
INTRODUCTION:Chronic kidney disease (CKD) is a major determinant of adverse cardiovascular outcomes. Patients with CKD undergoing percutaneous coronary intervention (PCI) represent a particularly high-risk population; however, data on the long-term prognostic impact of CKD in patients treated with PCI for left main coronary artery disease (LM CAD) remain limited. OBJECTIVES:This study aimed to evaluate the long-term impact of CKD on outcomes after left main PCI. PATIENTS AND METHODS:This single-center, prospective registry study analyzed 1321 patients who underwent left main PCI. Propensity score matching based on age, sex, diabetes mellitus, left ventricular ejection fraction, and SYNTAX score was performed among patients treated between January 2015 and December 2020, yielding a matched cohort of 344 patients (177 with CKD and 177 without CKD). CKD was defined as an estimated glomerular filtration rate <60 mL/min/1.73 m². RESULTS:During a median follow-up of 2199 days, CKD was associated with significantly higher all-cause mortality (HR 1.75, 95% CI 1.30-2.34; P <0.001), cardiac death (HR 2.10, 95% CI 1.33-3.33; P = 0.001), stroke and major adverse cardiovascular events rates. In contrast, no significant long-term differences were observed between CKD and non-CKD patients in the incidence of myocardial infarction. Procedural characteristics, periprocedural complications, and procedural success rates were comparable between groups. CONCLUSIONS:In patients undergoing PCI for LM CAD, CKD predicts worse long-term survival despite comparable procedural and ischemic outcomes. The excess mortality appears driven by systemic rather than revascularization-related factors, underscoring the need for intensified long-term multidisciplinary management in this high-risk population.
INTRODUCTION:Malar rash is a hallmark manifestation of systemic lupus erythematosus (SLE); however, its clinical and immunological significance remains incompletely understood. OBJECTIVES:To investigate the associations of malar rash with clinical phenotype, serological profile, comorbidities, and treatment patterns in SLE. PATIENTS AND METHODS:We retrospectively analyzed 1039 patients with SLE who fulfilled the 2019 EULAR/ACR classification criteria and were treated at a tertiary referral center between 2012 and 2022. Patients were stratified according to the presence or absence of malar rash. RESULTS:Malar rash was present in 444 patients (42.7%). Patients with malar rash had an earlier disease onset (32 vs 37 years) and a longer disease duration (14 vs 11 years; both P <0.001). Constitutional symptoms were more frequent in patients with malar rash (81.8% vs 73.2%, P = 0.001), including fever, fatigue, myalgia, and weight loss. Mucocutaneous and musculoskeletal manifestations were also more common in this group (all P <0.001). Leukopenia occurred more frequently in patients with malar rash, whereas hemolytic anemia was more common in those without malar rash. Pulmonary involvement was less frequent in patients with malar rash, while renal and neurological manifestations did not differ significantly between the groups. Anti-Sm and anti-RNP antibodies were more frequently detected in patients with malar rash. Patients with malar rash were also more likely to receive antimalarial agents and azathioprine. CONCLUSIONS:Malar rash is associated with an earlier SLE onset and a distinct clinical phenotype characterized by increased constitutional, mucocutaneous, and musculoskeletal involvement, specific serological features, and less frequent pulmonary manifestations.
Patients undergoing maintenance hemodialysis face annual mortality rates of 15-27%, with cardiovascular causes accounting for more than half of all deaths. Despite advances in dialytic technology, conventional prognostic models derived from the general population systematically underestimate risk in end-stage renal disease, failing to capture the complexity of uremic pathophysiology that drives this excess mortality: immune dysregulation, chronic inflammation, oxidative stress, vascular calcification, uremic cardiomyopathy, protein-energy wasting, and accelerated vascular aging. This narrative review synthesizes current evidence on biomarkers predicting all-cause and cardiovascular mortality in haemodialysis patients, spanning established markers (albumin, CRP, ferritin, hemoglobin, high-sensitivity troponins, and NT-proBNP) to an emerging frontier encompassing IL-6, PTX3, sST2, galectin-3, FGF-23, Klotho, and multi-omics signatures. We further examine composite neutrophil-derived indices, adipokines, and mineral metabolism markers as tools for pathway-specific risk interrogation. The evidence converges on a clear practical message: combination and dynamics outperform single, static measurements. Multi-biomarker models consistently outperform individual markers, and longitudinal trajectories carry prognostic information, with divergence between survivors and non-survivors detectable many months before death, that a single time-point value cannot replicate. Advances in artificial intelligence and multi-omics further support this shift toward dynamic, personalized risk stratification, though these approaches remain at an early, largely exploratory stage. Critically, clinical translation remains limited by the lack of dialysis-specific thresholds, poor standardization, and the absence of randomized evidence demonstrating that biomarker-guided strategies improve outcomes. Bridging this gap between prognostic insight and clinical application remains the central challenge of precision nephrology.