Chronic kidney disease (CKD) and chronic obstructive pulmonary disease (COPD) are common conditions associated with increased risks of mortality and cognitive impairment. However, the association between COPD and dementia outcomes in patients with CKD remains incompletely understood. We conducted a retrospective observational cohort study using the TriNetX Global Collaborative Network, including patients aged 18–80 years with CKD stages 3–5, excluding those with prior dialysis, transplantation, dementia, or mild cognitive impairment before cohort entry. Two cohorts were identified: CKD with COPD, defined using classical ICD-10 COPD codes (J41–J44), and CKD without COPD. A secondary sensitivity analysis used a broader respiratory disease definition including asthma, bronchiectasis, and other chronic respiratory conditions. Cohorts were propensity score matched (1:1) for demographic characteristics, comorbidities, smoking exposure, and laboratory parameters. Outcomes included all-cause mortality, non-Alzheimer’s dementia, and Alzheimer’s disease, assessed over a maximum follow-up of 5 years using Kaplan–Meier and Cox proportional hazards analyses. Two cohorts were identified: CKD with COPD (n = 270 566) and CKD without COPD (n = 821 399). After propensity score matching, 234 317 patients remained in each cohort. CKD with COPD was associated with a higher observed risk of mortality compared with CKD alone (18.5

Post-coronavirus disease 2019 (COVID-19) condition describes a constellation of persistent or fluctuating symptoms and organ dysfunction following severe acute respiratory syndrome coronavirus 2 infection. Patients with end-stage kidney disease (ESKD) on dialysis and kidney transplant recipients (KTR) inhabit a landscape of immune dysfunction, multimorbidity, and high healthcare interaction, which may amplify both the risk and consequences of post-COVID condition (PCC). In this article, we aimed to review current evidence on PCC and related post-acute sequelae in dialysis patients and KTR-focusing on symptom burden, risk factors, functional outcomes, health-related quality of life (HRQoL), kidney and graft outcomes, and recovery trajectories. It was found that dialysis patients and KTR experience a substantial burden of PCC superimposed on already complex symptoms and risk profiles. Long COVID in these groups encompasses not only fatigue, dyspnea and a "brain fog" phenomenon but also impaired HRQoL, reduced functional recovery, and potential acceleration of kidney and graft decline. Harmonized PCC definitions, kidney-specific outcome measures, and prospective multicentre studies in ESKD and kidney transplant populations are urgently required to inform prevention and management strategies embedded within the dialysis and kidney transplantation pathways.

INTRODUCTION:This study assesses the impact of functional iron deficiency (FID) on outcomes, including all-cause mortality, hospitalizations and non-fatal cardiovascular events in patients with non-dialysis chronic kidney disease (CKD) and hemodialysis (HD). METHODS:In HD, absolute iron deficiency (AID) was defined as ferritin < 200 µg/L and TSAT (transferrin saturation) ≤ 20%, and FID ferritin ≥200 µg/L with TSAT ≤20%. In CKD, AID was ferritin < 100 µg/L and TSAT ≤ 20%, and FID ferritin ≥ 100 µg/L with TSAT ≤ 20%. Prevalent HD patients as of January 2012 and incident patients between January 2012 and December 2014 were included (n = 512) and followed to 31/12/2018 (median 36.5 months). CKD patients who received iron infusions between January 2017 and December 2019 were included (n = 831) and followed until 31/12/2023 (median 38.5 months). RESULTS:In the HD cohort, 71% of the FID patients were dead at the end of follow-up (vs No Iron Deficiency, NID: 52%, AID: 48%; p = 0.008). In the CKD cohort, 62% of the FID group died by the end of follow-up (vs AID: 49.5%, NID: 46.2%; p = 0.001). The hazard ratio for FID for all-cause mortality was 1.89 (p < 0.001) in HD and 1.48 (p < 0.001) in CKD. Multivariate analysis found FID was independently associated with all-cause mortality (HD HR:1.50, p = 0.015; CKD HR: 1.46, p = 0.017). Patients with FID on HD were more likely to be hospitalized (median episodes 2.5 FID vs 2 in AID and NID, p = 0.041; FID: 22.5 days vs AID: 10, NID:14 days, p = 0.019). CONCLUSION:FID was associated with all-cause mortality in patients with non-dialysis CKD and HD, and with higher rates of hospitalization and prolonged length of stay in HD.

ABSTRACT Patients referred to specialist hypertension clinics often have complex disease characterized by secondary causes, treatment resistance and coexisting kidney disease. Real‐world outcome data in this setting remain limited. We conducted a retrospective cohort study of 199 patients attending a tertiary hypertension clinic between January 2017 and December 2023. Baseline demographics, comorbidities, antihypertensive therapy, and blood pressure (BP) were recorded. BP changes were assessed annually for up to 3 years. Subgroup analyses examined outcomes by age, sex, diabetes, chronic kidney disease, obesity, resistant hypertension, secondary hypertension, and baseline systolic BP. Cardiovascular events were identified from clinical records. Mean age of patients was 44.1 ± 14.0 years and 61.3% were male. Secondary hypertension was present in 32.7% and resistant hypertension in 17.2%. Median follow‐up was 13.8 months (IQR 4.7–30.1), with follow‐up BP available for 146 patients. Mean baseline BP was 156/97 mmHg. At final follow‐up, significant reductions were observed, with mean systolic and diastolic BP decreases of −13.6 and −8.8 mmHg, respectively (both p < 0.001). BP improvements were consistent across clinical subgroups. Qualitative urine antihypertensive drug screening identified medication non‐adherence in a subset of patients, with targeted interventions associated with subsequent BP improvement. Cardiovascular events were infrequent (6.5%). This study shows that specialist hypertension care achieves substantial BP reductions in complex real‐world patients. Objective assessment of medication adherence appears clinically valuable, although BP control remains challenging and residual cardiovascular risk persists. Larger multicenter studies with longer follow‐up are needed to define predictors of cardiovascular outcomes and optimize care pathways.

Cite this article as: Morgans-Slader F, Suliman O, H.L. Wu H, Chinnadurai R. Human metapneumovirus infection in kidney transplant recipients. Turk J Nephrol. 2026;35(1):82-83.

Introduction:Patients with chronic kidney disease (CKD) have an increased risk of cardiovascular morbidity. Circulating endostatin is associated with both cardiovascular morbidity and impaired kidney function in the general population, but the utility of endostatin as a prognostic marker for CKD progression and mortality in patients with CKD is not well studied. The aim was to study association between serum endostatin and mortality, and also kidney function decline in a cohort of CKD patients (Salford Kidney Study [SKS]). Methods:Analyses were performed on baseline and annual follow-up samples from 970 adults in the SKS cohort with CKD stage 3-5. Association with mortality was studied using Cox proportional hazard models adjusted for age, gender, systolic and diastolic blood pressure, smoking status, diabetes mellitus, prior cardiovascular disease, creatinine-based estimated glomerular filtration rate (eGFR), and urine protein-to-creatinine ratio (uPCR). Associations between endostatin and eGFR decline were studied with linear regression analyses. eGFR decline was defined as the percentage difference between baseline eGFR and follow-up eGFR (median follow-up, 6.2 years). Results:Median age of the cohort was 66 years, with a median eGFR of 30 mL/min/1.73 m2. Multivariate Cox regression models revealed an association between higher endostatin levels and mortality with adjustments for established cardiovascular risk factors (HR: 1.14; CI: 1.02-1.28; p = 0.02) but was attenuated and nonsignificant after adjustments for baseline eGFR and uPCR. Baseline levels of endostatin were associated with eGFR decline but were nonsignificant after adjustments for baseline eGFR and uPCR. Changes of endostatin concentrations during the study were significantly associated with eGFR decline in all models (regression coefficient 0.0023% decrease per month [95% confidence intervals 0.0012-0.0034, p < 0.001]). Conclusion:The clinical utility of plasma endostatin for risk prediction in CKD patients seems limited. Importantly, longitudinal changes of endostatin were significantly associated with eGFR decline. The clinical relevance of this warrants further studies.

Peritoneal dialysis (PD) has long been an established modality of renal replacement therapy for patients with end-stage kidney disease (ESKD). Despite the modality’s advantages, significant inter-individual variability exists in peritoneal membrane transport characteristics, ultrafiltration capacity, and long-term technique survival. While PD therapy-related factors, such as dialysis solution composition, peritonitis episodes, and duration of therapy, contribute to these outcomes, genetic factors also play important roles in peritoneal membrane biology. Genetic studies have identified polymorphisms in genes involved in angiogenesis, inflammation, fibrosis, and endothelial function that influence PD outcomes. Variants in genes such as vascular endothelial growth factor, interleukin-6, transforming growth factor-β1, angiotensin-converting enzyme, endothelial nitric oxide synthase, and aquaporin-1 have all been reported to be associated with differences in peritoneal transport and susceptibility to membrane failure. These genetic discoveries provide significant insights into the pathways that lead to alterations in the PD membrane structure and function. This review article aims to explore current evidence on key genetic determinants of peritoneal membrane transport, inflammatory responses, and fibrotic transformation in PD, and to discuss their potential implications for personalised dialysis therapy and future research.

IgA nephropathy (IgAN), IgA vasculitis (IgAV), focal segmental glomerulosclerosis (FSGS), membranous nephropathy (MN), and minimal change disease (MCD) account for the majority of idiopathic glomerulo-nephropathies (GN). These disorders involve immune system dysregulation and have a complex genetic architecture. Currently, there are no adequately powered blood transcriptomic datasets coupled to genetic data from patients with GN that can delineate disease-context specific genetic effects on the blood immune cell transcriptome. We performed whole genome sequencing coupled with bulk blood transcriptome sequencing on 1,822 participants from the CureGN study, a prospective cohort of participants with a kidney biopsy diagnosis of primary GN. We generated disease-context specific transcriptome-wide maps of gene expression QTL (eQTL), splicing QTL (sQTL), and double strand RNA-editing QTL (edQTL) for FSGS (N=447), IgAN (N=403), IgAV (N=123), MCD (N=408), and MN (N=441), as well as cross-disease maps for all 1,822 participants. Our QTL mapping identified 16,068 eGenes, 4,644 sGenes and 4,611 edQTLs with an FDR<0.05 in at least one GN type. Approximately 5-10% of the QTL signals were unique to a specific GN type, while ~90% were shared between at least two conditions. Colocalization analysis demonstrated that ~80% of shared eGenes between traits also shared the same causal variants, whereas ~2% had distinct causal variants, suggesting context-specific regulatory effects. Cross-phenotype QTL mapping uncovered 6,466 eGenes, 2,705 sGenes and 5,321 edQTLs not previously detected in GTEx. Age, eGFR, and proteinuria-interaction QTL analyses identified hundreds of loci modified by age or disease severity. Lastly, integrative analyses with GWAS nominated new candidate genes for each of the five GN types under study. In summary, we generated comprehensive maps of GN-context-specific genetic effects on the blood transcriptome, providing a powerful new resource for integrative gene discovery studies of primary GN.

INTRODUCTION:Chronic kidney disease (CKD) frequently coexists with cardiovascular disease (CVD), diabetes, and obesity through shared biological pathways encompassed within the American Heart Association cardiovascular-kidney-metabolic (CKM) construct. Whether adverse cardiovascular and renal outcomes in CKD are driven predominantly by cumulative multimorbidity burden or by distinct CKM disease phenotypes remains uncertain. METHODS:We conducted a retrospective longitudinal cohort study of participants in the Salford Kidney Study with non-dialysis-dependent CKD and at least one other CKM comorbidity. Patients were evaluated according to CKM multimorbidity burden (2, 3, or 4 conditions) and in predefined CKM phenotypes. Co-primary outcomes were major adverse cardiovascular event (MACE: cardiovascular mortality, non-fatal myocardial infarction, non-fatal cerebrovascular accident, or heart failure event), composite kidney endpoint (CKE: ≥40% eGFR decline, eGFR <15 mL/min/1.73 m2, or renal replacement therapy initiation), and all-cause mortality. Associations were evaluated using multivariable time-to-event models. RESULTS:Among 2,003 participants (mean age 68 years; median follow-up 4.7 years), 279 (13.9%) experienced MACE and 1,010 (50.4%) reached the CKE. Compared with 2 CKM conditions, 4 conditions conferred an almost two-fold higher MACE risk (HR 1.93, 95% CI: 1.48-2.53), with the CKD-CVD-diabetes-obesity phenotype demonstrating the highest MACE risk. Diabetes-containing phenotypes were consistently associated with higher CKE risk, whereas increasing multimorbidity burden showed limited discriminatory value for kidney progression. The CKD-diabetes-CVD phenotype had the highest all-cause mortality (27.1 deaths per 100 patient-years). CONCLUSIONS:Increasing CKM multimorbidity burden predicted cardiovascular events and mortality in keeping with the American Heart Association staging framework, but kidney progression was more strongly determined by disease phenotype, particularly diabetic kidney disease. This cardiovascular-renal dissociation suggests that phenotypic refinement of the CKM staging model may improve risk stratification in advanced CKD populations with CKM multimorbidity.

BackgroundSocioeconomic deprivation is an established determinant of adverse health outcomes. However, UK-specific data examining its impact on peritoneal dialysis (PD) outcomes remains generally unknown. This study evaluated associations between socioeconomic deprivation and clinical outcomes among patients receiving PD at a single UK center over a 10-year period.MethodsThis retrospective observational study included 648 adult patients who underwent PD catheter insertion between January 2015 and December 2024. Socioeconomic deprivation was assessed using the Index of Multiple Deprivation (IMD), with study cohorts categorized into quintiles from the least to the most deprived. Primary outcomes included all-cause mortality, transfer to hemodialysis (HD), and kidney transplantation. Secondary outcomes included cardiovascular events and PD-related infections, that is, peritonitis and exit-site infections. A 1:1 propensity score matching was performed to match for age, ethnicity, and smoking history to compare between the most deprived quintiles (MDQ) (i.e., quintiles 1 and 2) and the least deprived quintiles (LDQ) (i.e., quintiles 4 and 5). Cox proportional hazards models were used to evaluate associations between socioeconomic deprivation and outcomes.ResultsOf the 648 patients included, 41.7% resided in quintile 1. Patients in LDQ were significantly younger (median = 54 [IQR 42-67] vs. 64 [51-74] years, p < 0.001) and more likely to belong to ethnic minority backgrounds (24% vs. 7.7%, p < 0.001) compared to those in MDQ. Across all quintiles, no significant associations were observed between deprivation and all-cause mortality, transfer to HD, or kidney transplantation. In the propensity-matched cohort (n = 298), all-cause mortality was significantly higher among patients from MDQ compared to the LDQ (39.6% vs. 24.8%, p = 0.006). Social deprivation was noted to be an independent risk factor associated with all-cause mortality in the matched cohort (adjusted HR 2.08, 95% CI 1.37-3.10, p = 0.001). No significant associations were identified in relation to cardiovascular events, transfer to HD, kidney transplantation, or PD-related infections.ConclusionIn a propensity score-matched cohort from this single-center study, socioeconomic deprivation was independently associated with increased mortality among patients receiving PD. No significant associations were observed between socioeconomic deprivation with transfer to HD or kidney transplantation and PD-related infection complications.

INTRODUCTION:Tolvaptan slows disease progression of autosomal dominant polycystic kidney disease (ADPKD) in clinical trials, but real-world effectiveness remains uncertain. We evaluated the association between tolvaptan use and kidney function decline in a large tertiary-centre cohort. METHODS:This retrospective cohort study evaluated adults with ADPKD attending a specialist polycystic kidney disease clinic. Patients with <1 year of follow-up or <3 estimated glomerular filtration (eGFR) measurements were excluded. eGFR slopes were estimated using piecewise linear mixed-effects models separating acute (<60 days) and chronic (≥60 days) phases, with the chronic slope defined as the primary outcome. Multivariable mixed-effects models and propensity score overlap weighting were used to adjust for baseline differences in covariates. Complete case analysis was performed as the primary analysis; multiple imputation was used as a sensitivity analysis. Patients receiving <6 months of tolvaptan were excluded from the primary slope analyses but retained for intention-to-treat comparisons. RESULTS:Of 327 patients, 119 initiated tolvaptan and 208 did not; mean duration of study follow-up was 61.4 months. Tolvaptan-treated patients had a lower baseline eGFR and trended towards a faster pre-study eGFR decline. After full adjustment, tolvaptan was associated with a modest slowing in the chronic eGFR slope of +0.45 mL/min/1.73 m2/year; however, confidence intervals (CIs) were wide (95% CI: -0.37 to +1.18) and therefore compatible with clinically meaningful benefit or no effect. Findings were directionally consistent across complete-case, overlap-weighted, and multiple-imputation analyses with similarly imprecise CIs. A total of 61 (52.1%) patients discontinued therapy within 12 months of initiation, primarily due to aquaretic side effects. In subgroup analyses, tolvaptan patients treated for ≥1 year and tolvaptan responders treated for ≥2 years showed greater magnitudes of benefit with chronic slopes of +0.58 and +0.78 mL/min/1.73 m2/year, respectively, when compared to untreated matched cohorts. CONCLUSION:Tolvaptan was not associated with a statistically significant slowing of kidney function decline. Point estimates suggest a modest potential benefit which is attenuated when compared to controlled trials. Treatment discontinuation substantially limited treatment exposure. Further real-world evidence is required to clarify tolvaptan's true effectiveness outside controlled trial settings.

Background Nonattendance at scheduled hemodialysis (HD) sessions is a frequent form of treatment nonadherence. Psychosocial factors are known contributors, yet the psychological profiles of frequent non-attenders remain underexplored. We conducted a retrospective analysis of patients with recurrent HD nonattendance, defined as missing more than four dialysis sessions during the two-year study period, who were referred to renal psychology services.Methods Data were extracted from psychological case notes using a structured pro forma designed by the renal psychology team, and included reason for referral, preexisting mental health issues and history of adverse childhood experiences (ACEs). Information recorded by the dialysis nurses on the electronic patient record on the day of nonattendance for all patients referred to psychology was retrieved and analyzed to identify and categorize recurring themes. Descriptive analysis was conducted for both datasets.Results Of 464 patients in the original cohort, 54 met criteria for frequent nonattendance. Twenty-two (40.7%) were referred to psychology, of whom 17 engaged with at least one session. Fifteen out of 17 (88%) of these patients had preexisting mental health conditions, primarily depression (n = 12, 71%) and anxiety (n = 8, 47%). Confirmed or possible adverse childhood experiences were identified in 88% of assessed patients. Nursing records cited concurrent illness, limited disease understanding, family obligations, and logistical barriers as common reasons for missed sessions.Conclusions This study underscores the need for early, integrated psychological assessment within the dialysis care pathway. A trauma-informed, multidisciplinary model may improve access to support and sustain adherence over time and should be prospectively investigated.

Background:Fabry disease (FD) is an X-linked lysosomal storage disorder caused by deficient α-galactosidase A (α-Gal) activity, leading to progressive renal, cardiac, and cerebrovascular involvement. Migalastat, an oral pharmacological chaperone, is indicated for patients with amenable GLA variants. Although efficacy has been demonstrated in clinical trials, long-term real-world data remain necessary, particularly in mixed groups of treatment-naïve and ERT-switch patients and genotype-phenotype subgroups. Methods:Eighty-seven adults with FD (55 males, 32 females) carrying GLA variants were retrospectively analysed at a single regional centre. Patients received migalastat as treatment naïve (TN) (n = 48) or treatment switch (TS) (n = 39). Demographic, genotypic, biochemical, renal, and cardiac parameters, and clinical outcomes were evaluated. Results:Variants were predominantly late-onset (67%), most commonly c.644 A > G (p.Asn215Ser)/p.N215S; 14% were classical and 19% unclassified. Plasma globotriaosylsphingosine (lyso-Gb3) declined in both groups (TN: 5.1 (3.7-7.9) to 2.2 (1.3-3.6) ng/mL; TS: 7.2 (3.8-13.0) to 3.3 (1.4-6.7) ng/mL). Renal function remained above clinically relevant thresholds in most patients, with a modest reduction in the proportion maintaining eGFR >90 mL/min/1.73 m2. Blood pressure, and echocardiographic measurements were largely stable; however, a significant reduction (P = 0.009) in left ventricular mass index (LVMI) was observed in TS patients when restricting analysis to variants classified as amenable according to the Galafold® amenability table (United Kingdom (UK), 2024 version). In TS patients, QTc increased significantly (P < 0.001) but remained within normal or only mildly prolonged limits. Sex-stratified analyses showed higher LVMI in males than females at baseline, with non-significant reductions in both groups over time. The incidence of non-fatal cardiovascular events was 81 and 43.5 per 1000 person-years in TN and TS groups, respectively. Six male patients (6.9%) experienced adverse events; five discontinued treatment, and one Fabry-related death occurred in the TN group. Conclusion:Migalastat was well tolerated and maintained stable renal and cardiac parameters with plasma lyso-Gb3 improvement. However, a subset of patients showed progression or intolerance, underscoring that variant amenability alone may not predict clinical benefit.

Peritoneal dialysis (PD) offers greater flexibility, a better quality of life, a lower risk of infections, better preservation of residual kidney function, and lower healthcare costs in comparison to in-centre hemodialysis (HD). Despite the known advantages associated with PD, over 35% of patients transition from PD to HD annually in the UK. The most common reasons for PD dropouts include mechanical failure, infection, inadequate clearance and death whilst receiving PD. We conducted a retrospective observational study at our centre investigating the characteristics of patients who dropped out of their PD regimens and the reasons for PD dropout over a 3-year follow-up period. There were 114 adult patients under the care of the renal medicine department at Northern Care Alliance NHS Foundation Trust who dropped out of PD between January 2022 and September 2024. Specific patient characteristics and the reasons for PD dropout were evaluated over this time period. Data collated include patient demographic characteristics, Charlson comorbidity index (CCI) scores prior to PD catheter insertion, issues identified during home visit assessments prior to PD initiation, and attendance to dialysis education visits. PD catheter-related information including the catheter insertion method (i.e. medical vs surgical insertion), whether an elective outpatient vs inpatient procedure was received, and the occurrence of acute complications post PD catheter insertion (e.g. catheter malposition) were recorded. In this study, continuous variables are expressed as median (interquartile range) with p values calculated via the Kruskal–Wallis H test or Mann–Whitney U test. Categorical variables are expressed as numbers (percentage) with p values calculated by the Chi-squared test. Comparisons were made between PD dropouts after catheter removal due to ’undesirable cause’ (UC) (i.e. infection and/or PD catheter dysfunction) versus ’natural causes’ (NC) (i.e. death, receipt of kidney transplantation or patient choice). Logistic regression statistics were applied to represent the findings of this comparative analysis. There were 43 patients in 2022, 42 patients in 2023, and 29 patients in 2024 who dropped out of PD. The cohort’s median age was 55.3 years, in which patients were predominantly male (69%) and of White ethnicity (81.3%). Patient characteristics relating to the pre-PD assessments—including CCI scores, issues identified during home visit assessments prior to PD initiation, and attendance to dialysis education visits—were similar between 2022 and 2024. The rates of medical PD catheter insertion (81.4% in 2022 vs 81% in 2023 vs 75.9% in 2024, P = 0.826) and elective outpatient catheter insertion (70% in 2022 vs 76.2% in 2023 vs 79.3% in 2024, P = 0.630) were similar across the 3 years. No differences were observed in terms of peri-operative characteristics relating to PD catheter insertion between 2022 and 2024, including constipation issues post-procedure, pre-procedure CCI scores or the number of medications received. There were an increased proportion of patients who dropped out of PD due to availability for kidney transplantation between 2022 and 2024 (21% in 2022 vs 28.6% in 2023 vs 48% in 2024, P = 0.005). Nevertheless, PD dropouts because of UC appeared similar over the years (35% in 2022 vs 43% in 2023 vs 31% in 2024, P = 0.564). Of the 114 patients, 42 had PD drop off due to UC and 72 had a NC. A comparison between the two groups showed a higher proportion of patients who had an emergency PD catheter insertion as inpatients eventually dropped off PD due to an UC (40.5% UC vs 16.7% NC, P = 0.005) (Table 1). Binary logistic regression analysis noted emergency inpatient catheter insertion as a significant predictor of UC for PD removal/drop out (OR 3.40, 95% CI 1.41–8.14, P = 0.006). Our study highlights emergency inpatient PD catheter insertion as a risk factor that predicts for future ’undesirable‘ PD dropout. This study’s findings strengthen the stance that meticulous pre-procedure assessments in advanced kidney care services and dialysis preparation clinics are warranted to prevent ’undesirable‘ PD dropouts.

Introduction: Cardiac biomarkers, N-terminal pro-B-type natriuretic peptide (NT-proBNP), and high-sensitivity cardiac troponin-T (Hs-cTnT) are good prognostic indicators of long-term clinical cardiovascular outcomes in patients with chronic kidney disease (CKD). However, the clinical utility of combined biomarkers in predicting death and cardio-renal outcomes in patients with CKD remains unclear. This study examined the prognostic accuracy and incremental value of NT-proBNP and Hs-cTnT for all-cause mortality, major adverse cardiovascular event (MACE), and end-stage kidney disease (ESKD) in non-dialysis-dependent chronic kidney disease (NDD-CKD) patients. Methods: Data from 1,946 individuals with NDD-CKD prospectively included in the Salford Kidney Study were used to investigate the associations between NT-proBNP and Hs-cTnT with study endpoints. Hazard ratio or sub-hazard ratio and 95% confidence intervals (95% CIs) were estimated using multivariate Cox-regression and competing risk models. The discriminatory power of NT-proBNP and Hs-cTnT along with kidney biomarkers (eGFR and uACR) and Framingham risk score (FRS) were calculated using Harrell's C-index. Endpoint-specific risk scores were generated using regression coefficients obtained in a training dataset and confirmed in a validation one. Results: During median follow-up of 71.5 months, 931 (47.8%) deaths, 553 (28.4%) MACE, and 554 (28.5%) ESKD events occurred. Baseline NT-proBNP and Hs-cTnT elevations were associated with significant increased risk of mortality, MACE, and ESKD independently of FRS. Combining NT-proBNP, Hs-cTnT, and FRS yielded the highest prognostic accuracy for all-cause mortality and MACE (respective C-statistics: 0.713; 95% CI: 0.695-0.731, and 0.697; 95% CI: 0.673-0.721), while combining NT-proBNP and Hs-cTnT with eGFR and uACR performed best at predicting ESKD (C-statistics: 0.821; 95% CI: 0.786-0.826). Conclusion: In NDD-CKD patients, NT-proBNP and Hs-cTnT are predictors of all-cause mortality, MACE, and ESKD, independently of eGFR and uACR. Combining NT-proBNP and Hs-cTnT with eGFR and uACR outperformed risk prediction for ESKD compared to kidney biomarkers used alone or in combination.

INTRODUCTION:Nonattendance for prescribed hemodialysis (HD) sessions is a form of nonadherence that compromises the delivery of life-sustaining HD therapy and is associated with severe morbidity and mortality. In this study, we aimed to assess the characteristics and outcomes of HD nonattenders in a single renal center in the North West of England. METHODS:HD patients followed by the renal team at our unit between December 2020 and September 2022 were included in this study. Dialysis nonattendance data were retrieved from the incident reports (DATIX) between December 2020 and November 2022, excluding dialysis nonattendance due to concurrent hospitalization. The cohort was split into group 1: no dialysis nonattendance; group 2: two or fewer dialysis nonattendances; and group 3: more than two dialysis nonattendances for comparative analysis. All patients were followed up for outcomes including all-cause mortality, transplantation, and hospitalizations until the study endpoint date of 12/31/2023. Predictors of dialysis nonattendance were identified using logistic regression. RESULTS:Of the 464 patients, dialysis nonattendance was noted in 149 (32%) patients, of which 79 (17%) had two dialysis nonattendance episodes and 70 (15%) had more than two dialysis nonattendance episodes. Over a median follow-up of 35 months, patients in group 3 had a higher hospitalization episode (4 vs. 1 day, p < 0.001) and lower kidney transplantation rates (4.3% vs. 13%, p = 0.038) compared to patients in group 1. In multivariate regression analysis, younger age (OR: 0.97; 95% CI: 0.95-0.98; p = 0.001), history of smoking (OR: 2.01; 95% CI: 1.12-3.62; p = 0.019), alcohol excess history (OR: 3.49; 95% CI: 1.87-6.49; p < 0.001) and history of mental health illness (OR: 3.01; 95% CI: 1.61-5.62; p = 0.001) were significant predictors of dialysis nonattendance. CONCLUSION:Skipping HD is a common phenomenon associated with mental health issues and is associated with increased morbidity. Further research is required to understand the psychosocial determinants of nonadherence and effective models of intervention developed to improve outcomes.

Rationale & Objective:Trials failed to show that angioplasty and stenting of atherosclerotic renovascular disease (ARVD) conferred benefit when used as first-line therapy. However, some patients might benefit from kidney revascularization depending on their clinical phenotype and severity of renal artery stenosis (RAS). We investigated this hypothesis further. Study Design:Data from the Angioplasty and Stenting for Renal Artery Lesions (ASTRAL) randomized trial and Salford ARVD observational study were included in a single analysis. Setting & Participants:Patients were grouped based on RAS severity (≥70%) and whether unilateral or bilateral, with the bilateral group including RAS in a single functioning kidney. High-risk clinical phenotypes included advanced chronic kidney disease (CKD) (estimated glomerular filtration rate < 30 mL/min/1.73 m2), rapid CKD progression (creatinine increase >100 μmol/l or >20% per year), refractory systolic hypertension (≥150 mm Hg on ≥3 agents), and heart failure (chronic or decompensated). Exposures:Medical therapy alone versus medial therapy and kidney revascularization. Outcome:Composite of end stage CKD, cardiovascular events, or all-cause mortality. Analytical Approach:Cox proportional hazard model adjusted for age, self-reported gender, and estimated glomerular filtration rate. Analysis of all patients and selected subgroups. Results:In total, 1,644 patients (806 ASTRAL and 838 Salford). Median (IQR) age 72 (66-77) years. For bilateral severe RAS (≥70%) the HR for the composite outcome for revascularization compared with medical therapy was 0.70 (0.50-0.99), P = 0.048. The clinical phenotype where benefit appeared to be greatest in the presence of bilateral severe disease was people with rapidly progressive kidney disease with a HR of 0.39 (0.22-0.71]). In the absence of bilateral severe RAS, there was no benefit to revascularization for any clinical phenotype. Limitations:The analyses included observational data. Conclusions:The presence of bilateral severe RAS may be the best predictor of benefit for kidney revascularization.

Introduction: Cardiac biomarkers, N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high-sensitivity cardiac troponin-T (Hs-cTnT) are good prognostic indicators of long-term clinical cardiovascular outcomes in patients with chronic kidney disease. However, the clinical utility of combined biomarkers in predicting death and cardio-renal outcomes in patients with CKD remains unclear. This study examined the prognostic accuracy and incremental value of, NT-proBNP and Hs-cTnT for all-cause mortality, major adverse cardiovascular events (MACE), and end-stage kidney disease (ESKD) in non-dialysis dependent chronic kidney disease (NDD-CKD) patients. Methods: Data from 1946 individuals with NDD-CKD prospectively included in the Salford Kidney Study was used to investigate the associations between NT-proBNP and Hs-cTnT with study endpoints. Hazards ratio or sub-hazards ratio and 95% confidence intervals (95%CI) were estimated using multivariate Cox-regression and competing risk models. The discriminatory power of NT-proBNP and Hs-cTnT along with kidney biomarkers (RBMs: eGFR and UACR) and Framingham Risk score (FRS) were calculated using Harrell’s C-index. Endpoint-specific risk scores were generated using regression coefficients obtained in a training dataset and confirmed in a validation one. Results: During median follow-up of 71.5 months, 931 (47.8%) deaths, 553 (28.4%) MACE and 554 (28.5%) ESKD events occurred. Baseline NT-proBNP and Hs-cTnT elevations were associated with significant increased risk of mortality, MACE and ESKD independently of FRS and RBMs. Combining NT-proBNP, Hs-cTnT, and FRS yielded the highest prognostic accuracy for all-cause mortality and MACE (respective C-statistics:0.713; 95%CI:0.695-0.731, and 0.697;95%CI:0.673-0.721,), while combining NT-proBNP, and Hs-cTnT with RBMs performed best at predicting ESKD (C-statistics:0.821; 95%CI: 0.786-0.826). Conclusions: In NDD-CKD patients, NT-proBNP and Hs-cTnT are predictors of all-cause mortality, MACE, and ESKD, independently of RBMs. Combining NT-proBNP and Hs-cTnT with RBMs outperformed risk prediction for ESKD compared to RBMs used alone or in combination.