Search Results (428)

Peripheral arterial disease (PAD) is a major cardiovascular complication of hemodialysis (HD), during which inflammation and oxidative stress contribute to vascular injury. The role of spermine oxidase (SMOX), a polyamine-metabolizing enzyme generating hydrogen peroxide, in PAD is unknown in HD. This cross-sectional study included 142 patients on maintenance HD, including 115 with a normal ankle–brachial index (ABI) (≥0.9) and 27 with a low ABI (<0.9). Patients with a low ABI were older and had lower creatinine and albumin levels, fractional clearance index for urea, and urea reduction ratio but higher levels of glucose, C-reactive protein (CRP), and SMOX; diabetes mellitus was also more prevalent (p < 0.05 for all). In Firth-penalized multivariable logistic regression, SMOX (adjusted odds ratio [aOR] per 1 ng/mL increase, 1.063; 95% confidence interval [CI], 1.018–1.115; p = 0.001) and CRP (aOR per 0.1 mg/dL increase, 1.181; 95% CI, 1.079–1.321; p < 0.001) were independently associated with ABI-defined PAD. Conventional and penalized sensitivity analyses yielded similar estimates. The areas under the curve for SMOX and CRP were 0.790 and 0.804, respectively. SMOX was inversely correlated with bilateral ABI and positively correlated with CRP. SMOX may represent a candidate biomarker associated with ABI-defined PAD in patients undergoing HD, although further validation in larger prospective cohorts is required. Full article

Chronic kidney disease (CKD) is characterized by progressive renal dysfunction and endothelial injury. Thrombomodulin (TM), encoded by the THBD gene, is released into the circulation as soluble TM (sTM) following endothelial damage; however, its clinical significance in CKD remains unclear. To address this question, public bulk and single-cell transcriptomic datasets were analyzed to characterize THBD expression and cellular localization in kidney injury, and a retrospective cohort of 278 hospitalized patients was used to evaluate circulating sTM levels across CKD stages and their associations with renal function, coagulation, and cardiac biomarkers. The transcriptomic analyses showed that THBD was upregulated in injured kidneys, positively correlated with a fibrosis-related transcriptional signature, and predominantly expressed in renal endothelial cells. Consistent with these findings, circulating sTM was elevated as early as stage 1 CKD and increased progressively with advancing disease stage. Higher sTM levels were positively associated with serum creatinine, serum urea, and urinary albumin-to-creatinine ratio (UACR), and inversely associated with estimated glomerular filtration rate (eGFR). In addition, sTM showed weak-to-modest associations with coagulation, fibrinolytic, and cardiac biomarkers. Multivariable analysis showed that eGFR remained independently associated with log-transformed sTM after adjustment for major clinical covariates (β = −0.0116, 95% CI −0.0141 to −0.0090, p < 0.001). ROC analysis showed that sTM discriminated CKD from non-CKD (AUC = 0.971) and early-stage CKD from non-CKD (AUC = 0.854), outperforming eGFR (AUC 0.920 and 0.565, respectively) and performing comparably to UACR. Collectively, these findings support sTM as a candidate biomarker associated with CKD severity whose interpretation should integrate endothelial injury and reduced renal elimination and prospective validation is warranted. Full article

Background: Contemporary management of type 2 diabetes mellitus (T2DM) extends beyond glycemic control and requires comprehensive assessment of cardiovascular, renal, metabolic, and anthropometric factors. Nevertheless, clinical status is often summarized predominantly by glycated hemoglobin (HbA1c), potentially overlooking concurrent non-glycemic abnormalities. This study evaluated the prevalence and coexistence of cardiorenal-metabolic abnormalities among patients with HbA1c <7.0% at six months. Methods: This retrospective observational study included adults with T2DM routinely followed in a specialized outpatient diabetes clinic. The primary descriptive analysis included participants with HbA1c <7.0% at the six-month assessment (T1). Seven non-glycemic cardiorenal-metabolic domains were evaluated at T1: LDL cholesterol, HDL cholesterol, triglycerides, body mass index, blood pressure, estimated glomerular filtration rate, and urinary albumin-to-creatinine ratio. An unweighted descriptive count of domains outside study-defined analytical thresholds was calculated (range, 0–7). An exploratory Poisson regression model examined associations between selected baseline characteristics and the number of affected domains, excluding baseline variables that directly corresponded to components of the T1 count to minimize mathematical coupling. Results: Among 809 participants, 385 (47.6%) had HbA1c <7.0% at six months and were included in the primary descriptive analysis. Concurrent non-glycemic abnormalities were common, particularly for blood pressure, LDL cholesterol, triglycerides, body mass index, and HDL cholesterol. The median number of domains outside study-defined analytical thresholds was three (IQR 3–4), and only three participants (0.8%) had values within all seven thresholds. In the exploratory multivariable model, none of the evaluated demographic, glycemic, or treatment-related baseline characteristics was independently associated with the number of domains outside study-defined thresholds. Conclusions: HbA1c <7.0% at six months did not necessarily coincide with favorable values across other clinically relevant cardiovascular, metabolic, anthropometric, and kidney-related domains in patients with T2DM. The unweighted domain count provides a descriptive summary of concurrent non-glycemic abnormalities but should not be interpreted as a validated measure of risk, prognosis, or clinical risk stratification. These findings support comprehensive, individualized assessment beyond glycemic status alone. Full article

Albuminuria is routinely used to assess kidney damage in diabetes, but it also conveys cardiovascular risk across the urinary albumin-to-creatinine ratio (UACR) distribution, including within A1. Whether sex modifies this relationship remains uncertain. This narrative review prioritizes longitudinal studies in type 2 diabetes mellitus (T2DM), analyses within A1 particularly, and distinguishes this direct evidence from the general population or chronic kidney disease cohorts, surrogate-endpoint studies, and experimental mechanisms. A few studies report formal sex-by-UACR interactions for selected outcomes, including mortality in broad kidney-disease populations and heart failure in diabetes. Many other apparent differences derive only from sex-stratified analyses and therefore do not establish effect modification. Differences in urinary creatinine excretion, body composition, hormonal exposure, kidney injury pathways, cardiovascular phenotype, and health-care ascertainment may alter the observed association, but most mechanistic evidence is indirect. Current evidence supports UACR as a continuous prognostic marker in both sexes but does not justify sex-specific diagnostic cut-offs, therapeutic thresholds, or response targets. UACR should be measured systematically, confirmed when abnormal or borderline, preferably repeated under standardized conditions, and interpreted with eGFR and the overall cardiovascular risk profile. Sex may provide additional clinical context; treatment should continue to follow guideline-based indications. Full article

Loss of renal function is associated with premature aging of the immune system; however, earlier studies on this topic enrolled patients with reduced GFR and did not distinguish between those with or without proteinuria. Clinical observations suggest that proteinuria alone might also impair immune defense. It is thus an open question whether patients with a urinary albumin-to-creatinine ratio > 300 mg/g (severe albuminuria) independent of their eGFR have an inflammatory risk profile and a disturbed adaptive immune response. This cross-sectional study included 25 patients with severe albuminuria (uACR > 300 mg/g; P-Group), 19 patients with an eGFR < 60 mL/min 1.73 m2 and a uACR < 300 mg/g (G-Group), and 30 patients with adequate kidney function (C-group). All three cohorts have a similar cardiovascular background with arterial hypertension and coronary artery disease. PBMCs from the patients were challenged with the superantigen Staphylococcal enterotoxin B (SEB) as well as with CMV- and SARS-CoV-2-specific antigens. Monocyte subsets and CD86 and HLA-DR expression were determined through flow cytometry. Transcripts of CD28 and IFN-α and -γ were measured by qPCR. Compared to those in the C-group, patients in the G-group showed a higher polyclonal SEB response and had significantly elevated circulating numbers of inflammatory monocytes (subset CD14++CD16+). CD28 transcripts were decreased in the P-group and G-group compared to the C-group, reaching significance for the G-Group. The CMV- and SARS-CoV-2-specific immune response, as measured by the frequency of CD4+69+137+ T and CD8+69+137+ T cells, was comparable in all three groups. Severe albuminuria per se does not alter the antigen-specific immune response; however, patients with reduced GFR, but not those with proteinuria, show inflammatory and polyclonal immune activation. Full article

Background/Objectives: Abnormal nocturnal dipping (ND) in diabetes mellitus is linked to adverse outcomes. Its association with vitamin D (VD), cardiovascular autonomic neuropathy (CAN), and diabetic kidney disease (DKD) remains unclear. We aim to evaluate the association of VD status with ND loss as well as CAN in type 2 diabetes mellitus (T2DM) across different DKD stages. Methods: 83 T2DM patients were included in this cross-sectional study: 36 with early-stage DKD (urine albumin-to-creatinine ratio [UACR] 30–299 mg/g; Group 1) as well as 47 with advanced-stage DKD (UACR ≥ 300 mg/g; Group 2). Results: Patients with advanced DKD exhibited higher CAN prevalence (72.70% vs. 52.80%; p < 0.05), lower 25(OH)D (26.90 ± 9.90 vs. 29.60 ± 8.00 ng/mL; p = 0.05), and lower systolic ND (0.82 ± 8.40 vs. 4.50 ± 7%; p < 0.05). Among patients with advanced DKD, lower 25(OH)D levels, classified according to the Institute of Medicine (IOM) criteria (normal ≥ 20 ng/mL), were associated with reduced systolic ND (1.90 ± 7.80 vs. −5.60 ± 9.30%; p < 0.05), while the Endocrine Society criteria showed a progressive reduction in systolic ND across VD classification (insufficiency 20–29.9, deficiency <20, and sufficiency ≥30 ng/mL), (−5.60 ± 9.30 vs. −0.20 ± 7.30 vs. 3.30 ± 8%, respectively; p < 0.05). Patients with definite/severe CAN exhibited lower systolic ND (−4.38 ± 7.41 vs. 3.34 ± 8.00%; p < 0.01) than those with absent/early CAN. In addition, lower VD levels were associated with greater CAN severity according to both the Endocrine Society criteria (p < 0.01, r = 0.40), and the IOM criteria (p < 0.05, r = 0.30). In the regression model, VD remained an independent predictor of absence of diastolic ND (Rsqr = 0.393; p < 0.05). Conclusions: These findings suggest a potential link between vitamin D status, autonomic dysfunction, and ND in patients with T2DM and advanced DKD. Full article

Chronic kidney disease (CKD) requires assessment of both glomerular filtration and kidney damage, particularly albuminuria, for diagnosis, risk stratification, and longitudinal care. Point-of-care testing (POCT) can shorten turnaround time and improve access when conventional laboratory testing is unavailable or would delay a clinical pathway. This narrative review summarizes established and emerging POCT approaches for kidney assessment in CKD, with emphasis on creatinine/eGFR and urine albumin-to-creatinine ratio (UACR), and distinguishes analytical validity from workflow utility and patient-level clinical utility. Evidence is strongest for rapid creatinine measurement in selected workflows, especially pre-imaging assessment and decentralized screening, while quantitative/semiquantitative UACR POCT can support CKD detection when abnormal results are appropriately confirmed. Cystatin C microfluidic systems remain investigational, and kidney injury/stress or molecular biomarkers such as NGAL, KIM-1, L-FABP, [TIMP-2]·[IGFBP7], extracellular vesicles, and microRNAs should be regarded primarily as a research horizon rather than direct measures of GFR. Important implementation requirements include assay-specific validation, calibration traceability, quality assurance, recognition of biological and analytical interference, and confirmation of results near major clinical decision thresholds. Evidence that POCT improves long-term CKD outcomes, safety, adherence, or cost-effectiveness remains limited. Future studies should prioritize prospective clinical utility, implementation, cost-effectiveness, home-use validation, and patient-centered outcomes. Full article

Background: Type 2 diabetes mellitus (T2DM) is clinically heterogeneous, and routinely available renal, inflammatory, and hepatic measures may add information beyond glycemic assessment. Methods: Among 811 screened adults, 809 had a standardized baseline assessment and six-month follow-up; two were excluded because a required baseline clustering variable was missing, leaving 807 complete cases for phenotype derivation. Twelve-month data were available for 320 participants. Nine baseline variables were standardized, with UACR and CRP analyzed after ln(x + 1) transformation. Candidate two- to six-cluster solutions were assessed using silhouette, Calinski–Harabasz, and Davies–Bouldin indices, 200 bootstrap resamples, and a consistent-transformation sensitivity analysis. Longitudinal outcomes were evaluated using generalized estimating equations including time, phenotype, and their interaction. Results: The final stored four-cluster solution comprised a comparatively favorable-profile phenotype (n = 294), a cardiorenal–fibrotic phenotype (n = 239), an inflammatory–metabolic phenotype (n = 141), and a severe hyperglycemic–obesity phenotype (n = 133). Internal separation was modest (silhouette 0.118; Calinski–Harabasz 87.6; Davies–Bouldin 2.118), bootstrap agreement was moderate (median adjusted Rand index 0.445), and the consistent ln(x + 1) sensitivity solution showed substantial agreement with the stored assignment (adjusted Rand index 0.776). Significant phenotype-by-time interactions were observed for HbA1c, BMI, TyG, triglycerides, UACR, eGFR, FIB-4, and CRP after false-discovery-rate correction, but not for LDL cholesterol. Baseline characteristics did not differ detectably between participants with and without twelve-month follow-up after correction. Marked treatment changes occurred by T2, particularly increased use of GLP-1 receptor agonists and SGLT2 inhibitors. Conclusions: The four phenotypes provide an exploratory multidimensional description of this cohort. Longitudinal differences should not be attributed to phenotype biology alone because regression to the mean and treatment intensification are plausible contributors; external validation remains necessary. Full article

Background/Objectives: Inflammation contributes to atherosclerotic progression and may intensify after percutaneous coronary intervention (PCI). In stable coronary artery disease (CAD), whether post-procedural inflammation is prognostically distinct from baseline inflammatory status and post-procedural renal function remains unclear. Methods: We studied 496 consecutive patients with stable CAD undergoing elective PCI. The primary outcome was a composite of death, myocardial infarction, stroke, or repeat revascularization. Post-PCI high-sensitivity C-reactive protein (hs-CRP) and creatinine were measured 18–24 h after PCI. Multivariable Cox models used clinically prespecified covariates, with hs-CRP log-transformed (hazard ratio [HR] per doubling) and additionally adjusted for its pre-PCI level; discrimination was assessed by ROC analysis with bootstrap internal validation. Results: The endpoint occurred in 43 patients (8.7%) over a median follow-up of 10 months. Post-PCI hs-CRP was independently associated with the endpoint after adjustment for pre-PCI hs-CRP, post-PCI creatinine, and albumin (HR 1.43 per doubling, 95% CI 1.05–1.96, p = 0.025), and after further adjustment for angiographic and procedural characteristics (HR 1.54, p = 0.008); pre-PCI hs-CRP was not independent (p = 0.083). Post-PCI creatinine was independently associated in every model (HR 1.16 per 0.1 mg/dL, p = 0.001) and identified a largely non-overlapping high-risk group. Conclusions: After elective PCI in stable CAD, post-PCI hs-CRP was independently associated with adverse outcomes and provided prognostic information beyond baseline hs-CRP and procedural characteristics in the fitted models, rather than merely reflecting baseline inflammatory status. Post-PCI renal function was a complementary, largely independent risk signal. Full article

Objectives: Individuals with type 2 diabetes (T2D) remain at high cardiovascular disease (CVD) risk. The pan-immune-inflammation value (PIV) integrates circulating neutrophils, monocytes, platelets, and lymphocytes but does not capture albumin-related nutritional and inflammatory reserve. We investigated associations between the PIV-to-albumin ratio (PIVA) and incident CVD, cardiovascular mortality, and disease progression in individuals with T2D. Methods: This prospective study included 15,355 UK Biobank participants with T2D and no baseline CVD. PIVA was calculated from peripheral blood cell counts and serum albumin and was natural log-transformed. Fine–Gray competing-risk and cause-specific Cox models were used to evaluate incident CVD and cardiovascular mortality. Multi-state models characterized transitions from T2D to CVD and death. We also examined nonlinear associations, renal biomarker mediation, joint associations with the CVD polygenic risk score and triglyceride–glucose index, sensitivity analyses, and external validation of cardiovascular mortality in the National Health and Nutrition Examination Survey. Results: During median follow-ups of 12.94 years for incident CVD and 14.49 years for cardiovascular mortality, 4829 incident CVD events and 514 cardiovascular deaths occurred. Each 1-unit increase in lnPIVA was associated with higher risks of incident CVD (subdistribution hazard ratio [sHR], 1.140; 95% confidence interval [CI], 1.088–1.194) and cardiovascular mortality (sHR, 1.449; 95% CI, 1.247–1.684). Associations were nonlinear. Higher lnPIVA was also associated with transitions from T2D to CVD, from T2D directly to cardiovascular death, and from incident CVD to cardiovascular death. Cystatin C explained a larger proportion of these associations than creatinine. Elevated lnPIVA identified excess cardiovascular risk across strata of genetic susceptibility and insulin resistance, and the findings were generally supported by sensitivity and external validation analyses. Conclusions: lnPIVA was associated with incident CVD, cardiovascular mortality, and adverse cardiovascular transitions in individuals with T2D. As an immune-inflammatory and albumin-based index, PIVA may help identify high-risk individuals beyond conventional cardiometabolic and genetic risk profiles. Full article

Background/Objectives: The study aimed to investigate the significance of laboratory biomarkers, particularly the lactate-to-hemoglobin ratio at admission in predicting 30-day mortality in patients with acute upper gastrointestinal bleeding (UGIB). Methods: Patients who presented to the emergency department due to acute UGIB between January and December 2024 were included in the study. The laboratory parameters at the time of admission, medication usage, endoscopic diagnoses, and 30-day mortality rates of the patients were investigated. It was investigated whether there were differences in biochemical parameters such as hemoglobin, hematocrit, neutrophil, lymphocyte, platelet, international normalized ratio (INR), pH, lactate, blood urea nitrogen (BUN), creatinine, C-reactive protein (CRP), albumin, BUN to creatinine ratio, and lactate to hemoglobin ratio between patients with and without 30-day mortality. In addition, the relationship between mortality, drug use, and endoscopic diagnoses was examined. Results: A total of 241 patients participated in the study. Of the participants in the study, 79 (32.8%) were women and 162 (67.2%) were men. The average age of the patients was 70 years. The most common causes of bleeding were, in order, bulbar ulcer (n = 84, 34.9%) and gastric ulcer (n = 79, 32.8%). A total of 15 (6.2%) patients developed mortality within 30 days. In the mortality group, lymphocyte (p = 0.016) and albumin (p = 0.026) values were statistically low, while INR (p = 0.041), creatinine (p = 0.020), CRP (p < 0.01), lactate (p = 0.014) and lactate to Hb ratio (LHR) (p = 0.012) values were significantly high. In cases of bleeding due to malignancy, mortality was higher. No association was found between medication use and mortality. Conclusions: In this exploratory study, the LHR showed potential as an adjunctive biomarker for estimating 30-day mortality in patients with non-variceal acute UGIB. It can be readily calculated based on common laboratory values, does not necessitate complex scoring systems, and can help with quick risk assessment in emergency conditions. Large, multicenter prospective studies are required to confirm prediction accuracy as well as identify optimum cutoff values for clinical application. Full article

This study evaluated graded dietary doses of Saccharomyces cerevisiae postbiotic (0, 1.25, 2.5 and 5 g kg⁻¹) on growth, feed utilization, serum biochemistry, expression of IGF-1, SOD2, IL-1β, IL-10 and IgM, and resistance to Fusarium oxysporum in Nile tilapia (Oreochromis niloticus; 35.1 ± 0.9 g) after 30 and 60 days of feeding. Although the 5 g Kg⁻¹ inclusion significantly increased WG (59.4 ± 0.9) and SGR (1.5 ± 0.0) and decreased FCR (0.8 ± 0.0), significant positive effects on multiple endpoints were also recorded at 1.25 and 2.5 g/kg. Serum total protein and globulin rose with increasing dose and feeding duration, while albumin showed limited change, lowering the A/G ratio. AST remained unchanged. Creatinine and glucose declined with postbiotic supplementation; the glucose reduction effect was dose-dependent, whereas creatinine was unaffected by feeding duration. The highest gene expression of hepatic IGF-1, SOD2, IL-1β, and IL-10 and splenic IL-1β, IL-10, and IgM was in T3 at both checkpoints; however, the highest gene expression of intestinal IL-1β, IL-10, and IgM expression was in T1 at both time points. The pathogenicity experiment showed a significant survival against F. oxysporum (p < 0.0001) compared to controls. The results suggested that dietary S. cerevisiae postbiotic improved growth, biochemical and molecular responses, and survival of Nile tilapia against F. oxysporum. Full article

Background/Objectives: Type 2 diabetes (T2D) is a major risk factor for cardiovascular disease and chronic kidney disease (CKD), yet the extent of longitudinal CKD screening in routine clinical practice remains unclear. This study aimed to assess long-term cardiorenal outcomes and CKD screening practices in patients with T2D managed across primary care and endocrinology settings, evaluating the feasibility of risk stratification in real-world practice. Methods: We conducted a retrospective cohort study using anonymized data from the Telotrón database (2.2 million patients). Adults with T2D attended across primary and endocrinology care were followed from 1 January 2018 to 31 December 2022. Frequency of estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) measurements, and cumulative proportion of kidney and cardiovascular events, hospitalizations, and mortality were assessed. Results: Among 13,600 individuals, 31.1% experienced a kidney event and 18.6% a cardiovascular event over 5 years. All-cause hospitalization occurred in 24.9% and 16.1% died. First occurrence of an abnormal eGFR or UACR measurement occurred in 37.0% of participants without baseline CKD, and 45.4% with baseline CKD showed progression. Annual monitoring was limited, with 39.1% and 16.6% undergoing at least one yearly assessment, and 2.9 and 1.5 mean number of measurements per patient for eGFR and UACR, respectively. Conclusions: Despite receiving endocrinology care, kidney disease progression and cardiovascular events remain a major concern in T2D, and yet suboptimal albuminuria and eGFR assessment limit early detection and risk stratification, thereby hindering risk-directed management. Full article

Background/Objectives: DEFA3 and DEFA5 are alpha-defensins, which are small cationic antimicrobial peptides that are part of the innate immune system. DEFA3 encodes human neutrophil peptide-3 (HNP-3), primarily expressed in neutrophils, while DEFA5 encodes human defensin-5 (HD-5), predominantly expressed in Paneth cells of the small intestine. Both defensins show elevated levels in diabetes and are strongly associated with diabetic nephropathy, with the highest concentrations found in patients with this complication. We evaluated serum levels of DEFA3 and DEFA5 in 160 participants (93 patients with T2DM and 67 controls without carbohydrate disturbances) and their associations with diabetic nephropathy, as well as peripheral and cardiac autonomic neuropathy and anthropometric and metabolic parameters. Methods: This was a monocentric, cross-sectional, observational study conducted at the Endocrinology and Metabolic Disorders Clinic of Alexandrovska Hospital in Sofia. Main methods included detailed clinical and anthropometric assessments, diagnosis of peripheral neuropathy via the Neuropathy Disability Score (NDS), evaluation of cardiac autonomic neuropathy using heart rate variability analysis and Ewing cardiovascular reflex tests, comprehensive laboratory investigations with fasting blood samples, and measurement of serum DEFA3 and DEFA5 levels by ELISA kits. Results: Serum DEFA3 and DEFA5 levels did not differ significantly between patients with T2DM and controls without carbohydrate disturbances, nor by sex or menopausal status. Patients with diabetic nephropathy showed significantly higher levels of both DEFA3 (345.7 ± 77.9 pg/mL vs. 299.2 ± 100.3 pg/mL; p = 0.042) and DEFA5 (5.3 ± 10.1 pg/mL vs. 2.9 ± 2.9 pg/mL; p = 0.044). DEFA5 levels were also elevated in participants with increased albumin-to-creatinine ratio (4.9 ± 9.9 pg/mL vs. 2.2 ± 1.5 pg/mL; p = 0.043). No significant differences were observed in patients with peripheral neuropathy, cardiac autonomic neuropathy, retinopathy, or macroangiopathy, although a non-significant trend toward higher values was noted. DEFA3 demonstrated moderate discriminatory ability for diabetic nephropathy (AUC = 0.641; p = 0.037), superior to DEFA5 (AUC = 0.570; p = 0.303). DEFA3 showed multiple weak positive correlations with diabetes duration, body weight, BMI, total and LDL-cholesterol, serum creatinine, and uric acid, while DEFA5 correlated only with total cholesterol. Conclusions: Circulating DEFA3 and DEFA5 are associated with diabetic nephropathy and selected metabolic and renal parameters in patients with type 2 diabetes, with DEFA3 showing moderate discriminatory capacity. The associations were largely attenuated after covariate adjustment, suggesting that these alpha-defensins likely reflect downstream innate immune activation and renal stress rather than acting as independent drivers of complications. Full article

Background: Chronic kidney disease (CKD) is highly prevalent in older adults, yet distinguishing pathological CKD from age-related decline in kidney function remains challenging. KDIGO guidelines recommend combined assessment of estimated glomerular filtration rate (eGFR) and urinary albumin-to-creatinine ratio (uACR), but implementation in primary care is uncertain. We evaluated CKD screening patterns, KDIGO risk categories, and the prognostic value of eGFR and albuminuria for all-cause mortality in adults aged ≥75 years. Methods: We conducted a retrospective population-based cohort study of 587,603 community-dwelling adults aged ≥75 years using Primary Care electronic records. Complete CKD screening was defined as at least two eGFR and two uACR measurements ≥ 3 months apart during 2015–2019. CKD prevalence, KDIGO risk categories, and 40-month all-cause mortality were assessed. Multivariable Cox regression models evaluated the independent and joint associations of eGFR and albuminuria with mortality. Results: Only 19.0% of participants underwent complete KDIGO-recommended screening, mainly because of limited albuminuria testing. Among screened individuals, CKD prevalence was 25.7%, with over half classified as high or very high KDIGO risk. Mortality increased progressively with declining eGFR, increasing albuminuria, and worsening KDIGO risk. Macroalbuminuria (HR 1.87, 95% CI 1.75–2.00) and eGFR < 30 mL/min/1.73 m² (HR 1.91, 95% CI 1.79–2.04) were independently associated with mortality. Conclusions: Complete KDIGO-recommended screening was performed in only one in five adults aged ≥75 years, identifying a major implementation gap in primary care. Albuminuria provided prognostic information beyond eGFR, improving identification of older adults at highest risk of death. These findings support systematic combined eGFR–uACR assessment to improve risk stratification, guide kidney-protective management, and inform healthcare planning for ageing populations. Full article