Clinical Kidney Journal最新文献

Background: Acute kidney injury (AKI) is associated with increased morbidity and mortality but is likely underrecorded in health registers. This study examined the sensitivity and positive predictive value (PPV) of AKI diagnoses compared with laboratory-identified AKI.

Methods: In this observational study we analysed data from the Danish National Patient Register and laboratory databases from January 2007 through November 2023. Diagnoses of AKI according to the International Classification of Diseases, 10th Revision (ICD-10) were compared with laboratory-identified AKI episodes defined by the Kidney Disease: Improving Global Outcomes (KDIGO) creatinine criteria. Sensitivity was defined as the proportion of laboratory-identified AKI episodes captured by ICD-10 codes within 30 days before or after the episode's index date and PPV was the proportion of ICD-10-coded AKI episodes confirmed by the KDIGO criteria within a ±30-day window. Analyses were stratified by sex, age, AKI stage, setting, comorbidity and short-term mortality.

Results: A total of 947 209 laboratory-identified AKI episodes and 80 649 ICD-10-coded AKI episodes were included. Overall, sensitivity was 7.5% [95% confidence interval (CI) 7.4-7.5], varying by stage (4.0% for stage 1 versus 21.7% for stage 3) and setting (6.0% for hospital acquired versus 8.6% for community acquired). The overall PPV was 90.6% (95% CI 90.4-90.9), with little variation across subgroups.

Conclusion: ICD-10 codes of AKI demonstrate a high PPV, ensuring accuracy in identifying true AKI episodes. However, the low sensitivity highlights a risk of underestimating AKI occurrence. Laboratory data should be prioritized for comprehensive AKI identification and potential biases addressed when relying on diagnosis codes in research.

Background: Myelodysplastic syndromes(MDSs) have been known to be associated with various forms of kidney disease; however, whether they predispose to a longitudinal decrease in kidney function in the general population is unknown. This study aimed to investigate the association between MDSs and the risk of kidney function decline using a large-scale population-based cohort.

Methods: We retrospectively analysed nationwide administrative claims and health checkup data collected between April 2014 and August 2024. MDSs were identified using International Classification of Diseases, 10th Revision codes. Individuals were categorized into two groups according to the presence of MDSs. 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 years [interquartile range (IQR) 61-72]; 41.9% male}, MDSs were identified in 901 individuals (0.05%). During a median follow-up of 1092 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 MDSs compared with those without MDSs (P < .001, logrank test). In multivariable Cox regression analysis, the presence of MDSs 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, MDSs were significantly associated with an increased risk of kidney function decline, positioning MDSs as a clinically relevant kidney risk condition and supporting closer kidney monitoring in this population.

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 ∼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.

Background: Tunnelled catheter-related bloodstream infections (CRBSIs) in haemodialysis (HD) 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 HD patients with suspected or confirmed CRBSI. Patients received either 70% ELT 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 ELT (78.6% versus 57.1%; P = .035). Recurrence was lower with ELT at day 60 (20.5% versus 53.7%; P = .002). The median catheter survival was longer (15 versus 8 days), although not statistically significant (P = .283). Fever resolution by day 7 was significantly higher in the ELT group compared with controls (64.3% versus 35.7%; P = .009). Adverse events were infrequent and mild. In multivariate analysis, higher serum albumin was independently associated with an increased likelihood of catheter salvage [odds ratio (OR) 2.43, P = .038], while longer dialysis vintage (OR 0.90, P = .035) and Pseudomonas infection (OR 0.05, P = .014) were associated with reduced salvage rates.

Conclusion: Adjunctive ELT 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.

Muscle cramps are common in patients undergoing haemodialysis, but their pathophysiology is not well understood. The effect of regional blood flow reduction on the neuromuscular compartment as a result of a 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.

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 etiology. Whole-exome sequencing (WES) was performed on peripheral blood DNA. Variants were curated and classified per the American College of Medical Genetics and Genomics/Association for Molecular Pathology (ACMG/AMP) 2015 and Association for Clinical Genomic Science (ACGS) guidelines, with only "pathogenic" or "likely pathogenic" findings considered diagnostic.

Results: The cohort was 59% male, mean ESKD onset 53.2 ± 14.3 years. A definitive monogenic diagnosis emerged in 7.3% (23/317) of patients, in line with multicenter and international studies. Genes 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 and Alport syndrome as major genetic contributors in adult ESKD. Notably, mutations in ACTN4, PAX2, COQ8B or INF2, causing hereditary steroid-resistant nephrotic syndrome, led to significantly earlier ESKD onset (mean 31.3 years) compared with PKD1 or COL4-related cases. Inconclusive 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 therapy. These 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.