Search Results (4,874)

Background: Medication adherence is a critical component of effective management in type 2 diabetes mellitus (T2DM). Although previous studies have explored the relationship between adherence and clinical outcomes, the strength and consistency of these associations have not been fully elucidated and remain unclear. In particular, evidence derived from patient-reported measures of adherence is limited, and the prognostic significance of adherence as assessed from the patient perspective is not clearly defined. Methods: We conducted a prospective observational cohort study consisting of adult patients with T2DM who received regular outpatient follow-up. Medication adherence was assessed at the time of enrollment using the eight-item Morisky Medication Adherence Scale (MMAS-8) and was categorized as good, moderate, or poor. Participants were subsequently followed for five years to ascertain clinical outcomes. Primary outcomes were assessed longitudinally and included the occurrence of nonfatal myocardial infarction, heart failure, nonfatal stroke, and progression to end-stage kidney disease (ESKD), as well as all-cause mortality. Secondary outcomes included changes in glycated hemoglobin (HbA1c), estimated glomerular filtration rate (eGFR), and low-density lipoprotein (LDL) levels. Results: No statistically significant differences were observed in the incidence of nonfatal myocardial infarction, heart failure, nonfatal stroke, or progression to ESKD across adherence groups. In contrast, all-cause mortality was significantly higher among patients with poor adherence. With respect to metabolic outcomes, HbA1c and eGFR at five years were comparable across adherence groups, whereas LDL levels were significantly higher in patients with poor adherence. Conclusions: Poor medication adherence as assessed at baseline may be related to a higher risk of all-cause mortality and poorer lipid control, while no statistically significant differences were observed for nonfatal cardiovascular or renal outcomes. Full article

Background and Objectives: Chronic kidney disease (CKD) is associated with severe coronary calcification and increased procedural risks. We aimed to evaluate the impact of CKD on contrast-induced nephropathy (CIN), bleeding, and clinical outcomes in patients undergoing rotational atherectomy (RA). Materials and Methods: This study retrospectively analyzed 652 patients who underwent RA for calcified coronary lesions from the multicenter ROCK registry and a single-center extension between 2010 and 2025. Patients were classified into CKD (eGFR < 60 mL/min/1.73 m², n = 66) and non-CKD (n = 586) groups, excluding those on dialysis. The primary endpoint was a composite of CIN and in-hospital bleeding. Secondary endpoints included 3-year target vessel failure (TVF), myocardial infarction (MI), and total bleeding. Results: The primary composite outcome occurred more frequently in the CKD group (16.7% vs. 5.1%, p = 0.001). Specifically, CIN was significantly higher in CKD patients (15.2% vs. 1.7%, p < 0.001), while in-hospital bleeding did not differ significantly. In multivariate analysis, CKD was an independent predictor of the primary outcome (adjusted OR 3.02; 95% CI 1.36–6.69; p = 0.006). At 3-year follow-up, total bleeding (10.6% vs. 3.9%, p = 0.008) and MI (6.1% vs. 2.1%, p = 0.024) were higher in the CKD group, whereas TVF and cardiac death showed no significant difference. Conclusions: CKD is a robust independent risk factor for CIN and long-term bleeding in patients undergoing RA. However, comparable clinical efficacy outcomes suggest that RA remains a feasible strategy in CKD patients when early complications are carefully managed with contrast-minimizing strategies. Full article

Cytokine storm is a central pathogenic mechanism underlying sepsis-induced acute lung injury (SALI) and severe coronavirus disease 2019 (COVID-19), yet effective therapeutic strategies remain limited. Eupatorium lindleyanum DC. (EL), a traditional Chinese medicinal herb, has been reported to possess anti-inflammatory, antioxidant, and antiviral-related activities; however, its protective mechanisms in SALI and virus-associated inflammatory lung injury remain incompletely understood. In this study, an integrated strategy combining computational prediction and experimental validation was employed to investigate the therapeutic potential and underlying mechanisms of EL. The chemical constituents of EL were characterized by UPLC–Q–TOF/MS, followed by network pharmacology, molecular docking, and molecular dynamics analyses to predict key targets and signaling pathways. A cecal ligation and puncture (CLP)-induced SALI rat model was used to evaluate lung histopathology, pulmonary edema, cytokine production, and inflammatory signaling activation. In parallel, LPS-stimulated RAW264.7 macrophages were used to assess cytokine secretion and pathway regulation in vitro. In addition, a SARS-CoV-2 pseudovirus-induced mouse model was employed to further evaluate the in vivo relevance of the representative bioactive compound hyperoside in pseudovirus-associated lung injury. A total of 32 active compounds and 697 putative targets were identified, among which 116 were associated with sepsis and COVID-19. In vivo, EL markedly alleviated lung injury, reduced the lung coefficient and wet/dry ratio, and suppressed excessive production of proinflammatory cytokines and activation of key signaling proteins. In vitro, EL dose-dependently inhibited TNF-α and IL-6 secretion and regulated the PI3K–Akt and NF-κB signaling pathways. Notably, hyperoside showed favorable predicted interactions with PI3K–Akt pathway-related targets (EGFR, PI3K, and Akt), while molecular dynamics simulations supported stable interactions with several COVID-19-related targets, including ACE2, Mpro, and RdRp. Furthermore, hyperoside significantly alleviated SARS-CoV-2 pseudovirus-associated lung injury, reduced ACE2 protein expression, and downregulated EGFR, PI3K, and Akt mRNA levels in vivo. Collectively, these findings indicate that EL exerts protective effects through multi-component, multi-target, and multi-pathway mechanisms, and support its potential value for further investigation in SALI and virus-associated inflammatory lung injury. Full article

Background: Liquid biopsy using circulating tumor DNA (ctDNA) is rapidly reshaping gastrointestinal (GI) oncology. The highest-impact applications are molecular residual disease (mRD) detection after curative-intent therapy and early recognition of progression or resistance during systemic treatment. Methods: We performed a structured, clinically oriented narrative synthesis by using explicit search, eligibility, evidence prioritization, and clinical interpretation rules, integrating landmark prospective cohorts, randomized ctDNA-guided strategy trials where available, meta-analyses, key methodological research (e.g., pre-analytics, assay design, and clonal hematopoiesis (CH)/clonal hematopoiesis of indeterminate potential (CHIP)), and selected trial registries. Results: In resected colorectal cancer (CRC), postoperative ctDNA positivity is among the strongest known biomarkers of recurrence risk; large prospective studies demonstrate clear separation of disease-free survival (DFS)/overall survival (OS) between mRD+ and mRD− patients. In stage II colon cancer, randomized data (DYNAMIC) show that a ctDNA-guided strategy reduces adjuvant chemotherapy exposure without compromising long-term outcomes. In metastatic CRC, ctDNA supports early response monitoring and resistance tracking; ctDNA-selected anti-EGFR rechallenge provides a model of biomarker-driven actionability (CHRONOS). In gastroesophageal cancers, longitudinal ctDNA dynamics correlate with relapse risk and treatment efficacy, and in esophageal squamous cell carcinoma, ctDNA after neoadjuvant chemoradiotherapy informs residual disease risk and adjuvant stratification. In pancreatic ductal adenocarcinoma and hepatobiliary malignancies, sensitivity is constrained by low shedding and background cell-free DNA (cfDNA), yet ctDNA positivity remains clinically meaningful, and emerging data in resected extrahepatic cholangiocarcinoma (STAMP-linked analyses) show that ctDNA dynamics during adjuvant therapy predict recurrence. Conclusions: ctDNA is a clinically validated biomarker for mRD in CRC, whereas in other GI cancers, it remains a promising but methodologically heterogeneous tool whose clinical utility is tumor- and context-dependent. The next phase requires interventional trials demonstrating outcome improvement, harmonized sampling and reporting standards, and rigorous control of confounders (notably CH/CHIP). Full article

Background/Objectives: Fabry disease (FD) is a lysosomal storage disorder characterized by progressive renal and cardiac involvement and an increased burden of cardiovascular and cerebrovascular events. While cardiac magnetic resonance imaging (CMR) has significantly advanced structural assessment, circulating biomarkers reflecting disease-related cardiac manifestations remain incompletely understood. We therefore investigated adiponectin and leptin, two adipokines involved in inflammatory, metabolic, and fibrotic pathways, in relation to cardiac involvement and analyzed long-term lipid trajectories in FD. Methods: This longitudinal observational study included 49 patients with FD with 149 study visits. Circulating adiponectin, leptin, NT-proBNP, and conventional lipid parameters were assessed longitudinally and stratified by FD-specific therapy status and sex. Multivariable linear regression was performed to evaluate independent associations with log-transformed NT-proBNP values. Results: Adiponectin was positively associated with NT-proBNP, reflecting cardiac involvement, independent of age, sex, BMI, and eGFR (p < 0.001). Higher adiponectin levels were observed in patients with left ventricular hypertrophy or low T1 and those with fibrosis, detected by CMR (p = 0.009 and p < 0.001, respectively). This association was mainly seen in patients receiving FD-specific therapy, raising the question of whether this reflects underlying organ involvement or treatment effects. Leptin demonstrated weaker, inverse associations. Adiponectin, leptin, Triglycerides, total cholesterol, and HDL- and LDL-cholesterol levels remained stable over long-term follow-up, irrespective of FD-specific therapy or sex. Conclusions: In FD, adiponectin appears to be associated with cardiac involvement, and conventional lipid parameters remained unchanged over time. These findings suggest that alterations in adipokines, rather than progressive dyslipidemia, may reflect disease-related cardiac manifestations. Full article

Background: Ciltacabtagene autoleucel (cilta-cel) and idecabtagene vicleucel (ide-cel) have transformed the treatment landscape of relapsed/refractory multiple myeloma (RRMM). Given their recent regulatory approval and limited availability, mainly due to logistical issues, real-world data remain scarce. Methods: A retrospective study was conducted using the TriNetX database, identifying adult patients with RRMM treated with either cilta-cel or ide-cel. The clinical outcomes evaluated included overall survival (OS), progression-free survival (PFS), as well as the safety profile. Results: A total of 697 patients treated with cilta-cel and 575 with ide-cel were identified. The median age was 65 and 67 years, with ~16% being Black/African American. The 12-month OS was 89.6% for cilta-cel and 86.0% for ide-cel. In a descriptive subgroup analysis, renal impairment (eGFR < 60 mL/min/1.73 m²) seemed to be associated with significantly inferior OS in both cohorts (HR = 3.66, p < 0.001 for cilta-cel; HR = 1.73, p = 0.003 for ide-cel). Conversely, prior anti-CD38 exposure did not seem to impact survival in any of the two treatment groups. Any-grade CRS occurred in 45.9% (cilta-cel) and 41.8% (ide-cel), while any-grade ICANS was observed in 15.4% and 11.8%, respectively. Severe (grade ≥ 3) ICANS remained rare (<3%) in both cohorts. Hematologic toxicity was prevalent, with grade ≥ 3 neutropenia occurring in 76.0% (cilta-cel) and 68.0% (ide-cel). Notably, any-grade infections (28.5–40.1%) and hypogammaglobulinemia (41.1–43.1%) were frequent, highlighting a significant long-term immunosuppressive burden. Conclusions: In these real-world cohorts, both approved CAR T-cell therapies demonstrated favorable survival outcomes. While the incidence of severe hematologic and immune-related toxicities was high, these findings are compatible with published data from clinical trials and it seems that the clinical utility of these drugs overcomes the adverse safety profile. Full article

Metastatic colorectal cancer (mCRC) remains a major cause of cancer-related mortality worldwide. Advances in molecular profiling have transformed the therapeutic landscape, enabling biomarker-driven treatment strategies based on alterations in RAS, BRAF V600E, HER2 amplification, and mismatch repair status. Among these, dysregulation of the epidermal growth factor receptor (EGFR), BRAF, and HER2 signaling pathways represents a central driver of tumor progression and therapeutic resistance. Targeted agents directed against these pathways—including the anti-EGFR monoclonal antibody panitumumab, the selective BRAF inhibitor encorafenib, and the HER2-selective tyrosine kinase inhibitor tucatinib—have substantially expanded treatment options for molecularly defined subgroups of patients with mCRC. Anti-EGFR therapy remains a cornerstone of treatment for patients with RAS/BRAF wild-type, left-sided tumors. Panitumumab combined with chemotherapy has demonstrated significant improvements in response rates and overall survival compared with anti-angiogenic-based regimens in randomized clinical trials. For tumors harboring BRAF V600E mutations, which are associated with poor prognosis, combination strategies incorporating encorafenib with EGFR blockade have shown clinically meaningful survival benefits and represent an important therapeutic advance. In HER2-amplified colorectal cancer, HER2-targeted therapies have emerged as an effective treatment strategy. Trastuzumab-based combinations and HER2-selective tyrosine kinase inhibitors such as tucatinib have demonstrated durable responses and favorable safety profiles in heavily pretreated patients. This review summarizes current evidence from pivotal phase II and III clinical trials, translational studies, and real-world data evaluating EGFR-, BRAF-, and HER2-directed therapies in colorectal cancer. Particular emphasis is placed on biomarker-guided patient selection, mechanisms of resistance, and emerging combination strategies that continue to refine precision oncology approaches in mCRC. Full article

Background: Mindray BC-6800 Plus ^TM (Mindray, Shenzhen, China) measures reticulocyte counts and provides the reticulocyte hemoglobin (RHe, reticulocyte Hb expression) and mean reticulocyte volume (MRV). We studied the performance of those reticulocyte-derived parameters for the detection of iron-restricted erythropoiesis in older patients, compared with standard laboratory tests. Methods: A total of 220 anemic patients, age > 65 years, were recruited in the context of routine health controls. Group differences were assessed using analysis of variance (ANOVA), with p values < 0.05 considered statistically significant. Receiver operating characteristic (ROC) curve analysis was performed to assess the diagnostic performance of RHe and MRV for detecting iron-restricted erythropoiesis. The reference standard for iron deficiency was sTfR > 52 nmol/L. A multivariable logistic regression model was constructed for iron-restricted erythropoiesis, including MRV, Ret-He and s-ferritin as independent covariates, and adjusted for inflammatory status and renal function. Results: Overall, 30.1% in the group had IDA and 29.0% had mixed IDA/ACD, so 59.1% had absolute or functional iron deficiency, while 40.9% had adequate iron supply. RHe and MRV values differed significantly between both groups (p = 0.0001). For s-ferritin, ROC analysis yielded an AUC of 0.685 (95% CI 0.606–0.767), with the best Youden index at a cut-off of 100 µg/L, corresponding to 72.5% sensitivity and 65.9% specificity. An MRV cut-off of 97.4 fL identified iron-restricted erythropoiesis with 88.2% sensitivity and 82.7% specificity (AUC 0.878, 95% CI 0.799–0.957); RHe AUC 0.860, 95% CI 0.777–0.947; cut-off 30.4 pg; sensitivity 82.4%, specificity 79.8%). In multivariable logistic regression adjusted for CRP and eGFR, s-ferritin was not an independent predictor of iron-restricted erythropoiesis, whereas MRV and RHe remained significant. The overall model demonstrated good discrimination, with an AUC 0.808 (95% CI 0.804–0.814). Conclusions: RHe and MRV are reliable parameters for assessing iron supply to erythropoiesis in older patients and can assist in distinguishing iron-restricted erythropoiesis in complex, inflammation-driven settings. Full article

Targeted drug delivery (TDD), specifically through targeting ligand–drug conjugates, has reshaped oncology by enabling selective delivery of cytotoxic payloads to cancer cells while minimizing uptake by normal tissues. A key approach relies on exploiting overexpressed cell surface receptors (CSRs) to enable selective uptake of drug conjugates via receptor-mediated endocytosis. This review delineates four clinically validated CSRs (HER2, Trop-2, Nectin-4, and SSTR2) with several FDA-approved drug conjugates. Furthermore, emerging CSRs (EGFR, DLL3, and keratin 1) that may support next-generation TDD platforms for cancer treatment are also highlighted. We discuss how CSR type, density on cancer cells, and its mechanism of endocytosis, as well as the conjugate design for cellular uptake, tissue distribution, ligand size, and linker stability, collectively determine tumor drug accumulation and therapeutic efficacy. From representative examples, we elucidate the rationale for judicious refinement of these parameters, guiding the development of more potent ligands and drug conjugates to enhance the therapeutic efficacy of cytotoxic agents. Full article

Background: Recent advancements in heart failure (HF) therapy have significantly enhanced the management of patients across all phenotypes of left ventricular ejection fraction. However, these multidrug regimens frequently induce alterations in renal function by influencing intrarenal hemodynamics, thereby modifying glomerular capillary pressure. This phenomenon could result in a mild to moderate decline in estimated glomerular filtration rate (eGFR), often classified as “worsening kidney function.” This nomenclature stems from consistent observations of eGFR reductions recorded during HF treatment in clinical trials. This narrative review aims to elucidate why the observed eGFR declines in clinical practice may represent either loss of functioning glomeruli or pharmacologically mediated reductions in intraglomerular pressure that ultimately safeguards long-term renal and cardiovascular outcomes. Methods: By a comprehensive re-examination of data from HF clinical trials conducted with various classes of medications, all affecting eGFR, we sought to provide evidence that the decline in eGFR is associated with the activation of specific mechanisms that collectively contribute to a reduction in glomerular filtration pressure, a prominent factor in maladaptive neurohormonal responses. Results: From the investigation of angiotensin-converting enzyme inhibitors to the more recent non-steroidal mineralocorticoid receptor antagonist, the renal effects of these therapeutic regimens correlate with improvements in patient outcomes. The data consistently indicate that an early decline in eGFR, when coupled with an enhancement in HF outcomes, is associated with a more gradual decline in eGFR during long-term follow-up. Conclusions: Clinicians should recognize early declines in eGFR as indicators of favorable intraglomerular hemodynamic adjustments that mitigate maladaptive neurohormonal responses and contribute to improved long-term outcomes in patients with HF. Full article

Background: First-line chemoimmunotherapy (I + C) is the standard of care for advanced non-squamous non-small cell lung cancer (NSCLC) without oncogenic mutation. Bevacizumab has been shown to enhance the efficacy of chemotherapy in non-squamous NSCLC, yet its added value when combined with I + C (I + C + B) remains unclear. To address this gap, we conducted a real-world comparative study and a network meta-analysis to evaluate I + C + B versus I + C in this setting. Methods: This retrospective study included patients with advanced EGFR/ALK-negative non-squamous NSCLC treated with first-line I + C + B or I + C. Propensity score matching (PSM) was employed to balance baseline characteristics between groups. Efficacy endpoints were progression-free survival (PFS) and overall survival (OS). Subgroup analyses examined outcomes by PD-L1 expression, age, metastases, and chemotherapy, among other factors. In parallel, a network meta-analysis of four randomized trials (n = 2026) indirectly compared I + C + B against I + C for PFS, OS, and safety outcomes. Results: A total of 277 patients were included, with 167 (60.3%) receiving I + C + B and 110 (39.7%) receiving I + C. Before PSM, the I + C + B regimen significantly prolonged PFS versus I + C (hazard ratio [HR] = 0.69, 95% CI 0.52–0.92, p = 0.010), with this benefit maintaining post-matching (HR = 0.70, 95% CI 0.49–0.99, p = 0.045). However, OS did not differ significantly between groups in either the pre-PSM (HR = 0.93, 95% CI: 0.67–1.30; p = 0.665) or matched analyses (HR = 0.84, 95% CI: 0.54–1.29; p = 0.421). Subgroup analyses suggested greater PFS benefit from I + C + B among PD-L1-negative, older patients, those with brain metastases or multiple metastatic sites, and in patients receiving specific chemotherapy doublets. The network meta-analysis confirmed a PFS advantage for I + C + B over I + C (HR = 0.84, 95% CI: 0.71–0.98) without an OS benefit (HR = 0.95, 95% CI: 0.79–1.14). Toxicity was higher with I + C + B; rates of grade 3–5 adverse events, serious adverse events, and treatment discontinuation were all significantly increased compared to I + C. Conclusions: In the first-line treatment of advanced EGFR/ALK-negative non-squamous NSCLC, adding bevacizumab to I + C improved PFS but did not translate into an OS gain. Although PFS benefits were observed in certain subgroups, these were accompanied by significantly increased treatment-related toxicities. Our findings suggest that no clear subgroup has been identified where the benefit outweighs the risks, necessitating extreme clinical caution. Full article

Before the American Heart Association introduced the cardiovascular–kidney–metabolic (CKM) syndrome concept in 2023, clinical care was largely organ-specific. This retrospective study analyzed diagnostic patterns and gaps in 406 patients with hypertension referred to and evaluated at the University Hospital Basel Hypertension Centre in 2017, 2019, or 2022 to identify blind spots in the assessment of cardio–kidney–liver–metabolic health. Electronic health records were used to assess CKM-relevant diagnostics, including lipid profiles, N-terminal pro-B-type natriuretic peptide (NT-proBNP), echocardiography, kidney function (estimated glomerular filtration rate: eGFR, urinary albumin-to-creatinine ratio: uACR), and hepatic assessment (Fib-4 score, abdominal ultrasound). Previously undetected conditions were identified according to contemporary criteria for dyslipidemia, chronic kidney disease (CKD), suspected heart failure (HF), diabetes, and suspected metabolic dysfunction-associated steatotic liver disease (MASLD). Although 94% of participants had laboratory data, key CKM parameters were inconsistently assessed. Of the participants, 39% had neither NT-proBNP measurement nor echocardiography, and 27% lacked hepatic ultrasound or sufficient data for Fib-4 calculation. Previously unrecognized comorbidities were common (suspected HF 21%, CKD 6%, suspected MASLD 3%). Lipoprotein(a) testing increased from 0% in 2017 to 23.7% in 2022, indicating growing awareness. Despite specialized care, diagnostic fragmentation persisted, underlining the need for systematic, interdisciplinary screening and informing the design of prospective registries such as the Swiss CKLM Registry to integrate patient-centered cardio–kidney–liver–metabolic care. Full article

Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer deaths, with resistance to targeted therapies posing a major clinical challenge. Drug-tolerant persister (DTP) cells are key contributors to resistance, and targeting them offers new strategies to enhance existing treatments. MicroRNAs (miRNAs), particularly the tumour-suppressive miR-15/107 family, offer promise due to their ability to target multiple oncogenic pathways. This study evaluated a synthetic consensus miRNA mimic, conmiR-15/107, in NSCLC cell line models. Dose–response assays showed robust, dose-dependent growth inhibition in both EGFR-mutant (PC9) and KRAS-mutant (H358 and A549) lung adenocarcinoma cells, but not in the human bronchial epithelial cell line BEAS-2B. When combined with EGFR inhibitors (osimertinib and gefitinib) in PC9 cells, the mimics showed a higher rate of growth inhibition compared with the controls and reduced IC₅₀ values. Similarly, conmiR-15/107 enhanced growth inhibition by the KRAS inhibitors sotorasib and adagrasib in H358 cells. RT-qPCR confirmed downregulation of conmiR-15/107 targets, including MEK1, BCL2 and BRCA1, suggesting a multi-target mechanism of action. Long-term assays showed that the mimics reduced the survival and delayed the proliferation of DTPs in osimertinib-treated PC9 cells as well as sotorasib-treated H358 cells. These findings support conmiR-15/107 as a potential adjunct to targeted therapy, capable of enhancing treatment efficacy and delaying resistance in lung adenocarcinoma. Full article

Introduction/Objectives: Body composition changes and diet quality may contribute to metabolic complications and graft outcomes after kidney transplantation. We evaluated the relationships between diet quality and CT-derived body composition components (skeletal muscle mass, muscle quality/myosteatosis, and visceral adiposity) and explored their associations with metabolic markers and graft function. Materials and Methods: In this single-center retrospective cross-sectional study, we included 161 adult first kidney transplant recipients (KTRs) with a functioning graft and ≥12 months of follow-up. Body composition was quantified on routine abdominal CT at the L3 level using skeletal muscle index (SMI), mean muscle attenuation (Hounsfield units) for myosteatosis, and visceral adipose tissue area (VAT). Diet quality was scored using the Revised Diet Quality Index (DQI-R). Graft function was followed with creatinine-based estimated glomerular filtration rate (eGFR) calculated by the CKD-EPI equation. Results: Mean age was 45.7 ± 13.2 years and 58% were men. The prevalence of low muscle mass was 26.0%, myosteatosis 73.5%, and visceral obesity (VAT ≥ 100 cm²) 45.6%. No participant had “good” diet quality; 48.4% had poor diet quality. DQI-R showed a weak positive correlation with SMI (r = 0.157; p = 0.047) but was not significantly related to VAT, subcutaneous adipose tissue (SAT), Kidney transplant recipient (VSR) or myosteatosis. In multivariable models, age and VAT were associated with HbA1c, whereas body composition and diet quality variables were not independent predictors of eGFR. Myosteatosis was independently associated with older age. Conclusions: Visceral adiposity and impaired muscle quality frequently clustered and were linked to metabolic status. These findings support post-transplant follow-up strategies that go beyond BMI and integrate body composition and nutritional assessment within a multidisciplinary care model. Full article

Background: In patients with diabetes or hypertension, if appropriate intervention is not initiated early in the course of kidney disease, not only does the risk of progressing to end-stage renal failure increase, but mortality associated with vascular complications also rises as the disease progresses; therefore, there is an urgent need to develop urinary biomarkers that enable early diagnosis and prediction of disease progression. Methods: This two-year prospective observational study involved 185 outpatients. Patients were classified into two groups based on their baseline urinary L-FABP levels relative to the reference value of 8.4 μg/g·Cr at the start of the study. The rate of eGFR decline during the observation period was evaluated. Results: The results showed an interaction (synergistic effect) between urinary L-FABP and time in patients with diabetes or hypertension who had an eGFR of at least 60 mL/min/1.732 m²/kg/1.732 m². Patients with high urinary L-FABP levels (>8.4 μg/g·Cr) exhibited a notably faster eGFR decline compared with those with low levels (≤8.4 μg/g·Cr). This finding suggests the potential of urinary L-FABP as a predictor of renal function decline; we evaluated this utility using the area under the ROC curve (AUC) and logistic regression analysis. The results indicate that urinary L-FABP holds potential as a predictor of renal function decline in diabetic or hypertensive patients with preserved eGFR. Conclusions: Among the analysis groups in which the validation was conducted, it was demonstrated that urinary L-FABP holds potential as a predictor of renal function decline in patients with diabetes or hypertension who have a maintained eGFR. Given that urinary L-FABP is thought to reflect tubulointerstitial damage associated with renal microcirculatory impairment, its future utility as a urinary biomarker for the early diagnosis and prognosis of chronic kidney disease (CKD) is anticipated. Full article