Kidney international最新文献

{"title":"An observational cohort study of kidney function evolution following increased BK viral replication.","authors":"Evert Cleenders, Maarten Coemans, Olga Mineeva-Sangwo, Priyanka Koshy, Dirk Kuypers, Geert Verbeke, Maarten Naesens","doi":"10.1016/j.kint.2024.10.013","DOIUrl":"https://doi.org/10.1016/j.kint.2024.10.013","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142503093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Presentation and outcome in carriers of pathogenic variants in SLC34A1 and SLC34A3 encoding sodium-phosphate transporter NPT 2a and 2c.","authors":"Max Brunkhorst, Lena Brunkhorst, Helge Martens, Svetlana Papizh, Martine Besouw, Corinna Grasemann, Serap Turan, Przemyslaw Sikora, Milan Chromek, Elisabeth Cornelissen, Marc Fila, Marc Lilien, Jeremy Allgrove, Thomas J Neuhaus, Mehmet Eltan, Laura Espinosa, Dirk Schnabel, Ibrahim Gokce, Juan David González-Rodríguez, Priyanka Khandelwal, Mandy G Keijzer-Veen, Felix Lechner, Maria Szczepańska, Marcin Zaniew, Justine Bacchetta, Francesco Emma, Dieter Haffner","doi":"10.1016/j.kint.2024.08.035","DOIUrl":"https://doi.org/10.1016/j.kint.2024.08.035","url":null,"abstract":"<p><p>Pathogenic variants in SLC34A1 and SLC34A3 encoding sodium-phosphate transporter 2a and 2c are rare causes of phosphate wasting. Since data on presentation and outcomes are scarce, we collected clinical, biochemical and genetic data via an online questionnaire and the support of European professional organizations. One hundred thirteen patients (86% children) from 90 families and 17 countries with pathogenic or likely pathogenic variants in SLC34A1 or SLC34A3 and a median follow-up of three years were analyzed. Biallelic SLC34A1 variant carriers showed polyuria, failure to thrive, vomiting, constipation, hypercalcemia and nephrocalcinosis in infancy, while biallelic SLC34A3 carriers presented in childhood or even adulthood with rickets/osteomalacia and/or osteopenia/osteoporosis, hypophosphatemia and, less frequently, nephrocalcinosis, while the prevalences of kidney stones were comparable. Adult biallelic SLC34A3 carriers had a six-fold increase chronic kidney disease (CKD) prevalence compared to the general population. All biallelic variant carriers shared a common biochemical pattern including elevated 1,25(OH)₂D and alkaline phosphatase levels, suppressed parathyroid hormone (PTH), and hypercalciuria. Heterozygous carriers showed similar but less pronounced phenotypes. In biallelic SLC34A1 carriers, an attenuation of clinical features was observed after infancy, independent of treatment. Phosphate treatment was given in 55% of patients, median duration two years, and resulted in significant reduction, although not normalization, of alkaline phosphatase and of hypercalciuria but an increase in PTH levels, while 1,25(OH)₂D levels remained elevated. Thus, our study indicates that biallelic SLC34A1 and SLC34A3 carriers show distinct, albeit overlapping phenotypes, with the latter having an increased risk of CKD in adulthood. Phosphate treatment may promote kidney phosphate loss and enhance 1,25(OH)₂D synthesis via increased PTH production.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142503096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnosis and Management of Immune Checkpoint Inhibitor-Associated Nephrotoxicity: A Position Statement from the American Society of Onco-nephrology.","authors":"Sandra M Herrmann, Ala Abudayyeh, Shruti Gupta, Prakash Gudsoorkar, Nattawat Klomjit, Shveta S Motwani, Sabine Karam, Verônica T Costa E Silva, Sheikh B Khalid, Shuchi Anand, Jaya Kala, David E Leaf, Naoka Murakami, Arash Rashidi, Rimda Wanchoo, Abhijat Kitchlu","doi":"10.1016/j.kint.2024.09.017","DOIUrl":"https://doi.org/10.1016/j.kint.2024.09.017","url":null,"abstract":"<p><p>Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of cancer and are now the backbone of therapy for several malignancies. However, ICIs can cause a spectrum of renal immune-related adverse events including acute kidney injury (AKI), most commonly manifesting as acute interstitial nephritis (AIN), though glomerular disease and electrolyte disturbances have also been reported. In this position statement by the American Society of Onco-nephrology (ASON), we summarize the incidence and risk factors for ICI-AKI, pathophysiological mechanisms and clinicopathological features of ICI-AKI. We also discuss novel diagnostic approaches and promising biomarkers for ICI-AKI. From expert panel consensus, we provide clinical practice points for the initial assessment and diagnosis of ICI-AKI, management and immunosuppressive therapy, and consideration for re-challenge with ICI following AKI episodes. In addition, we explore ICI use in special populations such as kidney transplant recipients and propose key areas of focus for future research and clinical investigation.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142503094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Avoiding Arrythmias by Personalizing Dialysate Concentration: A Case for Precision Medicine in Dialysis Patients.","authors":"T Alp Ikizler, Tilman B Drueke, Jürgen Floege, Germaine Wong","doi":"10.1016/j.kint.2024.10.009","DOIUrl":"https://doi.org/10.1016/j.kint.2024.10.009","url":null,"abstract":"<p><p>Cardiac arrythmias are common in patients undergoing maintenance hemodialysis (HD). In this issue of the journal, Charytan et al showed that, in HD patients with hyperkalemia (5.1 - 6.5 mEq/l), a dialysate concentration of 3 mEq/l combined with sodium zirconium cyclosilicate (SZC) on dialysis-free days is associated with a less rate of atrial fibrillation compared to a dialysate concentration of 2 mEq/l over 8 weeks. Despite the obvious limitations such as the small sample size, short treatment period and the absence of information on longer-term impact regarding patient important outcomes such as sudden death, this well-conceived pilot study provides impetus for larger prospective trials to test whether this personalized approach reduces major cardiovascular events and mortality.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of dialysate potassium concentration of 3.0mEq/l with sodium zirconium cyclosilicate on dialysis-free days versus dialysate potassium concentration of 2.0mEq/l alone on rates of cardiac arrhythmias in hemodialysis patients with hyperkalemia.","authors":"David M Charytan, Wolfgang C Winkelmayer, Christopher B Granger, John P Middleton, Charles A Herzog, Glenn M Chertow, James M Eudicone, Jeremy D Whitson, James A Tumlin","doi":"10.1016/j.kint.2024.10.010","DOIUrl":"https://doi.org/10.1016/j.kint.2024.10.010","url":null,"abstract":"<p><p>The optimal approach towards managing serum potassium and hemodialysate potassium concentrations is uncertain. To study this, adults receiving hemodialysis for three months or more with hyperkalemia (pre-dialysis serum potassium (sK⁺) 5.1-6.5 mEq/l) had cardiac monitors implanted and were randomized to either eight weeks of 2.0 potassium/2.5 calcium mEq/l dialysate without sodium zirconium cyclosilicate (SZC) (2.0 potassium/noSZC) or 3.0 potassium/2.5 calcium mEq/l dialysate combined with SZC (3.0 potassium/SZC) on non-dialysis days to maintain pre-dialysis sK⁺ 4.0-5.5 mEq/l, followed by treatment crossover for another eight weeks. The primary outcome was the rate of adjudicated atrial fibrillation (AF) episodes of 2 minutes or more duration. Secondary outcomes included clinically significant arrhythmias (bradycardia, ventricular tachycardia, and/or asystole) and the proportion of sK⁺ measurements within an optimal window of 4.0- 5.5 mEq/l. Among 88 participants (mean age: 57.1 years; 51% male; mean pre-dialysis sK⁺: 5.5 mmol/l) with 25.5 person-years of follow-up, 296 AF episodes were detected in nine patients. The unadjusted AF rate was lower with 3.0 potassium/SZC versus 2.0 potassium/noSZC; 9.7 vs. 13.4/person-year (modeled rate ratio 0.52; 95% confidence interval: 0.41; 0.65). Clinically significant arrhythmias were reduced with 3.0 potassium/SZC vs. 2.0 potassium/noSZC 6.8 vs. 10.2/person-year modeled rate ratio 0.47: 0.38;0.58). Fewer sK⁺ measurements outside the optimal window occurred with 3.0 potassium/SZC (modeled odds ratio: 0.27:0.12, 0.35). Hypokalemia was less frequent (33 vs. 58 patients) with 3.0 potassium/SZC compared with 2.0 potassium/noSZC. Thus, in patients with hyperkalemia on maintenance hemodialysis, a combination of potassium 3.0 mEq/l and SZC on non-hemodialysis days reduced the rates of AF, other clinically significant arrhythmias, and post-dialysis hypokalemia compared with potassium 2.0/noSZC.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Acute kidney injury genetic risks: taking it 1 SNP at a time.” Kidney International 2024;106:188–190","authors":"","doi":"10.1016/j.kint.2024.08.006","DOIUrl":"10.1016/j.kint.2024.08.006","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142486261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Using prediction models to improve care and communicate risk: updated modeling for children with IgA nephropathy","authors":"","doi":"10.1016/j.kint.2024.08.029","DOIUrl":"10.1016/j.kint.2024.08.029","url":null,"abstract":"<div><div>Clinical risk prediction models are being generated at an increasing rate. One important component is the identification of groups for whom such models might require recalibration to retain their desired performance. To this end, an update of the postbiopsy International IgA Nephropathy Prediction Tool for children has been published in this issue of <em>Kidney International</em>. We review the methods used and generalizability in practice, along with broader concepts in model development and application.</div></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142486294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Looking into the cholesterol crystal ball: is complement the answer?","authors":"","doi":"10.1016/j.kint.2024.08.025","DOIUrl":"10.1016/j.kint.2024.08.025","url":null,"abstract":"<div><div>Cholesterol crystal embolism (CCE) is a complication of atherosclerosis and can cause microvascular obstruction in multiple organs. Because the consequences may be fatal, and there is no specific treatment, it is crucial to understand the mechanisms and identify treatment strategies. In this issue, Zhao <em>et al.</em>, using a mouse model of kidney CCE, demonstrated that inhibition of C5a/C5aR prevented and resolved CCE-induced renal thrombosis and angiopathy. Although these findings must be extended to human condition, they offer hope for management of CCE syndrome.</div></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142486303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Subscription Information","authors":"","doi":"10.1016/S0085-2538(24)00651-3","DOIUrl":"10.1016/S0085-2538(24)00651-3","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142538810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ULK1-regulated AMP sensing by AMPK and its application for the treatment of chronic kidney disease","authors":"","doi":"10.1016/j.kint.2024.08.024","DOIUrl":"10.1016/j.kint.2024.08.024","url":null,"abstract":"<div><div>Adenosine monophosphate (AMP)-activated protein kinase (AMPK) is a central kinase involved in energy homeostasis. Increased intracellular AMP levels result in AMPK activation through the binding of AMP to the γ-subunit of AMPK. Recently, we reported that AMP-induced AMPK activation is impaired in the kidneys in chronic kidney disease (CKD) despite an increase in the AMP/ATP ratio. However, the mechanisms by which AMP sensing is disrupted in CKD are unclear. Here, we identified mechanisms of energy homeostasis in which Unc-51-like kinase 1 (ULK1)-dependent phosphorylation of AMPKγ1 at Ser260/Thr262 promoting AMP sensitivity of AMPK. AMPK activation by AMP was impaired in Ulk1 knockout mice despite an increased AMP/ATP ratio. ULK1 expression is markedly downregulated in CKD kidneys, leading to AMP sensing failure. Additionally, MK8722, an allosteric AMPK activator, stimulated AMPK in the kidneys of a CKD mouse model (5/6th nephrectomy) via a pathway that is independent of AMP sensing. Thus, our study shows that MK8722 treatment significantly attenuates the deterioration of kidney function in CKD and may be a potential therapeutic option in CKD therapeutics.</div></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142468937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}