Abstract Background Myelodysplastic syndromes (MDS) have been associated with various forms of kidney disease; however, whether they predispose to a longitudinal decline in kidney function in the general population is unknown. This study aimed to investigate the association between MDS and the risk of kidney function decline using a large-scale population-based cohort. Methods We retrospectively analyzed nationwide administrative claims and health checkup data collected between April 2014 and August 2024. MDS were identified using International Classification of Diseases, 10th Revision codes. Individuals were categorized into two groups according to the presence of MDS. The primary outcome was a composite kidney outcome, defined as incident end-stage kidney disease, initiation of kidney replacement therapy, or a ≥30% decline in estimated glomerular filtration rate. Results Among 1,659,421 individuals (median age, 68 [IQR, 61–72] years; 41.9% male), MDS were identified in 901 individuals (0.05%). During a median follow-up of 1,092 days (IQR, 631–1520), 33,335 individuals experienced the composite kidney outcome. Cumulative incidence curves demonstrated a higher incidence of kidney function decline in individuals with MDS compared with those without MDS (P <0.001, log-rank test). In multivariable Cox regression analysis, the presence of MDS was independently associated with an increased risk of kidney function decline (hazard ratio 2.28 [95% confidence interval 1.66–3.13]). Conclusions In this large-scale nationwide cohort, MDS were significantly associated with an increased risk of kidney function decline, positioning MDS as a clinically relevant kidney risk condition and supporting closer kidney monitoring in this population.

Abstract Thrombotic microangiopathy (TMA) is a pathological condition characterized by microangiopathic hemolytic anemia, thrombocytopenia and ischemic organ dysfunction due to microvascular endothelial damage and thrombosis. It affects approximately 0.8-14% of kidney transplant recipients, and may manifest as either a recurrent or de novo disease. While systemic manifestations are commonly anticipated, kidney-limited TMA can also occur and is not rare. Histopathologic examination of allograft biopsies shows morphologic features indicating endothelial injury, and repeated episodes of TMA may result in coexisting acute and chronic lesions within the same patient. In transplant recipients, multiple triggers contribute to endothelial damage, including ischemia-reperfusion injury, antibody-mediated rejection, immunosuppressive agents (calcineurin and mTOR inhibitors) and infections. The risk is particularly important in individuals with genetic variants that dysregulate the alternative complement pathway. In de novo TMA, environmental triggers and transplant-related stressors play a central role, whereas genetic predisposition is the primary factor in recurrent cases. Notably, these mechanisms often overlap and may act synergistically. Recurrent atypical hemolytic uremic syndrome can successfully be managed with terminal complement inhibitors, and prophylactic use of eculizumab in the peri-transplant period has significantly reduced recurrence rates. Management of de novo TMA begins with the identification and removal of precipitating factors. In cases where no clear trigger is found, or when the disease proves refractory to conventional therapy, terminal complement inhibition may be an effective therapeutic option. The prognosis of recurrent TMA has improved substantially with the advent of complement targeting therapies but research is still needed to optimize management strategies.

Abstract Muscle cramps are common in patients undergoing hemodialysis, but their pathophysiology is not well understood. The effect of regional blood flow reduction on the neuro-muscular compartment as a result of high-flow arteriovenous fistula (HFAVF) was not previously implicated in dialysis-associated muscle cramps. We report a patient with HFAVF (Blood flow rate 2450 mL/min) causing high cardiac output failure, who developed severe muscle cramps during dialysis, significantly limiting ultrafiltration and causing fluid overload. Ligation of the fistula resulted in complete reversal of muscle cramps, allowing for adequate ultrafiltration. This case highlights the need for clinical vigilance and potential screening for HFAVF in dialysis patients presenting with persistent muscle cramps.

Abstract Background Monogenic causes are increasingly recognized in end-stage kidney disease (ESKD), but the real-world diagnostic efficacy of exome sequencing in unselected dialysis cohorts is still being defined. Methods We conducted a prospective study enrolling 317 adult ESKD patients from a single center in Taiyuan, China, regardless of presumed etiologyWhole-exome sequencing (WES) was performed on peripheral blood DNAVariants were curated and classified per the ACMG/AMP 2015 and ACGS guidelines, with only ‘pathogenic’ or ‘likely pathogenic’ findings considered diagnostic. Results The cohort was 59% male, mean ESKD onset 53.2 ± 14.3 yearsA definitive monogenic diagnosis emerged in 7.3% (23/317) of patients, in line with multicenter and international studiesGenes most frequently implicated were PKD1 (3.5% of cohort; 47.8% of genetically diagnosed) and COL4A3/4/5 (1.9%; 26.1% of diagnosed), reflecting global trends of autosomal dominant polycystic kidney disease (ADPKD) and Alport syndrome as major genetic contributors in adult ESKDNotably, mutations in ACTN4, PAX2, COQ8B or INF2, causing hereditary steroid-resistant nephrotic syndrome (SRNS), led to significantly earlier ESKD onset (mean 31.3 years) compared to PKD1 or COL4-related casesInconclusive genetic findings were present in 7.9% (25/317)Most patients reported no family history of kidney disease, indicating the limitations of clinical suspicion alone. Conclusions In a real-world Chinese dialysis cohort, WES provided a molecular diagnosis in 7.3% of cases, demonstrating clinical utility for risk stratification, family counseling, donor selection, and actionable therapyThese findings underscore the need for routine integration of genetic testing in ESKD care irrespective of family history, especially to clarify ambiguous cases and optimize management.

Abstract Background Tunnelled catheter-related bloodstream infections (CRBSIs) in haemodialysis are challenging to manage due to biofilm formation. Ethanol lock therapy (ELT) has demonstrated potential as an adjunct to antibiotics for catheter salvage, but robust evidence is limited. Methods We conducted a single-centre, open-label, randomised controlled trial of adult haemodialysis patients with suspected or confirmed CRBSI. Patients received either 70% ethanol lock therapy plus intravenous antibiotics or intravenous antibiotics alone. Primary outcome was catheter salvage at Day 7. Secondary outcomes included recurrence at Day 60, catheter survival, and adverse events. Results Eighty-four patients were randomised (42 per arm). Coagulase-negative Staphylococcus was the most common pathogen (34.5%). Early catheter salvage was higher with ethanol lock (78.6% vs 57.1%; P = 0.035). Recurrence was lower with ethanol lock at Day 60 (20.5% vs 53.7%; P = 0.002). Median catheter survival was longer (15 vs 8 days), though not statistically significant (P = 0.283). Fever resolution by Day 7 was significantly higher in the ethanol lock group compared to control (64.3% vs. 35.7%, P = 0.009). Adverse events were infrequent and mild. In multivariate analysis, higher serum albumin was independently associated with increased likelihood of catheter salvage (OR 2.43, P = 0.038), while longer dialysis vintage (OR 0.90, P = 0.035) and Pseudomonas infection (OR 0.05, P = 0.014) were associated with reduced salvage rates. Conclusion Adjunctive ethanol lock therapy improved early catheter salvage and reduced recurrence without significant adverse effects. These findings support its use as part of salvage protocols in tunnelled catheter infections.

Abstract Chronic kidney disease (CKD) affects approximately 10% of adults worldwide and is associated with an elevated risk of cardiovascular disease, such as heart failure, and increased prevalence of comorbidities such as type 2 diabetes (T2D). Early CKD diagnosis and intervention are crucial to prevent progression to advanced kidney disease, which imposes a significant clinical and economic burden on health systems and patients alike. Despite the availability of global CKD management guidelines, adherence remains low, particularly with respect to the use of sodium-glucose cotransporter 2 inhibitors (SGLT2is), which offer strong cardiorenal benefits particularly when initiated in a timely manner. This gap underscores the urgent need for practical solutions to translate existing guideline recommendations into improved clinical practice across the CKD management pathway, encompassing screening, treatment initiation and referral. This manuscript highlights successful global initiatives in CKD management, presenting a ‘call-to-action’ to support healthcare systems and providers in achieving improved CKD management worldwide. By bringing together eight diverse ‘Champions of Change’ initiatives from various health systems, this paper presents innovative, and transformative solutions across the entire CKD management pathway, from early diagnosis to treatment. These case studies underscore the potential of tailored, context-specific strategies to transforming CKD care. By adopting core principles such as proactive screening, risk stratification strategies, multidisciplinary collaboration, knowledge-sharing, and patient-centred approaches, healthcare systems and providers can adapt these successful models to their local settings, thereby advancing global efforts to prevent CKD progression and improve patient outcomes.

Abstract Immunoglobulin A nephropathy (IgAN) is an immune-mediated disease of B-cell origin and the most common primary glomerulonephritis worldwide, which often progresses to kidney failure within 10–20 years of diagnosis. Microscopic hematuria is frequently observed in IgAN; it is thought to result from damage to the glomerular filtration barrier caused by pathogenic immune complex deposits, allowing red blood cells to leak into the urinary space. Emerging evidence suggests that microscopic hematuria in IgAN may be linked to active glomerular inflammation, poorer disease prognosis, and progressive kidney function decline. Despite this, it remains an underutilized biomarker for IgAN because of a lack of standardization (which can lead to preanalytical errors), challenging logistical considerations in large multicenter trials, and non-glomerular hematuria as a confounding factor. The ‘proteinuria-centric’ approach by the nephrology community may overlook that active forms of glomerulonephritis manifest with both proteinuria and hematuria, in contrast to primary podocytopathies where proteinuria is the main feature. When properly assessed, microscopic hematuria is a prognostically relevant biomarker in IgAN that may improve risk stratification and assessment of therapeutic response when evaluated alongside traditional biomarkers. This review evaluates the methods of assessment, pathophysiology, and clinical utility of microscopic hematuria in IgAN.