Background. One of the primary reasons for high mortality in end-stage renal disease (ESRD) is cardiovascular disease in patients with renal replacement therapy (RRT). Left ventricular hypertrophy (LVH) significantly predicts mortality and cardiovascular events. Objectives. We assess the left ventricular mass index change in two dialysis methods: hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD). The factors associated with increased left ventricular mass index (LVMI). Materials and Methods. We recruit more than 50 HD patients and 45 CAPD patients with LVH of similar age, gender, dialysis duration, and LVMI for one-year follow-up. Results. The LVMI in the group of HD patients after one year increased from 180.2845.32g/m² to 212.5866.22g/m² (p=0.001), while the LVMI in the group of patients with CAPD increased from 190.1666.01g/m² to 197.4278g/m² (p=0.32). Multivariable logistic regression analysis, we demonstrated that dialysis by HD (β=1,167, 95 CI: 0.1040.938, p=0.036) and anemia treatment lower the goals (β=1.9566, 95 CI: 1.46634.094, p=0.015) were two factors associated with the progression of the LVMI. Conclusion. The LVH of end-stage renal disease patients with HD treatment is worse than CAPD treatment after a follow-up in oneyear. Dialysis by periodic hemodialysis and anemia treatment that fails to achieve the goal are risk factors associated with increased progression of LVMI in patients with ESRD.

Background: Disturbances in magnesium homeostasis and magnesium supplementation are common in critical illness; however, the association between early intravenous magnesium sulfate administration and clinical outcomes in critically ill patients with pneumonia remains unclear. Methods: This retrospective observational cohort study used data from the Medical Information Mart for Intensive Care IV (version 3.1) database and included critically ill patients admitted to the intensive care unit (ICU) with pneumonia. Patients were classified according to early exposure to intravenous magnesium sulfate, defined as administration from 6 h before to 24 h after ICU admission, or no exposure during this period. The primary outcome was 30-day all-cause mortality, with secondary outcomes including 60-day and 90-day mortality. Associations were evaluated using multivariable Cox proportional hazards models, with prespecified subgroup, interaction, and sensitivity analyses, including propensity score matching. Results: Among 9203 eligible patients, 2975 (32.3%) received early intravenous magnesium sulfate. Magnesium sulfate administration was associated with lower 30-day mortality after multivariable adjustment (adjusted hazard ratio [aHR] 0.84; 95% confidence interval [CI] 0.76-0.94; p = .002). Similar associations were observed for 60-day mortality (aHR 0.86; 95% CI 0.78-0.95; p = .002) and 90-day mortality (aHR 0.87; 95% CI 0.80-0.96; p = .004). Subgroup analysis identified a significant interaction for sepsis status (p for interaction = .007). In a propensity score–matched cohort, magnesium sulfate administration remained associated with lower 30-day mortality (aHR 0.85; 95% CI 0.74-0.96; p = .012). Conclusions: In critically ill patients with pneumonia, early intravenous magnesium sulfate administration was associated with lower mortality. These findings are hypothesis-generating and suggest the need for prospective studies to clarify causality and define optimal dosing and duration of magnesium supplementation in this population.

The 2024 global redefinition of acute respiratory distress syndrome (ARDS) broadens diagnostic criteria to include patients on non-invasive respiratory support. While this inclusivity enhances early recognition, it also introduces heterogeneity in disease severity, inflammatory burden, and treatment responsiveness–complicating the use of corticosteroids. Although recent guidelines recommend corticosteroids for moderate-to-severe ARDS, they fall short of specifying optimal timing, dosing, and patient selection. The DEXA-ARDS trial showed that high-dose dexamethasone reduced mortality in moderate-to-severe ARDS regardless of etiology, but its generalizability to less severe or non-intubated patients remains unclear. Conversely, in severe community-acquired pneumonia (CAP), hydrocortisone regimens used in CAPE-COD and APROCCHSS trials demonstrated mortality benefits, suggesting a particular therapeutic niche for corticosteroids in non-viral, infection-associated ARDS. A recent network meta-analysis suggests that low-dose methylprednisolone may reduce ARDS mortality, though phenotype-specific efficacy is not well defined. Despite these encouraging signals, key questions persist: Which corticosteroid? At what dose? For which ARDS phenotype? As evidence accumulates unevenly across ARDS subtypes, guideline-endorsed recommendations may inadvertently mask the nuances required for individualized therapy. Until precision approaches are better defined, clinicians must balance empirical benefit with thoughtful restraint in applying corticosteroids to non-viral ARDS. This concise review summarizes current evidence, key limitations, and pragmatic phenotype-informed strategies for corticosteroid use in non-viral ARDS.

Đặt vấn đề: Biến chứng tim mạch là nguyên nhân chính dẫn đến tử vong trên bệnh nhân thẩm phân phúc mạc (TPPM) [5]. Phì đại thất trái (PĐTT) thường gặp ở bệnh nhân lọc máu định kỳ và là yếu tố nguy cơ độc lập tiên lượng tỉ lệ tử vong. Mục tiêu nghiên cứu: Mô tả và so sánh tỷ lệ, một số yếu tố liên quan đến phì đại thất trái ở bệnh nhân thẩm phân phúc mạc và thận nhân tạo (TNT). Đối tượng và phương pháp nghiên cứu: Nghiên cứu cắt ngang mô tả có so sánh với nhóm chứng trên 148 bệnh nhân ≥ 18 tuổi, thời gian lọc máu định kỳ ≥ 3 tháng tại Bệnh viện Đa khoa thành phố Cần Thơ, trong đó có 74 bệnh nhân TPPM và 74 bệnh nhân TNT (nhóm chứng). Kết quả: Tỷ lệ PĐTT ở bệnh nhân TPPM là 86,5% (90,6% là PĐTT đồng tâm, 9,4% là PĐTT lệch tâm) tương đương với nhóm chứng (TNT) là 90,5% (86,6% là PĐTT đồng tâm, 13,4% là PĐTT lệch tâm). Chỉ số khối cơ thất trái (LVMI) ở bệnh nhân TPPM có mối tương quan thuận với thời gian lọc máu (r=0,2), huyết áp tâm thu (r=0,54), huyết áp tâm trương (r=0,419) và tương quan nghịch với Hb (r=-0,363), thể tích nước tiểu 24 giờ (r=-0,448) trong phân tích đơn biến. Trên mô hình hồi quy logistic đa biến, mất chức năng thận tồn dư (CNTTD) là yếu tố nguy cơ độc lập của PĐTT ở bệnh nhân TPPM. Không có sự khác biệt về các yếu tố liên quan đến PĐTT giữa nhóm bệnh nhân TPPM và nhóm chứng (TNT) (p<0,05). Kết luận: PĐTT ở bệnh nhân TPPM và TNT chiếm tỷ lệ cao, tương đương nhau; không có sự khác biệt về một số yếu tố liên quan đến PĐTT ở hai nhóm. Mất CNTTD là yếu tố nguy cơ độc lập của PĐTT ở bệnh nhân TPPM.