Peritoneal inflammation precedes encapsulating peritoneal sclerosis: results from the GLOBAL Fluid Study

BACKGROUND: Encapsulating peritoneal sclerosis (EPS) is an uncommon condition, strongly associated with a long duration of peritoneal dialysis (PD), which is itself associated with increased fibrosis in the peritoneal membrane. The peritoneal membrane is inflamed during PD and inflammation is often associated with fibrosis. We hypothesized that patients who subsequently develop EPS might have a more inflamed peritoneal membrane during PD. METHODS: We performed a nested, case-control study identifying all EPS cases in the UK arm of the GLOBAL Fluid Study and matching them by centre and duration of PD with two to three controls. Dialysate and plasma samples were taken during repeated peritoneal equilibration tests prior to cessation of PD from cases and controls. Samples were assayed by electrochemiluminescence immunoassay for interleukin-1ß (IL-1ß), tumour necrosis factor a (TNF-a), interferon-? (IFN-?) and IL-6. Results were analysed by linear mixed models adjusted for age and time on PD. RESULTS: Eleven EPS cases were matched with 26 controls. Dialysate TNF-a {0.64 [95% confidence interval (CI) 0.23, 1.05]} and IL-6 [0.79 (95% CI 0.03, 1.56)] were significantly higher in EPS cases, while IL-1ß [1.06 (95% CI -0.11, 2.23)] and IFN-? [0.62 (95% CI -0.06, 1.29)] showed a similar trend. Only IL-6 was significantly higher in the plasma [0.42 (95% CI 0.07, 0.78)]. Solute transport was not significantly different between cases and controls but did increase in both groups with the duration of PD. CONCLUSIONS: The peritoneal cavity has higher levels of inflammatory cytokines during PD in patients who subsequently develop EPS, but neither inflammatory cytokines nor peritoneal solute transport clearly discriminates EPS cases. Increased systemic inflammation is also evident and is probably driven by increased peritoneal inflammation

Contested space: The contradictory political dynamics of food banking in the UK

This paper offers a critical reappraisal of the politics of food banking in the UK. Existing work has raised concerns about the institutionalisation of food banks, with charitable assistance apparently – even if inadvertently – undermining collectivist welfare and deflecting attention from fundamental injustices in the food system. This paper presents original ethnographic work that examines the neglected politics articulated within food banks themselves. Conceptualising food banks as potential spaces of encounter where predominantly middle-class volunteers come into contact with ‘poor others’ (Lawson and Elwood, 2013), we illustrate the ways food banks may both reinforce but also rework and generate new, ethical and political attitudes, beliefs and identities. We also draw attention to the limits of these progressive possibilities and examine the ways in which some food banks continue to operate within a set of highly restrictive, and stigmatising, welfare technologies. By highlighting the contradictory dynamics at work in food bank organisations, and among food bank volunteers and clients, we suggest the political role of food banks warrants neither uncritical celebration nor outright dismissal. Rather, food banks represent a highly ambiguous political space still in the making and open to contestatio

Nomenclature for kidney function and disease: report of a Kidney Disease:Improving Global Outcomes (KDIGO) Consensus Conference

The worldwide burden of kidney disease is rising, but public awareness remains limited, underscoring the need for more effective communication by stakeholders in the kidney health community. Despite this need for clarity, the nomenclature for describing kidney function and disease lacks uniformity. In June 2019, Kidney Disease: Improving Global Outcomes (KDIGO) convened a Consensus Conference with the goal of standardizing and refining the nomenclature used in the English language to describe kidney function and disease, and of developing a glossary that could be used in scientific publications. Guiding principles of the conference were that the revised nomenclature should be patient-centered, precise, and consistent with nomenclature used in the KDIGO guidelines. Conference attendees reached general consensus on the following recommendations: (i) to use "kidney" rather than "renal" or "nephro-" when referring to kidney disease and kidney function; (ii) to use "kidney failure" with appropriate descriptions of presence or absence of symptoms, signs, and treatment, rather than "end-stage kidney disease"; (iii) to use the KDIGO definition and classification of acute kidney diseases and disorders (AKD) and acute kidney injury (AKI), rather than alternative descriptions, to define and classify severity of AKD and AKI; (iv) to use the KDIGO definition and classification of chronic kidney disease (CKD) rather than alternative descriptions to define and classify severity of CKD; and (v) to use specific kidney measures, such as albuminuria or decreased glomerular filtration rate (GFR), rather than "abnormal" or "reduced" kidney function to describe alterations in kidney structure and function. A proposed 5-part glossary contains specific items for which there was general agreement. Conference attendees acknowledged limitations of the recommendations and glossary, but they considered standardization of scientific nomenclature to be essential for improving communication

Effects of rare kidney diseases on kidney failure: a longitudinal analysis of the UK National Registry of Rare Kidney Diseases (RaDaR) cohort

\ua9 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 licenseBackground: Individuals with rare kidney diseases account for 5–10% of people with chronic kidney disease, but constitute more than 25% of patients receiving kidney replacement therapy. The National Registry of Rare Kidney Diseases (RaDaR) gathers longitudinal data from patients with these conditions, which we used to study disease progression and outcomes of death and kidney failure. Methods: People aged 0–96 years living with 28 types of rare kidney diseases were recruited from 108 UK renal care facilities. The primary outcomes were cumulative incidence of mortality and kidney failure in individuals with rare kidney diseases, which were calculated and compared with that of unselected patients with chronic kidney disease. Cumulative incidence and Kaplan–Meier survival estimates were calculated for the following outcomes: median age at kidney failure; median age at death; time from start of dialysis to death; and time from diagnosis to estimated glomerular filtration rate (eGFR) thresholds, allowing calculation of time from last eGFR of 75 mL/min per 1\ub773 m2 or more to first eGFR of less than 30 mL/min per 1\ub773 m2 (the therapeutic trial window). Findings: Between Jan 18, 2010, and July 25, 2022, 27 285 participants were recruited to RaDaR. Median follow-up time from diagnosis was 9\ub76 years (IQR 5\ub79–16\ub77). RaDaR participants had significantly higher 5-year cumulative incidence of kidney failure than 2\ub781 million UK patients with all-cause chronic kidney disease (28% vs 1%; p<0\ub70001), but better survival rates (standardised mortality ratio 0\ub742 [95% CI 0\ub732–0\ub752]; p<0\ub70001). Median age at kidney failure, median age at death, time from start of dialysis to death, time from diagnosis to eGFR thresholds, and therapeutic trial window all varied substantially between rare diseases. Interpretation: Patients with rare kidney diseases differ from the general population of individuals with chronic kidney disease: they have higher 5-year rates of kidney failure but higher survival than other patients with chronic kidney disease stages 3–5, and so are over-represented in the cohort of patients requiring kidney replacement therapy. Addressing unmet therapeutic need for patients with rare kidney diseases could have a large beneficial effect on long-term kidney replacement therapy demand. Funding: RaDaR is funded by the Medical Research Council, Kidney Research UK, Kidney Care UK, and the Polycystic Kidney Disease Charity

Effects of rare kidney diseases on kidney failure: a longitudinal analysis of the UK National Registry of Rare Kidney Diseases (RaDaR) cohort

Background Individuals with rare kidney diseases account for 5–10% of people with chronic kidney disease, but constitute more than 25% of patients receiving kidney replacement therapy. The National Registry of Rare Kidney Diseases (RaDaR) gathers longitudinal data from patients with these conditions, which we used to study disease progression and outcomes of death and kidney failure. Methods People aged 0–96 years living with 28 types of rare kidney diseases were recruited from 108 UK renal care facilities. The primary outcomes were cumulative incidence of mortality and kidney failure in individuals with rare kidney diseases, which were calculated and compared with that of unselected patients with chronic kidney disease. Cumulative incidence and Kaplan–Meier survival estimates were calculated for the following outcomes: median age at kidney failure; median age at death; time from start of dialysis to death; and time from diagnosis to estimated glomerular filtration rate (eGFR) thresholds, allowing calculation of time from last eGFR of 75 mL/min per 1·73 m2 or more to first eGFR of less than 30 mL/min per 1·73 m2 (the therapeutic trial window). Findings Between Jan 18, 2010, and July 25, 2022, 27 285 participants were recruited to RaDaR. Median follow-up time from diagnosis was 9·6 years (IQR 5·9–16·7). RaDaR participants had significantly higher 5-year cumulative incidence of kidney failure than 2·81 million UK patients with all-cause chronic kidney disease (28% vs 1%; p<0·0001), but better survival rates (standardised mortality ratio 0·42 [95% CI 0·32–0·52]; p<0·0001). Median age at kidney failure, median age at death, time from start of dialysis to death, time from diagnosis to eGFR thresholds, and therapeutic trial window all varied substantially between rare diseases. Interpretation Patients with rare kidney diseases differ from the general population of individuals with chronic kidney disease: they have higher 5-year rates of kidney failure but higher survival than other patients with chronic kidney disease stages 3–5, and so are over-represented in the cohort of patients requiring kidney replacement therapy. Addressing unmet therapeutic need for patients with rare kidney diseases could have a large beneficial effect on long-term kidney replacement therapy demand. Funding RaDaR is funded by the Medical Research Council, Kidney Research UK, Kidney Care UK, and the Polycystic Kidney Disease Charity

Peritoneal inflammation precedes encapsulating peritoneal sclerosis: results from the GLOBAL fluid study

Background Encapsulating peritoneal sclerosis (EPS) is an uncommon condition, strongly associated with a long duration of peritoneal dialysis (PD), which is itself associated with increased fibrosis in the peritoneal membrane. The peritoneal membrane is inflamed during PD and inflammation is often associated with fibrosis. We hypothesized that patients who subsequently develop EPS might have a more inflamed peritoneal membrane during PD. Methods We performed a nested, case–control study identifying all EPS cases in the UK arm of the GLOBAL Fluid Study and matching them by centre and duration of PD with two to three controls. Dialysate and plasma samples were taken during repeated peritoneal equilibration tests prior to cessation of PD from cases and controls. Samples were assayed by electrochemiluminescence immunoassay for interleukin-1β (IL-1β), tumour necrosis factor α (TNF-α), interferon-γ (IFN-γ) and IL-6. Results were analysed by linear mixed models adjusted for age and time on PD. Results Eleven EPS cases were matched with 26 controls. Dialysate TNF-α {0.64 [95% confidence interval (CI) 0.23, 1.05]} and IL-6 [0.79 (95% CI 0.03, 1.56)] were significantly higher in EPS cases, while IL-1β [1.06 (95% CI −0.11, 2.23)] and IFN-γ [0.62 (95% CI −0.06, 1.29)] showed a similar trend. Only IL-6 was significantly higher in the plasma [0.42 (95% CI 0.07, 0.78)]. Solute transport was not significantly different between cases and controls but did increase in both groups with the duration of PD. Conclusions The peritoneal cavity has higher levels of inflammatory cytokines during PD in patients who subsequently develop EPS, but neither inflammatory cytokines nor peritoneal solute transport clearly discriminates EPS cases. Increased systemic inflammation is also evident and is probably driven by increased peritoneal inflammation