggesting that a better understanding of these markers may contribute to the development of clinically relevant tools and enhance our comprehension of HFpEF. The findings from this study align with the current literature, which underscores the complexity of HFpEF and the need for innovative diagnostic, prognostic and therapeutic strategies.

Overhydration (OH) is a prevalent medical problem that occurs in patients with kidney failure, but a specific marker has still not been found. Patients requiring kidney replacement therapy suffer from a water imbalance, which is correlated with mortality rates in this population. Currently, clinicians employ techniques such as bioimpedance spectroscopy (BIS) and ultrasound (USG) markers of overhydration or markers of heart and kidney function, namely NT-pro-BNP, GFR, or creatinine levels. New serum markers, including but not limited to Ca-125, galectin-3 (Gal-3), adrenomedullin (AMD), and urocortin-2 (UCN-2), are presently under research and have displayed promising results. Ca-125, which is a protein mainly used in ovarian cancer diagnoses, holds great potential to become an OH marker. It is currently being investigated by cardiologists as it corresponds to the volume status in heart failure (HF) and ventricular hypertrophy, which are also associated with OH. The need to ascertain a more precise marker of overhydration is urgent mainly because physical examinations are exceptionally inaccurate. The signs and symptoms of overhydration, such as edema or a gradual increase in body mass, are not always present, notably in patients with chronic kidney disease. Metabolic disruptions and cachexia can give a false picture of the hydration status. This review paper summarizes the existing knowledge on the assessment of a patient’s hydration status, focusing specifically on kidney diseases and the role of Ca-125.

Overhydration (OH) is a prevalent medical problem occuring in patients with kidney failure, but a specific marker has still not been found. Currently, clinicians employ techniques such as bioimpedance spectroscopy (BIS), ultrasound (US) markers of fluid overload or markers of heart and kidney function such as NT-pro-BNP, GFR or creatinine levels. New serum markers, including but not limited to Ca-125, Galectin-3 (Gal-3), Adrenomedullin (AMD) and Urocortin-2 (UCN-2), are presently under research, displaying promising results. The necessity to ascertain a more precise marker of overhydration is urgent mainly because physical examination is exceptionally imprecise. Signs and symptoms of fluid overload, like edema or gradual increase of body mass, are not always present, notably in patients with chronic kidney disease. This review paper summarizes actual knowledge of a patient's hydration status estimation, focusing specifically on kidney diseases.

Acute kidney injury is a syndrome with a plethora of causes and not fully elucidated pathogenesis. Numerous attempts have been taken for many years to define and reliably diagnose this syndrome. The article is a review of recent advances in the diagnostics of acute kidney injury. Keywords: acute kidney injury diagnostics

IgA nephropathy (IgAN) is a progressive form of kidney disease defined by glomerular deposition of IgA. Here we performed a genome-wide association study of 10,146 kidney-biopsy-diagnosed IgAN cases and 28,751 controls across 17 international cohorts. We defined 30 genome-wide significant risk loci explaining 11% of disease risk. A total of 16 loci were new, including TNFSF4/TNFSF18, REL, CD28, PF4V1, LY86, LYN, ANXA3, TNFSF8/TNFSF15, REEP3, ZMIZ1, OVOL1/RELA, ETS1, IGH, IRF8, TNFRSF13B and FCAR. The risk loci were enriched in gene orthologs causing abnormal IgA levels when genetically manipulated in mice. We also observed a positive genetic correlation between IgAN and serum IgA levels. High polygenic score for IgAN was associated with earlier onset of kidney failure. In a comprehensive functional annotation analysis of candidate causal genes, we observed convergence of biological candidates on a common set of inflammatory signaling pathways and cytokine ligand–receptor pairs, prioritizing potential new drug targets.