Rajkumar Chinnadurai

Background: This study investigates the impact of deprivation and ethnicity on birth outcomes in a large area of Northwest England. It is a single-centre retrospective observational study of births from 22 weeks of gestation between January 2018 and December 2022 at the Northern Care Alliance NHS Foundation Trust (NCA), Greater Manchester, which has a level three maternity unit. Methods: Data for 24,045 pregnancies over a 5-year period were extracted from electronic databases. Index of Multiple Deprivation (IMD) quintiles were generated from patients’ residential postcodes, with lower IMD status indicating greater socioeconomic deprivation. Univariate and multivariate logistic regression identified predictors of poor outcomes with a focus on maternal deprivation and ethnic background. The primary outcome was an adverse birth outcome, which included stillbirth (after 24 weeks), early neonatal death (after any gestation), extreme prematurity (22–27 weeks gestation) and very premature (28–31 weeks) in singleton pregnancies. Results: 42.6% of pregnancies involved ethnic minority groups (EMG), and 61% of all mothers were living in the most socially deprived index of multiple deprivation (IMD) quintile. Poor outcomes, including stillbirth (0.7 vs. 0.4%, p = 0.03) and early neonatal death (0.3 vs. 0.2%, p = 0.018), were significantly higher in EMG than White women. Premature deliveries were more frequent in pregnancies from mothers living in areas of highest deprivation ( p < 0.001). In multivariate logistic regression analysis, EMG (OR: 1.25, p = 0.042), higher maternal age (OR: 1.03, p = 0.006), hypertension history (OR: 2.18, p < 0.001) and a lower IMD status (OR: 1.81, p = 0.002) were all shown to be independent predictors of an adverse birth outcome. Conclusions: The study reinforces the link between ethnicity, deprivation and pregnancy outcomes, with women from both lower IMD and EMG backgrounds being at risk of poorer outcomes.

Peritoneal dialysis (PD)-associated peritonitis remains a major cause of treatment failure, hospitalisation, catheter loss and transition to haemodialysis despite reductions in incidence over the decades. This narrative review examines the global evolution of microbiological epidemiology and pharmacological management of PD-associated peritonitis, looking at global trends in microbiological epidemiology and exploring how treatment recommendations have evolved in response to changing pathogen distribution, antibiotic resistance patterns and associated clinical outcomes. Although Gram-positive organisms remain the predominant pathogens in most PD programmes, recent evidence demonstrates marked geographical and centre-level heterogeneity with rising clinical importance of Gram-negative, polymicrobial, fungal and culture-negative infections in certain regions. Antibiotic resistance has emerged as an additional challenge, including methicillin-resistant staphylococci, vancomycin-resistant enterococci, extended-spectrum β-lactamase-producing Enterobacterales and multidrug-resistant non-fermenting Gram-negative organisms. These changes challenge conventional empirical regimens and emphasise the importance of programme-specific microbiological surveillance. In parallel, pharmacological management has evolved considerably from relatively standardised empirical antibiotic combinations towards an individualised approach incorporating intraperitoneal administration, local susceptibility profiles, organism-directed therapy, pharmacokinetic optimisation, therapeutic drug monitoring and antifungal prophylaxis. However, substantial evidence gaps remain, particularly regarding antibiotic resistance patterns globally, optimal dosing in automated PD, intraperitoneal stability and clinical efficacy of newer antimicrobial agents.

Introduction Chronic kidney disease (CKD) frequently coexists with cardiovascular disease, 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.

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.

Background: Socioeconomic 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. Methods: This 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. Results: Of 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. Conclusion: In 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: 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.

Background: 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 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 confidence intervals. 61 patients (52.1%) 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. Conclusions: 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.

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.

Introduction: Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a systemic condition usually affecting small blood vessels, commonly causing kidney disease. It has a reported incidence of around 20–25 per million per year. AAV includes both granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA). Here, we describe the epidemiology of this condition at our renal centre over a 23-year period, compare GPA and MPA and compare the overall cohort by era of diagnosis. Methods: We identified all patients with AAV with renal involvement between January 2000 and December 2022 through our biopsy database and electronic patient record. The cohort after exclusions totaled 278. We collected demographic data, baseline laboratory values, treatment received and outcomes including progression to renal replacement therapy (RRT), relapse rates and mortality. We performed subgroup analysis comparing those with GPA and MPA, and created 4 groups by era of diagnosis. Results: Median age of the cohort was 63.5 years (interquartile range [IQR] 52–72), 52.5% were male and 92.4% White. GPA was seen in 49.3% and MPA in 42.1%. There was advanced renal disease at presentation with median eGFR 18 mL/min/1.73 m2 (IQR 9–38) and 54 (19.4%) required RRT at presentation. Relapse occurred in 23%, progression to RRT in 26.6% and 1-year mortality was 3.2%. Median follow-up duration was 54 months (IQR 22–98). Those with GPA were younger, had higher incidence of ENT disease at presentation, were more likely to relapse and had greater 1- and 5-year survival. Mortality rate per hundred person years improved from 2010 onwards. Conclusions: This is one of the largest retrospective observational studies conducted on AAV. We demonstrate that there were more cases of GPA (49.2%) compared to MPA (42.1%) presenting to our centre; comorbidity rates were high; there was advanced renal disease at presentation and mortality rate appeared to improve in the more recent eras.