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The document titled "No association between vascular inflammation and estimated glomerular filtration rate in patients with rheumatoid arthritis: secondary analysis of the TARGET trial" explores the relationship between vascular inflammation and kidney function in patients with rheumatoid arthritis. The study found no significant association between aortic or carotid vascular inflammation and estimated glomerular filtration rate (eGFR) in patients with active rheumatoid arthritis. The results suggest that reducing vascular inflammation may not lead to temporal improvement in eGFR, and future studies should investigate the long-term impact of chronic vascular inflammation on kidney function in a larger population. [Extracted from the article]

Coronary artery disease (CAD), the build-up of atherosclerotic plaques on the wall of blood vessels, causes adverse cardiovascular events. Secondary prevention focuses on treating patients with existing plaques to prevent disease progression. Recent studies have shown that inflammation is an independent risk factor that drives disease progression, and targeting inflammation could be an effective therapeutic strategy for secondary prevention. In this review, we highlighted the roles of several inflammatory pathways in rupture and erosion, two major processes through which established plaques lead to adverse cardiovascular events. In the past 15 years, numerous clinical trials have tested the therapeutic potential of targeting these pathways, including neutralizing inflammatory cytokines and blocking signaling transduction of the inflammatory pathways. Only colchicine was approved for clinical use in patients with CAD. This is primarily due to the multifaceted roles of inflammatory pathways in disease progression. Commonly used pre-clinical models provided robust information for the onset of early disease but limited understanding of the inflammatory network in established plaques. This review will summarize lessons learned from successful and failed clinical trials to advocate for assessing inflammation in established plaques before designing therapeutics for secondary prevention. [ABSTRACT FROM AUTHOR]

Background Isolated tubulitis, borderline changes and isolated arteritis suspicious for histologic T-cell-mediated rejection (hTCMR) remain findings of uncertain significance. Although the Molecular Microscope Diagnostics System (MMDx) has not been trained on those lesions, it was suggested that MMDx might reclassify a subgroup to molecular TCMR (mTCMR). Methods In this single-center cohort of 326 consecutive, unselected kidney allograft biopsies assessed by histology and MMDx, we analyzed 249 cases with isolated tubulitis (i0, t1–3, v0; n  = 101), borderline changes (according to Banff 2022, v0; n  = 9), isolated arteritis (no borderline, v1; n  = 37), no inflammation (i0, t0, v0; n  = 67) and a positive control cohort (hTCMR, n  = 27; mixed histologic rejection, n  = 8; both according to Banff 2022; total n  = 35). The first three groups were summarized as TCMR-suspicion (n  = 147). Subcategorization included the presence and absence of microvascular inflammation (MVI); g+ptc ptc ≥2. Molecular rejection rates and differentiation were investigated. Results Molecular rejection rates were 37/147 cases (25.2%; 32 with MVI) in TCMR-suspicion, 6/67 (9%; 4 with MVI) in no inflammation and 30/35 (85.7%; 19 with MVI) in the positive control cohort. Molecular antibody-mediated rejection (mAMR) was present in 39/73 (53.4%) of cases. The presence of donor-specific antibodies at the time of the biopsy was high (127/249, 51%). Only 3 mAMR/TCMR and 0 pure mTCMR cases were detected in TCMR-suspicion and no inflammation, compared with 12 mAMR/TCMR and 10 mTCMR cases in the positive control cohort (P  < .001). Even though the TCMR-specific molecular (Classifier) score differentiated between TCMR-suspicion and no inflammation (P  = 0.005), rejection phenotype scores (R2 and R3) did not (P  = .157 and.121). Conclusions MMDx did not identify pure mTCMR among isolated tubulitis, borderline changes or isolated arteritis, likely due to low sensitivity for TCMR lesions. However, it identified mAMR or mAMR/TCMR, especially in cases with MVI. Subthreshold findings remain to be further studied. [ABSTRACT FROM AUTHOR]

Introduction: Chronic inflammation is a major risk factor for coronary artery disease (CAD). Currently, the inflammatory cardiovascular risk is assessed via C-reactive protein (CRP) levels measured using a high-sensitivity assay (hsCRP). Monomeric CRP (mCRP) is a locally produced form of CRP that has emerged as a potential biomarker of inflammation. Aim: This study investigated whether mCRP levels are associated with premature CAD. Materials and methods: This study comprised 103 participants of both sexes, including 50 patients 56 ± 7 years old with premature CAD and 53 patients 51 ± 10 years old without CAD. CAD was verified using coronary angiography, hsCRP levels were measured using a standard assay, and mCRP levels were measured using fluorescent cytometric beads conjugated with an anti-mCRP antibody. Results: The levels of hsCRP were 0.99 (0.59; 3.10) mg/L vs. 0.63 (0.35; 1.85) mg/L (p = 0.067), and mCRP 6.84 (4.20; 13.78) µg/L vs. 2.57 (0.32; 5.66) µg/L (p <0.001) in patients with CAD vs. patients without CAD, respectively. There was a weak positive correlation between the mCRP and hsCRP levels (ρ = 0.214; p = 0.030). hsCRP levels were below 2.0 mg/L (i.e., residual inflammatory cardiovascular risk should have been excluded) in 70% of patients with CAD and 79% of patients without CAD (p = 0.365). mCRP levels differed between the groups of patients with hsCRP levels below 2.0 mg/L: 5.14 (4.07; 10.68) µg/L vs. 2.77 (0.53; 5.00) µg/L in patients with or without CAD, respectively (p <0.001). Logistic regression analysis demonstrated that mCRP levels were independently associated with premature CAD. The adjusted odds ratio was 1.18 (95% CI 1.06-1.33, p = 0.004) per each µg/L increase in mCRP levels. Conclusion: Higher mCRP levels were associated with premature CAD, independent of hsCRP levels and traditional risk factors. [ABSTRACT FROM AUTHOR]

Objective: Acute cerebral infarction is a common complication of intracranial tuberculosis (TB), causing irreversible damage to brain tissue and significantly affecting patient prognosis. This study aims to explore the risk factors associated with acute cerebral infarction in patients with intracranial tuberculosis. Methods: We retrospectively analyzed data from eligible intracranial TB patients treated at our hospital between January 2020 and March 2023. Based on MRI findings, patients were categorized into a cerebral infarction group and a non-infarction group. Clinical data, cerebrospinal fluid (CSF) examinations, and imaging features (such as hydrocephalus, cerebral arteritis, and meningeal thickening) were compared between the two groups. Binary logistic regression analysis was used to identify risk factors for acute cerebral infarction in patients with intracranial TB. Results: A total of 102 patients were included, with 24 in the cerebral infarction group and 78 in the non-infarction group. Male patients accounted for 87.5% in the infarction group and 58.3% in the non-infarction group. Patients with a Glasgow Coma Scale (GCS) score of 3–10 accounted for 45.8% in the infarction group compared to 15.4% in the non-infarction group. The incidence of hydrocephalus, cerebral arteritis, and meningeal thickening was significantly higher in the infarction group (37.5, 54.2, and 79.2%, respectively) compared to the non-infarction group (6.4, 6.4, and 43.6%, respectively) (p < 0.05). The parenchymal type of intracranial TB was less frequent in the infarction group (20.8%) than in the non-infarction group (56.4%), while the mixed type was more frequent in the infarction group (62.5%) compared to the non-infarction group (26.9%) (p < 0.05). Patients with meningeal thickening involving the cisterns and basal cisterns had a higher risk of cerebral infarction (p < 0.05). Multivariate binary logistic regression analysis revealed that male sex (OR = 13.56; 95% CI 1.25–38.30) and cerebral arteritis (OR = 19.32; 95% CI 0.94–37.64) were independent risk factors for cerebral infarction in intracranial TB patients. Conclusion: Male sex and the presence of cerebral arteritis are independent risk factors for acute cerebral infarction in patients with intracranial tuberculosis. [ABSTRACT FROM AUTHOR]