This systematic review investigates the role of the gut microbiota in patients with advanced chronic kidney disease (CKD), specifically stages 4 and 5. Increasing evidence suggests that dysbiosis—an alteration in the normal balance of gut microbial populations—is not merely a secondary consequence of renal decline but a significant driver of disease progression. Such microbial imbalances are closely linked to a range of CKD-associated complications, including systemic inflammation, accumulation of uremic toxins, and heightened cardiovascular risk. Using PRISMA 2020 guidelines, we analyzed 87 peer-reviewed studies published between 2019 and 2025. The review revealed a consistent decline in beneficial microbes such as short-chain fatty acid-producing bacteria were markedly reduced, while populations of uremic toxin-generating microbes were notably increased. This microbial imbalance was associated with elevated concentrations of indoxyl sulfate and p-cresyl sulfate, heightened systemic inflammation, and impaired intestinal barrier integrity. Five conceptual frameworks—including the gut—kidney axis and endotoxemia—inflammation loop—were discussed. Ten microbiome assessment tools were reviewed, including 16S rRNA sequencing and LC-MS/MS for uremic toxin detection. Although probiotics, prebiotics, and synbiotics are gaining attention as potential therapeutic options, questions remain regarding their long-term efficacy and incorporation into standard clinical practice. Increasing scientific evidence underscores the gut microbiome’s pivotal role in CKD progression and management, reinforcing the need for carefully designed, long-term interventions aimed at restoring a healthier microbial balance to support renal function.

This systematic review examines chronic kidney disease-associated pruritus (CKD-aP) as a complex clinical manifestation in patients undergoing hemodialysis. Traditionally considered a secondary symptom of end-stage renal disease, emerging evidence now positions CKD-aP as a multidimensional disorder with substantial pathogenic influence on patient outcomes. Using the PRISMA 2020 methodology, we critically evaluated 54 peer-reviewed studies published between 2020 and 2025. Our synthesis highlights a convergence of five mechanistic frameworks underpinning CKD-aP: elevated levels of uremic toxins originating from gut microbial dysbiosis, immune activation driven by IL-31 and other pro-inflammatory cytokines, heightened peripheral and central neural sensitization, dysregulation of endogenous opioid receptor pathways favoring μ-receptor activation, and xerosis-related epidermal barrier dysfunction. These mechanisms contribute to a systemic cycle of microinflammation, pruritogenic signaling, and neural hyperexcitability. We also identified and compared validated assessment tools—including the NRS, VAS, Skindex-10, and the UP-Dial scale—that facilitate standardized quantification of disease burden. While available treatments such as gabapentinoids and phototherapy offer partial relief, targeted therapies—including κ-opioid receptor agonists—represent a major advancement, although long-term effectiveness and accessibility remain under investigation. Growing scientific consensus establishes CKD-aP as a priority therapeutic target in hemodialysis care, underscoring the need for integrated, mechanism-based management strategies to improve quality of life and clinical outcomes. This work represents a narrative systematic review, integrating evidence from mechanistic, translational, and clinical studies to critically examine the biological pathways underlying CKD-associated pruritus.

Background: End-stage renal disease (ESRD) patients on haemodialysis present a high burden of cardiovascular comorbidities and require anticoagulation, which increases bleeding risk. Methods: We performed a retrospective observational study (2021–2024) in the Haemodialysis Centre of The Clinical Emergency Hospital of Constanta County, Romania, including 50 adults with stage G5 CKD on haemodialysis for ≥3 months and receiving anticoagulant therapy. We collected from electronic medical records detailed demographic data (age, sex, place of residence), comorbidities (hypertension, atrial fibrillation, ischaemic heart disease, diabetes, deep-vein thrombosis, stroke, myocardial infarction, pulmonary embolism, cirrhosis), lifestyle factors (smoking and alcohol consumption), vascular access type (arteriovenous fistula or central venous catheter) and laboratory parameters (haemoglobin, haematocrit, creatinine, albumin, total protein, electrolytes, LDL- and HDL-cholesterol, total cholesterol, INR, APTT, D-dimer, BNP, CK-MB, troponin). All laboratory units were standardised and checked for plausibility. Results: Median age was 71 years; 48% were female. The most common comorbidities were: hypertension (100%), atrial fibrillation (100%) and ischaemic heart disease (62–81%). Patients exhibited severe anaemia (mean Hb ~9.7 g/dL), nephrotic-range proteinuria, hypoalbuminaemia, and impaired coagulation profiles (INR ~1.8–1.9; prolonged APTT in men). Female patients had higher platelet counts and D-dimer levels, suggesting a stronger prothrombotic profile, while males showed longer APTT. Cardiovascular strain was reflected by elevated BNP in men and also troponin/CK-MB. Correlations included smoking with leukocytosis, alcohol with increased urine density, diabetes with higher urea and lower protein, and subtherapeutic INR in cerebrovascular disease. Conclusions: Patients with ESRD on haemodialysis and anticoagulant therapy display a complex interplay of cardiovascular comorbidities, anemia, overlapping thrombotic and bleeding risks, with sex-specific differences. Therefore, systematic monitoring of proteinuria, haemoglobin, D-dimer, and coagulation markers is crucial to balance thrombotic and bleeding risks. Objective: To characterise the clinical and paraclinical profile and comorbidity–laboratory correlations of ESRD patients undergoing haemodialysis and anticoagulant therapy.

Background: Anticoagulation in patients with advanced chronic kidney disease (CKD) and atrial fibrillation (AF) remains challenging due to the concurrent risks of thrombosis and bleeding driven by endothelial dysfunction, uremic inflammation, and impaired hemostasis. Evidence comparing vitamin K antagonists (VKAs) with direct oral anticoagulants (NOACs) in this high-risk population, particularly in dialysis, is still limited. Methods: We conducted a single-center, retrospective observational study including 93 patients with CKD stages 4–5 and AF treated between January 2021 and February 2025. Fifty patients received apixaban (2.5–5 mg twice daily), and forty-three received acenocoumarol with a target INR of 2.0–3.0. Thirty-eight patients (41%) were on maintenance hemodialysis. Demographics, comorbidities, and risk scores (CHA₂DS₂-VASc and HAS-BLED) were analyzed. Bleeding events were classified per ISTH criteria. Statistical comparisons used t-tests and χ² tests, with p < 0.05 considered significant. Results: The mean age was 67.8 ± 9.1 years, and 51.6% were male. Major bleeding occurred in 9.7%, minor in 15.8%, and overdose-related bleeding in 10.0% of patients. The overall bleeding rate was significantly lower in the apixaban group (16.0%) than in the acenocoumarol group (53.5%; p = 0.01). No thromboembolic events were observed in either group. Dialysis patients had higher bleeding rates overall (13.2% vs. 7.4%), mainly among those on VKAs. The HAS-BLED score moderately correlated with bleeding incidence (r = 0.43, p < 0.01). Conclusions: Apixaban provided comparable thromboembolic protection with significantly fewer bleeding events than acenocoumarol, including in patients on dialysis. These findings support apixaban as a safer and more practical anticoagulant option in advanced CKD, consistent with its limited renal clearance and reduced influence on the inflammation–coagulation axis. Further multicenter prospective studies are warranted to validate these real-world results.

Advanced chronic kidney disease (CKD) presents a complex hemostatic paradox, characterized by a simultaneous increase in bleeding and thromboembolic risks. This study aimed to evaluate and compare the safety and efficacy of apixaban versus acenocoumarol in a real-world cohort of patients across advanced CKD stages (pre-dialysis and hemodialysis). We conducted a retrospective observational study including 84 adults with CKD stages 4 and 5 (40.5% in stage 4; 59.5% in stage 5, of whom 86.0% were on chronic hemodialysis) receiving oral anticoagulation for at least 3 months. Patients were stratified by CKD stage and anticoagulant type (apixaban vs. acenocoumarol). Clinical outcomes included major and clinically relevant bleeding, anticoagulant overdose, and thromboembolic events. Bleeding events were more frequent in CKD stage 5 than in stage 4 (66.0% vs. 44.1%, p = 0.06), highlighting a pronounced hemorrhagic burden that increases with disease progression. Apixaban was associated with significantly fewer total bleeding events (44.4% vs. 66.7%, p = 0.04) and a lower rate of anticoagulant overdoses (5.6% vs. 18.8%, p = 0.04) compared with acenocoumarol. Thromboembolic event rates did not differ significantly between the two anticoagulant groups (13.9% vs. 16.7%, p = 0.72). Conventional risk scores (CHA₂DS₂-VASc and HAS-BLED) showed limited discriminatory capacity for actual clinical events in this advanced CKD population. In patients with advanced CKD, oral anticoagulation is associated with a high hemorrhagic burden that intensifies as renal function declines. Apixaban demonstrated a more favorable safety profile than acenocoumarol without a loss of thromboembolic protection. These findings suggest that stage-specific biological factors, rather than conventional risk models alone, should guide anticoagulation strategies in this population.

Background: Sapropelic mud from Techirghiol Lake has been used therapeutically under medical supervision for more than 170 years; however, its comprehensive physicochemical characterization under application-relevant conditions remains insufficiently documented. This study aimed to evaluate the physicochemical properties, mineral and organic composition, ion-exchange capacity, and potential therapeutic mechanisms of Techirghiol sapropelic mud. Methods: Mud samples were analyzed using standardized physicochemical and analytical techniques to determine pH, water content, granulometry, mineral composition, organic fraction, and trace elements. Results: The results indicate that Techirghiol mud is a highly hydrated alkaline peloid characterized by a complex mineral–organic system. Major elements included sodium, calcium, and magnesium, while trace elements such as manganese, iron, and zinc were present in relevant concentrations. The organic fraction, composed of humic substances, lipids, and proteins, reflected advanced but incomplete humification processes. Conclusions: The findings demonstrate the complex physicochemical composition of Techirghiol sapropelic mud and provide a scientific basis for further studies regarding its properties and applications.