Journal of Nephrology最新文献

Diabetic kidney disease (DKD) is a significant complication of type 2 diabetes, posing a global health risk. Detecting and predicting diabetic kidney disease at an early stage is crucial for timely interventions and improved patient outcomes. Artificial intelligence (AI) has demonstrated promise in healthcare, and several tools have recently been developed that utilize Machine Learning with clinical data to detect and predict DKD. This review aims to explore the current landscape of AI and machine learning applications in DKD, specifically examining existing literature on risk scores and machine learning approaches for predicting DKD development. A literature search was conducted using Medline (PubMed), Google Scholar, and Scopus databases until July 2023. Relevant keywords were used to extract studies that described the role of AI in DKD. The review revealed that AI and machine learning have been successfully used to predict DKD progression, outperforming traditional risk score models. Artificial intelligence-driven research for DKD extends beyond prediction models, offering opportunities for integrating genetic and epigenetic data, advancing understanding of the disease's molecular basis, personalizing treatment strategies, and fostering the development of novel drugs. However, challenges remain, including the requirement for large datasets and the lack of standardization in AI-driven tools for DKD. Artificial intelligence and machine learning have the potential to revolutionize the management and care of DKD patients, surpassing the limitations of traditional methods reliant on existing knowledge. Future research should address the challenges associated with AI and machine learning in DKD and focus on developing AI-driven tools for clinical practice.

Background: Systemic steroids are recommended for patients with IgA nephropathy (IgAN) and proteinuria. However, there are concerns about their safety due to an excess of serious adverse events (SAEs) in previous randomised trials. This study evaluates the incidence of SAEs in IgAN patients receiving different treatment regimens in clinical practice.

Methods: Multicentre, retrospective, observational cohort study of 1209 patients (M/F: 864/345, mean age: 41.73 ± 14.92 years) with biopsy-proven IgAN treated with renin angiotensin system (RAS) inhibitors (RASI) (n = 285), intravenous + oral steroids (n = 633), oral steroids (n = 99), steroids + immunosuppressants (n = 192).

Results: A total of 119 (9.8%) adverse events were reported, of which 67 (5.5%) were considered treatment-emergent, and 36 (2.9%) were SAEs (n = 23, 63.8% were infections). One patient died due to sepsis. A significant association was observed between AEs and immunosuppression [8 (2.8%) in RASI, 60 (9.4%) in steroids + immunosuppressants, 14 in oral steroids (14.1%) and 37 pts (19.2%) in steroids + immunosuppressants (p < 0.01)], age and estimated glomerular filtration rate (eGFR), but not with proteinuria and sex. On multivariate analysis, only older age was associated with the occurrence of SAEs.

Conclusions: According to our findings, the incidence of SAEs during therapy with steroids alone or associated with immunosuppressors is lower in everyday clinical practice than in randomised clinical trials.

Osimertinib is an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) effective in non- small cell lung cancer (NSCLC) with EGFR mutations. Since the drug is primally eliminated by the fecal route no dose adjustment is needed in patient with chronic-kidney disease (CKD); despite this there is limited data about its safety in cancer patients with end-stage renal disease (ESRD). Herein, we reported a case report of a 77-year-old woman, diagnosed in 2018 with lung adenocarcinoma EGFR mutated with lymph nodal and cerebral metastasis, who started Osimertinib 80 mg/day. She under- went 41 cycles of therapy with no Osimertinib interruptions, no severe toxicities and obtaining complete radiological response. We conclude that Osimertinib has an acceptable safety profile also in cancer patients with ESRD not undergoing hemodialysis (HD).

Background: α-Klotho deficiency may increase cardiovascular risks and worsen survival. We evaluated the association of α-Klotho with cardiovascular and all-cause mortality in pre-dialysis chronic kidney disease (CKD) patients.

Methods: In this prospective study, 75 non-diabetic CKD stage 3b-4 patients were followed-up for a median of 8 years. Primary and secondary outcomes were all-cause and cardiovascular mortality, respectively. Human soluble α-Klotho ELISA Assay (IBL-Takara 27,998-96Well), Human Fibroblast Growth Factor-23 ELISA Assay (intact FGF23, Merck Millipore MILLENZ FGF23-32 K), and Human Sclerostin ELISA kits (Biomedica, Vienna, BI-20492) were used to measure serum α-Klotho, FGF23 and sclerostin levels in the certified laboratory at the Sechenov University according to the manufacturers' protocols. All patients underwent echocardiography to evaluate left ventricular mass index (LVMI), left ventricular ejection fraction by Simpson method, and cardiac (valve) calcification score by a semi-quantitative point scale. Lateral abdominal radiography by Kauppila method was used to estimate calcification of the abdominal aorta. Cox multivariate regression and receiver-operating characteristic curve (ROC)-analysis were used to evaluate risk factors for death and their cut-off values.

Results: Primary and secondary endpoints were reached in 15 (20%) and 9 (12%) patients, respectively. Median α-Klotho levels in deceased and surviving patients were 344 and 484 pg/ml, respectively (p = 0.002). In a multivariate Cox regression model, baseline α-Klotho levels (HR 0.99, 95% CI 0.98-1.00, p = 0.023), aortic calcification (HR 1.18, 95% CI 1.02-1.36, p = 0.029) and left ventricular mass index (LVMI) (HR 1.04, 95% CI 1.00-1.08, p = 0.033) were associated with the primary endpoint, whereas α-Klotho (HR 0.99, 95% CI 0.98-1.00, p = 0.029), aortic calcification (HR 1.23, 95% CI 1.07-1.42, p = 0.003) and LVMI (HR 1.04, 95% CI 1.00-1.08, p = 0.021) were associated with the secondary endpoint. α-Klotho levels had the highest area under the curve (AUC) by ROC analysis, that is, 0.766 (95% CI 0.70-0.82) for the primary endpoint and 0.842 (95% CI 0.79-0.90) for the secondary endpoint with cut-off values of 412 pg/ml (HR 3.06, 95% CI 1.36-6.89, p = 0.007) and 368 pg/ml (HR 4.84, 95% CI 1.59-14.73, p = 0.005), respectively.

Conclusion: In pre-dialysis CKD patients, α-Klotho levels are associated with all-cause and cardiovascular mortality and may be considered an early prognostic marker.

Background: Chronic Kidney Disease (CKD) significantly increases the risk of cardiovascular diseases, including atrial fibrillation, which usually requires anticoagulant therapy. The effectiveness and safety of direct oral anticoagulants compared to vitamin K antagonists in patients with CKD remain insufficiently studied, particularly in the more advanced stages.

Methods: This systematic review, registered in PROSPERO (CRD42023410192), adhered to PRISMA guidelines and included randomized clinical trials and cohort studies comparing direct oral anticoagulants and vitamin K antagonists in CKD patients. Major databases were searched, and studies were selected based on strict inclusion criteria. A meta-analysis was performed using random-effects models.

Results: Twenty-three studies with a total of 465,673 CKD patients were included. Direct oral anticoagulants showed a significant reduction in major bleeding events compared to vitamin K antagonists (Relative Risk [RR] = 0.62, 95% Confidence Interval: 0.49-0.79, p < 0.01) and a non-significant trend toward reducing thromboembolic events (RR = 0.69, 95% Confidence Interval: 0.43-1.14, p = 0.11). Furthermore, direct oral anticoagulants were associated with a significant reduction in all-cause mortality (RR = 0.63, 95% Confidence Interval: 0.43-0.91, p = 0.02).

Conclusion: Direct oral anticoagulants may offer a safe alternative to vitamin K antagonists in CKD patients, particularly in terms of reducing bleeding risks and potentially improving survival. However, their role in preventing thromboembolic events remains uncertain, highlighting the need for further research, especially in patients with advanced CKD and kidney failure.