Pub Date : 2025-12-22DOI: 10.1053/j.ajkd.2025.09.024
Joanna Q Hudson,Alex R Chang,Amanda J Condon Martinez,Rebecca Maxson,Calvin J Meaney,Wendy L St Peter
Comprehensive medication management (CMM) is the standard of care that ensures medications are individually assessed to determine that each medication is appropriate, effective for the medical condition, safe given the patient's comorbidities and other medications, and able to be taken by the patient as intended. CMM helps improve all aspects of healthcare quality and is essential for individuals with chronic kidney disease (CKD). It specifically addresses the complexity of medication regimens in patients with multiple comorbid conditions that often lead to medication therapy problems. Provision of CMM is best optimized with a multidisciplinary team that includes a pharmacist. The importance of interprofessional and multidisciplinary practice in the care of individuals with kidney disease has been emphasized by nephrology organizations and within CKD related guidelines. The shift towards pay for performance and value-based care models within nephrology has created more opportunities for pharmacist integration into care teams. Other health care providers should view the inclusion of pharmacists in the kidney care team as a valuable opportunity to enhance patient support, reduce work-related stress and improve outcomes through collaborative teamwork. The Advancing Kidney Health through Optimal Medication Management initiative supports the involvement of pharmacists across practices and healthcare systems to ensure successful implementation of CMM for individuals with kidney disease.
{"title":"Optimizing Comprehensive Medication Management in CKD: An Opportunity to Integrate Pharmacists in the Kidney Care Team.","authors":"Joanna Q Hudson,Alex R Chang,Amanda J Condon Martinez,Rebecca Maxson,Calvin J Meaney,Wendy L St Peter","doi":"10.1053/j.ajkd.2025.09.024","DOIUrl":"https://doi.org/10.1053/j.ajkd.2025.09.024","url":null,"abstract":"Comprehensive medication management (CMM) is the standard of care that ensures medications are individually assessed to determine that each medication is appropriate, effective for the medical condition, safe given the patient's comorbidities and other medications, and able to be taken by the patient as intended. CMM helps improve all aspects of healthcare quality and is essential for individuals with chronic kidney disease (CKD). It specifically addresses the complexity of medication regimens in patients with multiple comorbid conditions that often lead to medication therapy problems. Provision of CMM is best optimized with a multidisciplinary team that includes a pharmacist. The importance of interprofessional and multidisciplinary practice in the care of individuals with kidney disease has been emphasized by nephrology organizations and within CKD related guidelines. The shift towards pay for performance and value-based care models within nephrology has created more opportunities for pharmacist integration into care teams. Other health care providers should view the inclusion of pharmacists in the kidney care team as a valuable opportunity to enhance patient support, reduce work-related stress and improve outcomes through collaborative teamwork. The Advancing Kidney Health through Optimal Medication Management initiative supports the involvement of pharmacists across practices and healthcare systems to ensure successful implementation of CMM for individuals with kidney disease.","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"22 1","pages":""},"PeriodicalIF":13.2,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145823888","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}
Pub Date : 2025-12-20DOI: 10.1053/j.ajkd.2025.10.013
Howard Trachtman,Sean Eddy,Matthias Kretzler
Focal segmental glomerulosclerosis (FSGS) is not a single disease. Instead, it is a histopathological entity that is the manifestation of a wide range of clinical insults that injure the podocyte, a key structural element in the glomerular filtration barrier. The current classification of FSGS includes four subtypes - primary immune-mediated, genetic, secondary, and undetermined cause. Based on this scheme, patients are treated empirically with a combination of non-specific renoprotective drugs and immunosuppressive agents in an effort to reduce proteinuria and preserve kidney function. However, there are no FDA-approved medications for FSGS. Moreover, current therapy is successful in achieving disease remission in less than a quarter of patients and all of the available options are associated with significant side effects that limit their use in practice. Ongoing research using a full array of muti-omics analytical tools including genomic, transcriptomic, proteomic and metabolomic assessment suggest that patients with FSGS can be characterized mechanistically by the primary process(es) initiating and promoting disease progression. This work is summarized in this review and raises the potential to individualize therapy for each patient with FSGS. This would usher in the potential for precision medicine to be applied in the treatment of those affected by this rare but serious glomerular disease.
{"title":"Current and Future Therapeutics for Focal Segmental Glomerular Sclerosis in the Era of Precision Medicine: A Review.","authors":"Howard Trachtman,Sean Eddy,Matthias Kretzler","doi":"10.1053/j.ajkd.2025.10.013","DOIUrl":"https://doi.org/10.1053/j.ajkd.2025.10.013","url":null,"abstract":"Focal segmental glomerulosclerosis (FSGS) is not a single disease. Instead, it is a histopathological entity that is the manifestation of a wide range of clinical insults that injure the podocyte, a key structural element in the glomerular filtration barrier. The current classification of FSGS includes four subtypes - primary immune-mediated, genetic, secondary, and undetermined cause. Based on this scheme, patients are treated empirically with a combination of non-specific renoprotective drugs and immunosuppressive agents in an effort to reduce proteinuria and preserve kidney function. However, there are no FDA-approved medications for FSGS. Moreover, current therapy is successful in achieving disease remission in less than a quarter of patients and all of the available options are associated with significant side effects that limit their use in practice. Ongoing research using a full array of muti-omics analytical tools including genomic, transcriptomic, proteomic and metabolomic assessment suggest that patients with FSGS can be characterized mechanistically by the primary process(es) initiating and promoting disease progression. This work is summarized in this review and raises the potential to individualize therapy for each patient with FSGS. This would usher in the potential for precision medicine to be applied in the treatment of those affected by this rare but serious glomerular disease.","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"29 1","pages":""},"PeriodicalIF":13.2,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145807587","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}
Pub Date : 2025-12-20DOI: 10.1053/j.ajkd.2025.11.002
Neetika Garg , Carrie Thiessen , Didier A. Mandelbrot
{"title":"Health-Related Quality of Life After Living Kidney Donation: Insights From a Contemporary Meta-Analysis","authors":"Neetika Garg , Carrie Thiessen , Didier A. Mandelbrot","doi":"10.1053/j.ajkd.2025.11.002","DOIUrl":"10.1053/j.ajkd.2025.11.002","url":null,"abstract":"","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"87 2","pages":"Pages 153-155"},"PeriodicalIF":8.2,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145786058","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}
Pub Date : 2025-12-19DOI: 10.1053/j.ajkd.2025.07.023
Jia Wei Teh,Sinead Stoneman,Michelle M O'Shaughnessy
Immunoglobulin A nephropathy (IgAN) is the most common immune-mediated glomerular disease worldwide. Advanced understanding of the role of complement in IgAN pathogenesis has motivated the development of complement inhibition as a therapeutic strategy. Iptacopan, a complement factor B inhibitor, is the first approved complement inhibitor for IgAN. Several other complement inhibitors are being studied in Phase II/III clinical trials. How best to integrate complement inhibition into the evolving treatment paradigm for IgAN remains a challenge. This review provides an overview of the role of complement in the pathogenesis and progression of IgAN and summarizes current and emerging complement-targeted IgAN therapies.
{"title":"Complement Inhibition in Immunoglobulin A Nephropathy: A Mini-Review.","authors":"Jia Wei Teh,Sinead Stoneman,Michelle M O'Shaughnessy","doi":"10.1053/j.ajkd.2025.07.023","DOIUrl":"https://doi.org/10.1053/j.ajkd.2025.07.023","url":null,"abstract":"Immunoglobulin A nephropathy (IgAN) is the most common immune-mediated glomerular disease worldwide. Advanced understanding of the role of complement in IgAN pathogenesis has motivated the development of complement inhibition as a therapeutic strategy. Iptacopan, a complement factor B inhibitor, is the first approved complement inhibitor for IgAN. Several other complement inhibitors are being studied in Phase II/III clinical trials. How best to integrate complement inhibition into the evolving treatment paradigm for IgAN remains a challenge. This review provides an overview of the role of complement in the pathogenesis and progression of IgAN and summarizes current and emerging complement-targeted IgAN therapies.","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"22 1","pages":""},"PeriodicalIF":13.2,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145801332","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}
Pub Date : 2025-12-19DOI: 10.1053/j.ajkd.2025.11.003
James O. Burton DM, MBChB , Katherine L. Hull MBChB
{"title":"Chronic Pain in Hemodialysis: Beyond the Biochemical Paradigm","authors":"James O. Burton DM, MBChB , Katherine L. Hull MBChB","doi":"10.1053/j.ajkd.2025.11.003","DOIUrl":"10.1053/j.ajkd.2025.11.003","url":null,"abstract":"","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"87 2","pages":"Pages 156-158"},"PeriodicalIF":8.2,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145786361","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}
Pub Date : 2025-12-19DOI: 10.1053/j.ajkd.2025.07.021
Robert Sanchez MPS
{"title":"Why This Research Matters","authors":"Robert Sanchez MPS","doi":"10.1053/j.ajkd.2025.07.021","DOIUrl":"10.1053/j.ajkd.2025.07.021","url":null,"abstract":"","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"87 2","pages":"Pages A8-A9"},"PeriodicalIF":8.2,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145792907","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}
Pub Date : 2025-12-18DOI: 10.1053/j.ajkd.2025.09.006
Telma Pais , José Oliveira da Costa , Mafalda Pinho , Dolores López-Presa , Sofia Jorge , José António Lopes , Joana Gameiro
{"title":"Purpura in a Patient With Nephritic Syndrome: A Quiz","authors":"Telma Pais , José Oliveira da Costa , Mafalda Pinho , Dolores López-Presa , Sofia Jorge , José António Lopes , Joana Gameiro","doi":"10.1053/j.ajkd.2025.09.006","DOIUrl":"10.1053/j.ajkd.2025.09.006","url":null,"abstract":"","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"87 1","pages":"Pages A21-A24"},"PeriodicalIF":8.2,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145765755","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}
Pub Date : 2025-12-18DOI: 10.1053/j.ajkd.2025.11.001
Ajay K. Israni , Jon Miller , Syed F. Hassan
{"title":"Toward Smarter Allocation by Rethinking Kidney Donor Profile Index","authors":"Ajay K. Israni , Jon Miller , Syed F. Hassan","doi":"10.1053/j.ajkd.2025.11.001","DOIUrl":"10.1053/j.ajkd.2025.11.001","url":null,"abstract":"","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"87 1","pages":"Pages 4-6"},"PeriodicalIF":8.2,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145765734","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}
Pub Date : 2025-12-13DOI: 10.1053/j.ajkd.2025.09.014
Laura Aponte Becerra, Sherry G. Mansour
Exercise triggers complex effects on kidney physiology that vary with intensity, duration, and environmental conditions. While moderate physical activity improves cardiovascular and renal outcomes, intense or prolonged exertion, particularly in endurance sports, can lead to acute kidney injury. Adaptations in kidney physiology during exercise include reduced plasma flow, altered glomerular filtration, and hormone-mediated fluid retention. These changes are protective but may become maladaptive with dehydration, heat stress, or excessive fluid intake. High-intensity exercise increases oxidative stress and proteinuria, while ultramarathon participation may cause transient creatinine elevation from muscle breakdown, complicating acute kidney injury diagnosis. Prevention strategies include individualized hydration plans, electrolyte replacement, and avoidance of nonsteroidal anti-inflammatory drugs. In special populations, such as children with chronic kidney disease or patients receiving dialysis, structured exercise enhances quality of life and physical function when implemented safely. Clinicians must balance the benefits of exercise with kidney-related risks, promote safe training practices, and recognize early signs of exertional complications to optimize renal and overall health in physically active individuals. This core curriculum reviews the physiology of exercise on kidney function and provides evidence-based strategies for patient counseling and risk reduction.
{"title":"Exercise and Kidney Health: Core Curriculum 2026","authors":"Laura Aponte Becerra, Sherry G. Mansour","doi":"10.1053/j.ajkd.2025.09.014","DOIUrl":"10.1053/j.ajkd.2025.09.014","url":null,"abstract":"<div><div>Exercise triggers complex effects on kidney physiology that vary with intensity, duration, and environmental conditions. While moderate physical activity improves cardiovascular and renal outcomes, intense or prolonged exertion, particularly in endurance sports, can lead to acute kidney injury. Adaptations in kidney physiology during exercise include reduced plasma flow, altered glomerular filtration, and hormone-mediated fluid retention. These changes are protective but may become maladaptive with dehydration, heat stress, or excessive fluid intake. High-intensity exercise increases oxidative stress and proteinuria, while ultramarathon participation may cause transient creatinine elevation from muscle breakdown, complicating acute kidney injury diagnosis. Prevention strategies include individualized hydration plans, electrolyte replacement, and avoidance of nonsteroidal anti-inflammatory drugs. In special populations, such as children with chronic kidney disease or patients receiving dialysis, structured exercise enhances quality of life and physical function when implemented safely. Clinicians must balance the benefits of exercise with kidney-related risks, promote safe training practices, and recognize early signs of exertional complications to optimize renal and overall health in physically active individuals. This core curriculum reviews the physiology of exercise on kidney function and provides evidence-based strategies for patient counseling and risk reduction.</div></div>","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"87 2","pages":"Pages 246-259"},"PeriodicalIF":8.2,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145732820","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}
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