Clinical Kidney Journal最新文献

Background: Despite the high suicide rates among patients with end-stage kidney disease (ESKD), there is no suicide prediction model specifically designed for this vulnerable population. Herein, we aimed to develop and validate a novel suicide risk score for ESKD patients.

Methods: We analyzed data from the National Health Insurance Service (NHIS) of South Korea, including 251 819 patients aged above 18 years diagnosed with ESKD between 2007 and 2022 in South Korea. The mean follow-up duration was 6.6 years. The cohort was randomly divided into derivation (70%) and validation (30%) sets. Using multivariate Cox proportional hazard regression, key variables were incorporated to develop the suicide risk score, which was converted into a 48-point scoring system, which is composed of easily identifiable clinical parameters.

Results: Among 176 273 patients in the derivation cohort, 1126 (0.64%) patients committed suicide. The suicide risk score demonstrated moderate discrimination in both the derivation (C-statistic, 0.694) and validation (C-statistic, 0.709) cohorts, with good calibration. In the validation cohort, patients scoring below 16, 17-32 and 33-48 had predicted 10-year suicide risk of 0.2%, 1.2% and 7.7%, respectively, while the observed 10-year risk were 0.3%, 0.8% and 3.9%. These findings highlight the model's ability to effectively stratify risk using routinely available clinical data.

Conclusions: The suicide risk score is a significant advancement in suicide risk prediction for ESKD patients. It is based on simple, routinely collected clinical indicators and provides an actionable tool for risk stratification and early intervention in daily practice.

Background: Diabetes is the leading cause of end-stage kidney disease (ESKD) worldwide. In particular, whether diabetes has a negative effect on the risk of transfer to haemodialysis (HD) remains controversial. This study was conducted to provide updated data on outcomes of patients with diabetes on peritoneal dialysis (PD).

Methods: This was a retrospective cohort study using data from the French Language Peritoneal Dialysis Registry, including patients starting PD between 2008 and 2018; the end of the study was 31 December 2021. Cox and Fine-Gray models examined associations between diabetes and mortality, transfer to HD, a composite outcome of death and HD transfer and kidney transplantation. In addition, the causes of transfer to HD were analysed separately. Mediation analyses were performed to assess the indirect effects of early peritonitis and assisted PD on HD transfer.

Results: Of 10 412 PD patients, 3473 (33%) were diabetics. Diabetes was associated with an increased risk of HD transfer {cause-specific hazard ratio [cs-HR] 1.69 [95% confidence interval (CI) 1.36-2.11]}, death [cs-HR 1.32 (95% CI 1.21-1.43)] and the composite outcome [cs-HR 1.23 (95% CI 1.15-1.31)] in Cox and Fine-Gray models [HD transfer subdistribution HR (sd-HR) 1.18 (95% CI 1.07-1.31); death sd-HR 1.25 (95% CI 1.15-1.35)]. Diabetic patients were less likely to receive a kidney transplant [cs-HR 0.52 (95% C: 0.41-0.66); sd-HR 0.44 (95% CI 0.35-0.56)]. At a 5% false discovery rate, diabetes was significantly associated with an increased risk of transfer to HD due to inadequate dialysis, other PD-related causes and non-PD-related causes. Mediation analyses showed no significant indirect effects via early peritonitis or assisted PD.

Conclusion: Diabetes has a higher risk of transfer to HD that was not explained by early peritonitis or not being assisted. Diabetic PD patients have a greater mortality risk and lower access to transplantation.

Background: The prevalence of depression is high among patients with end-stage kidney disease (ESKD). Recent studies have indicated under-recognition and -treatment of depression in this population, and little is known about how the specialty of the prescribing clinician may influence clinical outcomes. This study aimed to evaluate whether the prescribing clinician's specialty (psychiatrist vs. non-psychiatrist) is associated with clinical outcomes in patients with ESKD and comorbid depression who receive antidepressant treatment.

Methods: We extracted data from the Korean National Health Institute Database System from January 2004 to December 2022. Patients with ESKD and depression who underwent antidepressant therapy after their ESKD diagnosis were included. Patients were followed up for 4.7 ± 3.5 years.

Results: Among 16 756 patients with ESKD and depression [mean age, 67.3 years; 8614 (51.4%) men], 7841 (46.8%) patients were prescribed antidepressants by psychiatrists. After propensity score matching, the 5-year mortality was significantly lower in the psychiatrist (25.8%) than in the non-psychiatrist group (38.2%). After multivariable adjustment, prescription by a psychiatrist remained significantly associated with lower mortality (adjusted hazard ratio, 0.66; 95% confidence interval, 0.62-0.70; P < .001). All-cause mortality was consistent across various subgroups, such as age (above or below 75 years), sex, time from dialysis initiation to depression diagnosis, income level, region of residence, and comorbidity status. This trend remained in 6-month, 1-year, 2-year, and 3-year landmark analyses.

Conclusions: Our findings suggest a potential benefit of specialty psychiatric care for improving clinical outcomes in patients with ESKD and depression.

Despite advances and therapeutic progress, nephrotic syndrome (NS) in childhood remains challenging due to its heterogeneous presentation, variable response to treatment and the potential of adverse long-term kidney outcomes. The recently published KDIGO 2025 clinical practice guideline for the management of NS in children refines the definitions of relapse, infrequently- and frequently-relapsing NS and steroid-resistant NS. Herein we describe the revised definitions, summarize the key updates of the KDIGO 2025 guidelines and comment on the new treatment algorithm from a European viewpoint, highlighting the need for individualized approaches to minimize toxicity and optimize long-term kidney outcomes in NS in children.

Background: Patients undergoing hemodialysis frequently experience stress, physical discomfort, depressive symptoms and prolonged immobility during lengthy treatment sessions. Immersive virtual reality (VR) has shown promise as a non-pharmacological intervention to improve wellbeing in various clinical settings. However, no multicenter study has examined personalized immersive VR in dialysis patients. This study therefore aimed to assess the tolerability and effects of a single personalized VR session on wellbeing, pain and physiological parameters in patients undergoing hemodialysis.

Methods: In this pre-post single group pilot study, 148 participants from 12 dialysis centers (10 outpatient, 2 in-hospital) were enrolled. Each patient completed one personalized 20-min VR session, selecting from 20 immersive 360° options. Emotional wellbeing and pain were assessed before and after VR exposure, while treatment tolerance, perceived quality and feasibility were assessed post-session. Physiological parameters (blood pressure, heart rate, oxygen saturation) were recorded before, during and after exposure.

Results: Of the 148 enrolled participants, 143 completed the intervention (mean age 62.2 ± 14.5 years; 64.9% male and 35.1% female). Wellbeing improved significantly; among participants reporting pain, scores decreased by ∼50%. Systolic blood pressure declined from 135 to 128 mmHg and diastolic from 72 to 69 mmHg during VR exposure, with heart rate decreasing from a mean of 72 to 67 bpm (P < .0001 for all); values returned toward baseline afterwards. No serious adverse events were reported.

Conclusion: Personalized VR was well tolerated and produced measurable psychological and physiological benefits in dialysis patients, supporting its potential as a feasible non-pharmacological adjunct to routine care.

Amino acid metabolism is closely linked with kidney physiology and pathology. In acute kidney injury, chronic kidney disease, diabetic kidney disease, and autosomal dominant polycystic kidney disease, disturbances in the branched-chain amino acids, tryptophan, glutamine, taurine, and sulfur amino acids pathways are consistently observed. Specific metabolites such as D-serine, kynurenine intermediates, and branched-chain keto acids are associated with disease progression. Taurine and indoxyl sulfate have also been proposed as therapeutic targets. At the nephron level, transporters and enzymes controlling amino acid flux influence nitrogen balance, oxidative stress, fibrosis, inflammation, and tubular injury. In chronic kidney disease, impaired amino acid handling contributes to protein-energy wasting, altered muscle metabolism, and systemic complications. In autosomal dominant polycystic kidney disease, cyst fluid metabolomics has revealed alterations in tryptophan and polyamine metabolism. The use of nutritional interventions, microbiome modulation, and selective supplementation as therapeutic strategies is being explored, although clinical trial evidence remains limited. Several key issues remain unresolved, including the need for isotope tracer studies to define renal amino acid kinetics in humans, the rigorous validation of metabolite biomarkers across diverse populations, the integration of diet and microbiome-derived metabolites into mechanistic frameworks, and the systematic evaluation of sex-specific differences. Longitudinal studies are scarce, thus restricting predictive power and therapeutic translation. Further mechanistic clarification may support the development of biomarkers and targeted therapies.

Background: The administration of an adequate dialysis dose is a critical aspect for ensuring the effectiveness of hemodialysis (HD) treatment and improving survival. Kt is a key indicator to evaluate the dose, with two targets: based on sex (Kt-Sx) and body surface area (Kt-BSA).

Methods: This retrospective study (2022-23) was conducted across 15 HD centers analyzed 1829 prevalent patients and 317 842 HD sessions.

Results: It was found that 65.9% met both Kt targets, 21.2% met only Kt-Sx and 12.9% met neither. Failure to meet both of the targets was associated with being male, older age, shorter time on HD, higher comorbidity, low body mass index, use of a catheter, shorter sessions, conventional HD, low flow rates and small membranes. Meeting at least the Kt-Sx target was associated with a 41.6% reduction in 24-month mortality risk, and an even more favorable association was observed when both targets were met, reducing the risk by 61.7%.

Conclusions: These findings highlight the importance of personalizing dialysis considering both sex and BSA, particularly in overweight or obese patients, to improve survival.

Background: Patients with chronic kidney disease (CKD) are frequently hospitalized for heart failure. Sodium-glucose co-transporter 2 (SGLT2)-inhibitors improve cardiorenal outcomes in CKD and heart failure, at least in estimated glomerular filtration rate (eGFR) ranges 20-60 ml/min/1.73 m², possibly through direct cardiac effects. In the cardiac imaging sub-studies of the Renal Lifecycle Trial, we aim to establish the effects of SGLT2-inhibition on cardiac structure and function in patients with advanced CKD, kidney failure and in kidney transplant recipients.

Methods: In the Renal Lifecycle Trial, patients with advanced CKD (eGFR ≤25 ml/min/1.73 m²), those treated with hemodialysis or peritoneal dialysis (PD) or kidney transplant recipients (eGFR ≤45 ml/min/1.73 m²), are randomized to receive either dapagliflozin or placebo. The echocardiography sub-study (acronym: STOP-HF-in-PD) will enroll 100 PD-treated patients, who undergo echocardiography at baseline, and at 6 and 12 months post-randomization. In the cardiac magnetic resonance imaging (MRI) sub-study, 250 Renal Lifecycle Trial participants across all three groups (i.e. advanced CKD, dialysis, kidney transplant recipients), including a subset of STOP-HF-in-PD participants, will undergo cardiac MRI at baseline, and at 12 months post-randomization. The primary endpoint of STOP-HF-in-PD is the difference in left ventricular global longitudinal strain, a measure of cardiac function, after 6-months of dapagliflozin compared to placebo. For the cardiac MRI sub-study, the primary endpoint is the difference of indexed left ventricular mass after 12 months of dapagliflozin compared to placebo.

Conclusions: The Renal Lifecycle Trial cardiac imaging sub-studies will generate novel data on the effects of SGLT2-inhibition on cardiac structure and function in a population with advanced CKD, in whom SGLT2-inhibitor induced cardiovascular protection remains to be established.

Clinical trial registration: The Renal Lifecycle Trial and its sub-studies are registered at ClinicalTrials.gov under registration number NCT05374291.

Mucosal-associated invariant T (MAIT) cells are a distinct subset of innate-like lymphocytes that bridge microbial homeostasis and tissue immunity. These evolutionarily conserved cells are activated via the recognition of microbial metabolites presented by the MR1 molecule and establish stable residency in the kidney, where they profoundly influence local immune-metabolic processes. There is growing interest in the robust regulatory capacities of MAIT cells in renal physiology and pathology. This review systematically delineates their paradoxical roles in kidney diseases. Under specific conditions, they exert protective functions by suppressing inflammation and maintaining tissue homeostasis. Conversely, in distinct microenvironments, they adopt a pro-inflammatory phenotype, exacerbating pathological progression through the release of inflammatory cytokines and cytotoxic effector functions. The gut-kidney axis serves as a critical regulatory hub, wherein dysbiosis-derived signals can significantly amplify the renal impact of MAIT cells. Focusing on clinical translation, we provide an in-depth exploration of innovative strategies targeting MAIT cells, including adoptive cell therapy, receptor-targeting agents, and microbiome reconstruction. These approaches position MAIT cells as promising therapeutic targets for a new generation of immune-mediated kidney diseases.