Pub Date : 2024-11-07DOI: 10.1053/j.ajkd.2024.09.005
Pascale Khairallah , Elizabeth C. Lorenz , Amy Waterman , Nidhi Aggarwal , Akshta Pai , Wolfgang C. Winkelmayer , Jingbo Niu
<div><h3>Rationale & Objective</h3><div>The management and outcomes of kidney transplant recipients have evolved over the past 3 decades. This study of US patients whose first kidney allograft failed examined long-term trends in subsequent waitlisting, retransplantation, and all-cause mortality.</div></div><div><h3>Study Design</h3><div>Retrospective cohort study.</div></div><div><h3>Setting & Participants</h3><div>Patients recorded in the US Renal Data System (USRDS) whose first kidney allograft failed between 1990 and 2019.</div></div><div><h3>Exposure</h3><div>The 5-year period in which the allograft failure occurred: 1990-1994, 1995-1999, 2000-2004, 2005-2009, 2010-2014, or 2015-2019.</div></div><div><h3>Outcome</h3><div>(1) Waitlisting for retransplantation, (2) retransplantation, and (3) all-cause mortality following first allograft failure.</div></div><div><h3>Analytical Approach</h3><div>Competing risk survival analyses with the approach described by Fine and Gray used for the outcomes of waitlisting and retransplantation, and Cox proportional hazards models used for the outcome of all-cause mortality.</div></div><div><h3>Results</h3><div>The absolute number of patients whose allograft failed and who started dialysis increased from 3,197 in 1990 to 5,821 in 2019. Compared with 1990-1994, the rate of waitlisting for a second transplant increased with each subsequent 5-year period, peaking between 2005 and 2009 before decreasing again subsequently. The rate of retransplantation following allograft failure decreased by 9%, 14%, 18%, 7%, and 11% in the sequential 5-year eras; and the mortality rate was 25% lower in 2015-2019 (HR, 0.75 [95% CI, 0.72-0.77]) compared with 1990-1994. Women had a reduced rate of waitlisting (HR, 0.93 [95% CI, 0.91-0.95]) and lower rate of retransplantation (HR, 0.93 [95% CI, 0.91-0.95]) compared with men. Compared with White patients, African American and Hispanic patients had significantly lower rates of waitlisting, retransplantation, and mortality.</div></div><div><h3>Limitations</h3><div>Retrospective data that lacks granular clinical information.</div></div><div><h3>Conclusions</h3><div>During the past 3 decades, among patients whose first kidney allograft failed and subsequently initiated dialysis, the rates of waitlisting for retransplantation increased while the rates of retransplantation and mortality decreased. Disparities based on race, ethnicity, and sex in waitlisting and retransplantation were observed and warrant further investigation.</div></div><div><h3>Plain-Language Summary</h3><div>Kidney allograft failure constitutes the fourth most common cause of dialysis initiation in the United States, and it accounts for 4% to 10% of yearly new dialysis starts globally. Little is known about the trends in the outcomes of patients whose kidney allograft failed. We studied US patients whose first kidney allograft failed between 1990 and 2019 to understand trends in waitlisting for retransplantation,
理由和目标：在过去的三十年中，肾移植受者的管理和治疗效果发生了变化。本研究对首次肾脏异体移植失败的美国患者进行了调查，旨在了解他们在后续等待、再次移植和全因死亡率方面的长期趋势：研究环境和参与者：美国肾脏登记处记录的患者：美国肾脏数据系统（USRDS）中记录的1990年至2019年间首次肾脏同种异体移植失败的患者：1990-1994年、1995-1999年、2000-2004年、2005-2009年、2010-2014年或2015-2019年：1）等待再次移植，2）再次移植，3）首次同种异体移植失败后的全因死亡率：分析方法：采用Fine和Gray所描述的方法对等待移植和再移植结果进行竞争风险生存分析。对全因死亡率结果采用了Cox比例危险模型：异体移植失败并开始透析的患者绝对人数从1990年的3197人增加到2019年的5821人。与 1990-1994 年相比，第二次移植的等待率在随后的 5 年中逐年上升，在 2005-2009 年间达到顶峰，随后再次下降。异体移植失败后的再次移植率在随后的5年中分别下降了9%、14%、18%、7%和11%；与1990-1994年相比，2015-2019年的死亡率降低了25%（HR=0.75，95% CI，0.72-0.77）。与男性相比，女性的等待率降低（HR 0.93，95% CI 0.91-0.95），再次移植率降低（HR 0.93，95% CI 0.91，0.95）。与白人患者相比，非裔美国人和西班牙裔患者的候选率、再移植率和死亡率明显较低：局限性：回顾性数据，缺乏详细的临床信息：结论：过去三十年间，在首次肾脏异体移植失败并随后开始透析的患者中，等待再次移植的比例上升，而再次移植的比例和死亡率下降。在等待移植和再移植方面，观察到了种族、民族和性别差异，值得进一步研究。
{"title":"Trends in Kidney Allograft Failure Among First-Time Transplant Recipients in the United States","authors":"Pascale Khairallah , Elizabeth C. Lorenz , Amy Waterman , Nidhi Aggarwal , Akshta Pai , Wolfgang C. Winkelmayer , Jingbo Niu","doi":"10.1053/j.ajkd.2024.09.005","DOIUrl":"10.1053/j.ajkd.2024.09.005","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>The management and outcomes of kidney transplant recipients have evolved over the past 3 decades. This study of US patients whose first kidney allograft failed examined long-term trends in subsequent waitlisting, retransplantation, and all-cause mortality.</div></div><div><h3>Study Design</h3><div>Retrospective cohort study.</div></div><div><h3>Setting & Participants</h3><div>Patients recorded in the US Renal Data System (USRDS) whose first kidney allograft failed between 1990 and 2019.</div></div><div><h3>Exposure</h3><div>The 5-year period in which the allograft failure occurred: 1990-1994, 1995-1999, 2000-2004, 2005-2009, 2010-2014, or 2015-2019.</div></div><div><h3>Outcome</h3><div>(1) Waitlisting for retransplantation, (2) retransplantation, and (3) all-cause mortality following first allograft failure.</div></div><div><h3>Analytical Approach</h3><div>Competing risk survival analyses with the approach described by Fine and Gray used for the outcomes of waitlisting and retransplantation, and Cox proportional hazards models used for the outcome of all-cause mortality.</div></div><div><h3>Results</h3><div>The absolute number of patients whose allograft failed and who started dialysis increased from 3,197 in 1990 to 5,821 in 2019. Compared with 1990-1994, the rate of waitlisting for a second transplant increased with each subsequent 5-year period, peaking between 2005 and 2009 before decreasing again subsequently. The rate of retransplantation following allograft failure decreased by 9%, 14%, 18%, 7%, and 11% in the sequential 5-year eras; and the mortality rate was 25% lower in 2015-2019 (HR, 0.75 [95% CI, 0.72-0.77]) compared with 1990-1994. Women had a reduced rate of waitlisting (HR, 0.93 [95% CI, 0.91-0.95]) and lower rate of retransplantation (HR, 0.93 [95% CI, 0.91-0.95]) compared with men. Compared with White patients, African American and Hispanic patients had significantly lower rates of waitlisting, retransplantation, and mortality.</div></div><div><h3>Limitations</h3><div>Retrospective data that lacks granular clinical information.</div></div><div><h3>Conclusions</h3><div>During the past 3 decades, among patients whose first kidney allograft failed and subsequently initiated dialysis, the rates of waitlisting for retransplantation increased while the rates of retransplantation and mortality decreased. Disparities based on race, ethnicity, and sex in waitlisting and retransplantation were observed and warrant further investigation.</div></div><div><h3>Plain-Language Summary</h3><div>Kidney allograft failure constitutes the fourth most common cause of dialysis initiation in the United States, and it accounts for 4% to 10% of yearly new dialysis starts globally. Little is known about the trends in the outcomes of patients whose kidney allograft failed. We studied US patients whose first kidney allograft failed between 1990 and 2019 to understand trends in waitlisting for retransplantation,","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"85 3","pages":"Pages 273-283.e1"},"PeriodicalIF":9.4,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611770","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}
Pub Date : 2024-11-07DOI: 10.1053/j.ajkd.2024.09.006
Hakan R Toka, Marializa Bernardo, Steven K Burke, Wenli Luo, Roberto Manllo-Karim, Irfan Ullah, Zhihui Yang, Zhiqun Zhang, James Tumlin
<p><strong>Rationale & objective: </strong>Hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs) may offer an alternative to erythropoiesis-stimulating agents (ESAs) for the treatment of anemia in the setting of chronic kidney disease (CKD). The objective of this study was to investigate the efficacy and safety of conversion from the long-acting ESA methoxy polyethylene glycol-epoetin-ß (MPG-EPO) to the oral HIF-PHI vadadustat 3 times weekly versus maintenance therapy with MPG-EPO.</p><p><strong>Study design: </strong>Phase 3b, open-label, noninferiority trial.</p><p><strong>Setting & participants: </strong>Multicenter study in the United States in 456 adult participants with anemia and dialysis-dependent CKD.</p><p><strong>Intervention: </strong>Participants were randomized 1:1:1 to vadadustat at a starting dose of 600mg thrice weekly, vadadustat at a starting dose of 900mg thrice weekly, or MPG-EPO for up to 52 treatment weeks and 4 safety follow-up weeks after the end of treatment or early termination.</p><p><strong>Outcomes: </strong>Primary and secondary efficacy end points were the mean change in hemoglobin concentration from baseline during primary (weeks 20-26) and secondary (weeks 46-52) evaluation periods, respectively. Noninferiority was specified as a lower bound of the 95% CI above -0.75g/dL for the difference in mean change in hemoglobin concentration from baseline. Other efficacy end points were the proportion of participants with hemoglobin levels within the target range and the proportions of participants requiring ESA or red blood cell transfusion rescue for anemia during the evaluation periods. Primary safety end points were any treatment-emergent and serious adverse events (AEs).</p><p><strong>Results: </strong>After combining the vadadustat groups (600mg and 900mg thrice weekly; n=304), vadadustat was noninferior to MPG-EPO (n=152) for primary (least-squares mean treatment difference, -0.33; 95% CI, -0.53 to-0.13) and secondary (-0.33; -0.56 to-0.09) efficacy end points. Mean hemoglobin concentrations were stable for all groups except for an initial slight decrease in the vadadustat 600mg group, which stabilized by week 12. ESA rescue for anemia was more frequent in the MPG-EPO group (primary evaluation period, 27.7%; secondary evaluation period, 16.2%) than in the combined vadadustat (14.2%; 7.3%) groups. Transfusion rates were low and occurred at similar rates across treatment groups (2.7% and 4.0% in the combined vadadustat and MPG-EPO groups, respectively). The incidences of any treatment-emergent and serious treatment-emergent AEs were similar across treatment groups.</p><p><strong>Limitations: </strong>Potential errors in attribution of AEs as drug-related.</p><p><strong>Conclusions: </strong>Three-times-weekly vadadustat was noninferior to MPG-EPO in its effect on hemoglobin levels without detectable differences in AEs.</p><p><strong>Funding: </strong>Funding from a private entity (Akebia Therapeutics, Inc)
{"title":"Vadadustat Three Times Weekly in Patients With Anemia Due to Dialysis-Dependent CKD.","authors":"Hakan R Toka, Marializa Bernardo, Steven K Burke, Wenli Luo, Roberto Manllo-Karim, Irfan Ullah, Zhihui Yang, Zhiqun Zhang, James Tumlin","doi":"10.1053/j.ajkd.2024.09.006","DOIUrl":"10.1053/j.ajkd.2024.09.006","url":null,"abstract":"<p><strong>Rationale & objective: </strong>Hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs) may offer an alternative to erythropoiesis-stimulating agents (ESAs) for the treatment of anemia in the setting of chronic kidney disease (CKD). The objective of this study was to investigate the efficacy and safety of conversion from the long-acting ESA methoxy polyethylene glycol-epoetin-ß (MPG-EPO) to the oral HIF-PHI vadadustat 3 times weekly versus maintenance therapy with MPG-EPO.</p><p><strong>Study design: </strong>Phase 3b, open-label, noninferiority trial.</p><p><strong>Setting & participants: </strong>Multicenter study in the United States in 456 adult participants with anemia and dialysis-dependent CKD.</p><p><strong>Intervention: </strong>Participants were randomized 1:1:1 to vadadustat at a starting dose of 600mg thrice weekly, vadadustat at a starting dose of 900mg thrice weekly, or MPG-EPO for up to 52 treatment weeks and 4 safety follow-up weeks after the end of treatment or early termination.</p><p><strong>Outcomes: </strong>Primary and secondary efficacy end points were the mean change in hemoglobin concentration from baseline during primary (weeks 20-26) and secondary (weeks 46-52) evaluation periods, respectively. Noninferiority was specified as a lower bound of the 95% CI above -0.75g/dL for the difference in mean change in hemoglobin concentration from baseline. Other efficacy end points were the proportion of participants with hemoglobin levels within the target range and the proportions of participants requiring ESA or red blood cell transfusion rescue for anemia during the evaluation periods. Primary safety end points were any treatment-emergent and serious adverse events (AEs).</p><p><strong>Results: </strong>After combining the vadadustat groups (600mg and 900mg thrice weekly; n=304), vadadustat was noninferior to MPG-EPO (n=152) for primary (least-squares mean treatment difference, -0.33; 95% CI, -0.53 to-0.13) and secondary (-0.33; -0.56 to-0.09) efficacy end points. Mean hemoglobin concentrations were stable for all groups except for an initial slight decrease in the vadadustat 600mg group, which stabilized by week 12. ESA rescue for anemia was more frequent in the MPG-EPO group (primary evaluation period, 27.7%; secondary evaluation period, 16.2%) than in the combined vadadustat (14.2%; 7.3%) groups. Transfusion rates were low and occurred at similar rates across treatment groups (2.7% and 4.0% in the combined vadadustat and MPG-EPO groups, respectively). The incidences of any treatment-emergent and serious treatment-emergent AEs were similar across treatment groups.</p><p><strong>Limitations: </strong>Potential errors in attribution of AEs as drug-related.</p><p><strong>Conclusions: </strong>Three-times-weekly vadadustat was noninferior to MPG-EPO in its effect on hemoglobin levels without detectable differences in AEs.</p><p><strong>Funding: </strong>Funding from a private entity (Akebia Therapeutics, Inc)","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":" ","pages":""},"PeriodicalIF":9.4,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611782","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 : 2024-10-29DOI: 10.1053/j.ajkd.2024.07.004
Sehoon Park , Jeong Min Cho , Dong Ki Kim
{"title":"Exploring the Causal Relationship Between Kidney Function and Cancer Risk: Insights and Limitations of Mendelian Randomization","authors":"Sehoon Park , Jeong Min Cho , Dong Ki Kim","doi":"10.1053/j.ajkd.2024.07.004","DOIUrl":"10.1053/j.ajkd.2024.07.004","url":null,"abstract":"","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"84 6","pages":"Pages 670-671"},"PeriodicalIF":9.4,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142543060","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 : 2024-10-23DOI: 10.1053/j.ajkd.2024.08.011
Laura H Mariani, Howard Trachtman, Aliza Thompson, Barbara S Gillespie, Michelle Denburg, Ulysses Diva, Duvuru Geetha, Peter J Greasley, Michelle A Hladunewich, Robert B Huizinga, Jula K Inrig, Radko Komers, Louis-Philippe Laurin, Dustin J Little, Patrick H Nachman, Kimberly A Smith, Liron Walsh, Keisha L Gibson
Focal segmental glomerulosclerosis (FSGS) is a characteristic histopathological lesion that is indicative of underlying glomerular dysfunction. It is not a single disease entity but rather a heterogeneous disorder that is an important cause of nephrotic syndrome and kidney failure in children and adults. The aim of this Kidney Health Initiative project was to evaluate potential end points for clinical trials in FSGS. Our focus is on the data supporting proteinuria as a surrogate end point. Available data support the use of complete remission of proteinuria in patients with heavy proteinuria as a surrogate end point for progression to kidney failure. Substantial treatment effects on proteinuria that are short of a complete remission may also predict the effect of a treatment on progression to kidney failure, but further work is needed to determine how such an end point should be defined. Fortunately, efforts are underway to bring together patient-level data from randomized controlled trials, observational studies, and registries to address this issue.
{"title":"Proteinuria as an End Point in Clinical Trials of Focal Segmental Glomerulosclerosis.","authors":"Laura H Mariani, Howard Trachtman, Aliza Thompson, Barbara S Gillespie, Michelle Denburg, Ulysses Diva, Duvuru Geetha, Peter J Greasley, Michelle A Hladunewich, Robert B Huizinga, Jula K Inrig, Radko Komers, Louis-Philippe Laurin, Dustin J Little, Patrick H Nachman, Kimberly A Smith, Liron Walsh, Keisha L Gibson","doi":"10.1053/j.ajkd.2024.08.011","DOIUrl":"10.1053/j.ajkd.2024.08.011","url":null,"abstract":"<p><p>Focal segmental glomerulosclerosis (FSGS) is a characteristic histopathological lesion that is indicative of underlying glomerular dysfunction. It is not a single disease entity but rather a heterogeneous disorder that is an important cause of nephrotic syndrome and kidney failure in children and adults. The aim of this Kidney Health Initiative project was to evaluate potential end points for clinical trials in FSGS. Our focus is on the data supporting proteinuria as a surrogate end point. Available data support the use of complete remission of proteinuria in patients with heavy proteinuria as a surrogate end point for progression to kidney failure. Substantial treatment effects on proteinuria that are short of a complete remission may also predict the effect of a treatment on progression to kidney failure, but further work is needed to determine how such an end point should be defined. Fortunately, efforts are underway to bring together patient-level data from randomized controlled trials, observational studies, and registries to address this issue.</p>","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":" ","pages":""},"PeriodicalIF":9.4,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142492822","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 : 2024-10-22DOI: 10.1053/j.ajkd.2024.10.003
Ladan Golestaneh , Abby Basalely , Andreas Linkermann , Tarek M. El-Achkar , Ryung S. Kim , Joel Neugarten
<div><h3>Rationale & Objective</h3><div>Animal models of kidney disease suggest a protective role for female sex hormones, but some authorities assert that female sex in humans is a risk factor for acute kidney injury (AKI). To better understand the risk of AKI, we studied the strength of association between sex and AKI incidence in hormonally distinct age groups across the life span.</div></div><div><h3>Study Design</h3><div>Prospective cohort study.</div></div><div><h3>Setting & Participants</h3><div>All patients hospitalized in the Montefiore Health System between October 15, 2015, and January 1, 2019, excluding those with kidney failure or obstetrics diagnoses.</div></div><div><h3>Exposure</h3><div>Male versus female sex.</div></div><div><h3>Outcome</h3><div>AKI occurring during hospitalization based on KDIGO definitions.</div></div><div><h3>Analytical Approach</h3><div>Generalized estimating equation logistic regression adjusted for comorbidities, sociodemographic factors, and severity of illness. Analyses were stratified into 3 age categories: 6 months to<!--> <!-->≤16 years,<!--> <!-->>16 years to<!--> <!--><55 years, and<!--> <!-->≥55 years.</div></div><div><h3>Results</h3><div>A total of 132,667 individuals were hospitalized a total of 235,629 times. The mean age was 55.2<!--> <!-->±<!--> <!-->23.8 (SD) years. The count of hospitalizations for women was 129,912 (55%). Hospitalization count among Black and Hispanic patients was 71,834 (30.5%) and 24,199 (10.3%), respectively. AKI occurred in 53,926 (22.9%) hospitalizations. In adjusted models, there was a significant interaction between age and sex (<em>P</em> <!--><<!--> <!-->0.001). Boys and men had a higher risk of AKI across all age groups, an association more pronounced in the age group<!--> <!-->>16 years to<!--> <!--><55 years in which the odds ratio for men was 1.7 (95% CI, 1.6-1.8). This age-based pattern remained consistent across prespecified types of hospitalizations. In a sensitivity analysis, women older than 55 years who received prescriptions for estrogen had lower odds of AKI than those without prescriptions.</div></div><div><h3>Limitations</h3><div>Residual confounding.</div></div><div><h3>Conclusions</h3><div>The greatest relative risk of AKI for males occurred during ages<!--> <!-->>16 to<!--> <!--><55 years. The lower risk among postmenopausal women receiving supplemental estrogen supports a protective role for female sex hormones.</div></div><div><h3>Plain-Language Summary</h3><div>Male sex is a risk factor for acute kidney injury (AKI) in animals, but in human studies this association is not as robust. We studied hospitalizations at a single center to examine the association of hospital-acquired AKI and sex. After controlling for various sources of potential bias and stratifying by age categories through the life course, we observed that men have a higher risk of AKI throughout life. This risk was especially high compared with women of f
{"title":"Sex, Acute Kidney Injury, and Age: A Prospective Cohort Study","authors":"Ladan Golestaneh , Abby Basalely , Andreas Linkermann , Tarek M. El-Achkar , Ryung S. Kim , Joel Neugarten","doi":"10.1053/j.ajkd.2024.10.003","DOIUrl":"10.1053/j.ajkd.2024.10.003","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Animal models of kidney disease suggest a protective role for female sex hormones, but some authorities assert that female sex in humans is a risk factor for acute kidney injury (AKI). To better understand the risk of AKI, we studied the strength of association between sex and AKI incidence in hormonally distinct age groups across the life span.</div></div><div><h3>Study Design</h3><div>Prospective cohort study.</div></div><div><h3>Setting & Participants</h3><div>All patients hospitalized in the Montefiore Health System between October 15, 2015, and January 1, 2019, excluding those with kidney failure or obstetrics diagnoses.</div></div><div><h3>Exposure</h3><div>Male versus female sex.</div></div><div><h3>Outcome</h3><div>AKI occurring during hospitalization based on KDIGO definitions.</div></div><div><h3>Analytical Approach</h3><div>Generalized estimating equation logistic regression adjusted for comorbidities, sociodemographic factors, and severity of illness. Analyses were stratified into 3 age categories: 6 months to<!--> <!-->≤16 years,<!--> <!-->>16 years to<!--> <!--><55 years, and<!--> <!-->≥55 years.</div></div><div><h3>Results</h3><div>A total of 132,667 individuals were hospitalized a total of 235,629 times. The mean age was 55.2<!--> <!-->±<!--> <!-->23.8 (SD) years. The count of hospitalizations for women was 129,912 (55%). Hospitalization count among Black and Hispanic patients was 71,834 (30.5%) and 24,199 (10.3%), respectively. AKI occurred in 53,926 (22.9%) hospitalizations. In adjusted models, there was a significant interaction between age and sex (<em>P</em> <!--><<!--> <!-->0.001). Boys and men had a higher risk of AKI across all age groups, an association more pronounced in the age group<!--> <!-->>16 years to<!--> <!--><55 years in which the odds ratio for men was 1.7 (95% CI, 1.6-1.8). This age-based pattern remained consistent across prespecified types of hospitalizations. In a sensitivity analysis, women older than 55 years who received prescriptions for estrogen had lower odds of AKI than those without prescriptions.</div></div><div><h3>Limitations</h3><div>Residual confounding.</div></div><div><h3>Conclusions</h3><div>The greatest relative risk of AKI for males occurred during ages<!--> <!-->>16 to<!--> <!--><55 years. The lower risk among postmenopausal women receiving supplemental estrogen supports a protective role for female sex hormones.</div></div><div><h3>Plain-Language Summary</h3><div>Male sex is a risk factor for acute kidney injury (AKI) in animals, but in human studies this association is not as robust. We studied hospitalizations at a single center to examine the association of hospital-acquired AKI and sex. After controlling for various sources of potential bias and stratifying by age categories through the life course, we observed that men have a higher risk of AKI throughout life. This risk was especially high compared with women of f","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"85 3","pages":"Pages 329-338.e1"},"PeriodicalIF":9.4,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142490427","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 : 2024-10-18DOI: 10.1053/j.ajkd.2024.08.010
Elaine Ku , Timothy P. Copeland , Charles E. McCulloch , Divya Seth , Christopher A. Carlos , Kerry Cho , Anna Malkina , Lowell J. Lo , Raymond K. Hsu
<div><h3>Rationale & Objective</h3><div>Optimal blood pressure (BP) targets in advanced chronic kidney disease (CKD) are controversial. More intensive BP lowering in the setting of advanced CKD is thought to be associated with risk of acute kidney injury, hyperkalemia, and end-stage kidney disease. We conducted a pilot trial of intensive BP control to determine if lower home systolic BP (SBP) targets can be safely achieved for patients with CKD through titration of BP medications using in-home measured BP.</div></div><div><h3>Study Design</h3><div>Nonblinded randomized controlled trial.</div></div><div><h3>Setting & Participants</h3><div>108 patients with advanced CKD (estimated glomerular filtration rate<!--> <!-->≤<!--> <!-->30<!--> <!-->mL/min/1.73<!--> <!-->m<sup>2</sup>) and hypertension.</div></div><div><h3>Interventions</h3><div>Participants were randomized either to a target SBP goal of<!--> <!--><120<!--> <!-->mm Hg (N<!--> <!-->=<!--> <!-->66) or a less intensive SBP goal (N<!--> <!-->=<!--> <!-->42). Antihypertensive medications were titrated to achieve the target home SBP range in the first 4 months of the study and maintained until the end of the study. Home BP was measured using a wireless Bluetooth-enabled monitor that transmitted readings to providers in real-time.</div></div><div><h3>Outcome</h3><div>The primary efficacy outcome was the difference in achieved clinic SBP between the 2 study arms from months 4-12. Safety outcomes included hyperkalemia, a composite outcome of falls or syncope, and onset of need for dialysis or kidney transplantation.</div></div><div><h3>Results</h3><div>The mean clinic SBP at month 12 was 124.7<!--> <!-->mm Hg in the intensive SBP group versus 138.2<!--> <!-->mm Hg in the less intensive SBP group. Averaged over months 4-12, the achieved mean clinic SBP in the intensive SBP arm was 11.7<!--> <!-->mm Hg ([95% CI, 7.5-16], <em>P</em> <!--><<!--> <!-->0.001), lower than the mean SBP achieved in the less intensive SBP arm. Primary safety outcomes were not statistically significantly different between the 2 arms (all <em>P</em> <!-->><!--> <!-->0.05).</div></div><div><h3>Limitations</h3><div>Small sample size, which may have limited our ability to detect clinically significant differences in rates of adverse outcomes, and single-center design.</div></div><div><h3>Conclusions</h3><div>A clinic SBP goal of<!--> <!--><120<!--> <!-->mm Hg is feasible to achieve with the help of real-time home BP monitoring and appears to be safe in this study population with advanced CKD. Larger trials to determine optimal BP targets in advanced CKD and the risks and benefits associated with more intensive BP control are warranted.</div></div><div><h3>Funding</h3><div>Grant from an educational institution (UCSF Research Allocation Program award).</div></div><div><h3>Trial Registration</h3><div>Registered at <span><span>ClinicalTrials.gov</span><svg><path></path></svg></span> with study number <span><span>N
{"title":"Intensive Home Blood Pressure Lowering in Patients With Advanced CKD","authors":"Elaine Ku , Timothy P. Copeland , Charles E. McCulloch , Divya Seth , Christopher A. Carlos , Kerry Cho , Anna Malkina , Lowell J. Lo , Raymond K. Hsu","doi":"10.1053/j.ajkd.2024.08.010","DOIUrl":"10.1053/j.ajkd.2024.08.010","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Optimal blood pressure (BP) targets in advanced chronic kidney disease (CKD) are controversial. More intensive BP lowering in the setting of advanced CKD is thought to be associated with risk of acute kidney injury, hyperkalemia, and end-stage kidney disease. We conducted a pilot trial of intensive BP control to determine if lower home systolic BP (SBP) targets can be safely achieved for patients with CKD through titration of BP medications using in-home measured BP.</div></div><div><h3>Study Design</h3><div>Nonblinded randomized controlled trial.</div></div><div><h3>Setting & Participants</h3><div>108 patients with advanced CKD (estimated glomerular filtration rate<!--> <!-->≤<!--> <!-->30<!--> <!-->mL/min/1.73<!--> <!-->m<sup>2</sup>) and hypertension.</div></div><div><h3>Interventions</h3><div>Participants were randomized either to a target SBP goal of<!--> <!--><120<!--> <!-->mm Hg (N<!--> <!-->=<!--> <!-->66) or a less intensive SBP goal (N<!--> <!-->=<!--> <!-->42). Antihypertensive medications were titrated to achieve the target home SBP range in the first 4 months of the study and maintained until the end of the study. Home BP was measured using a wireless Bluetooth-enabled monitor that transmitted readings to providers in real-time.</div></div><div><h3>Outcome</h3><div>The primary efficacy outcome was the difference in achieved clinic SBP between the 2 study arms from months 4-12. Safety outcomes included hyperkalemia, a composite outcome of falls or syncope, and onset of need for dialysis or kidney transplantation.</div></div><div><h3>Results</h3><div>The mean clinic SBP at month 12 was 124.7<!--> <!-->mm Hg in the intensive SBP group versus 138.2<!--> <!-->mm Hg in the less intensive SBP group. Averaged over months 4-12, the achieved mean clinic SBP in the intensive SBP arm was 11.7<!--> <!-->mm Hg ([95% CI, 7.5-16], <em>P</em> <!--><<!--> <!-->0.001), lower than the mean SBP achieved in the less intensive SBP arm. Primary safety outcomes were not statistically significantly different between the 2 arms (all <em>P</em> <!-->><!--> <!-->0.05).</div></div><div><h3>Limitations</h3><div>Small sample size, which may have limited our ability to detect clinically significant differences in rates of adverse outcomes, and single-center design.</div></div><div><h3>Conclusions</h3><div>A clinic SBP goal of<!--> <!--><120<!--> <!-->mm Hg is feasible to achieve with the help of real-time home BP monitoring and appears to be safe in this study population with advanced CKD. Larger trials to determine optimal BP targets in advanced CKD and the risks and benefits associated with more intensive BP control are warranted.</div></div><div><h3>Funding</h3><div>Grant from an educational institution (UCSF Research Allocation Program award).</div></div><div><h3>Trial Registration</h3><div>Registered at <span><span>ClinicalTrials.gov</span><svg><path></path></svg></span> with study number <span><span>N","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"85 3","pages":"Pages 320-328"},"PeriodicalIF":9.4,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142455777","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 : 2024-10-18DOI: 10.1053/j.ajkd.2024.08.010
Elaine Ku,Timothy P Copeland,Charles E McCulloch,Divya Seth,Christopher A Carlos,Kerry Cho,Anna Malkina,Lowell J Lo,Raymond K Hsu
RATIONALE & OBJECTIVEOptimal blood pressure (BP) targets in advanced CKD are controversial. More intensive BP lowering in the setting of advanced CKD is thought to be associated with risk of acute kidney injury, hyperkalemia, and ESKD. We aimed to conduct a pilot trial of intensive BP control to determine if lower SBP targets can be safely achieved for patients with CKD through titration of BP medications using in-home measured BP.STUDY DESIGNNon-blinded randomized controlled trial.SETTINGS & PARTICIPANTS108 patients with advanced CKD (eGFR ≤30 mL/min/1.73 m2) and hypertension.INTERVENTIONSParticipants were randomized either to a target home SBP goal of <120 mmHg (N=66) or a less intensive SBP goal (N=42). Antihypertensive medications were titrated to achieve the target home SBP range in the first 4 months of the study and maintained until the end of the study. Home BP was measured using a wireless Bluetooth-enabled monitor that transmitted readings to providers in real-time.OUTCOMESThe primary efficacy outcome was the difference in achieved clinic SBP between the two study arms from months 4-12. Safety outcomes included hyperkalemia, a composite outcome of falls or syncope, and onset of need for dialysis or kidney transplantation.RESULTSThe mean clinic SBP at month 12 was 124.7 mmHg in the intensive SBP group vs. 138.2 mmHg in the less intensive SBP group. Averaged over months 4-12, the achieved mean clinic SBP in the intensive SBP arm was 11.7 mmHg (95% CI 7.5 to 16 mmHg, p<0.001) lower than the mean SBP achieved in the less intensive SBP arm. Primary safety outcomes were not statistically significantly different between the two arms (all p>0.05).LIMITATIONSSmall sample size which may limit our ability to detect clinically significant differences in rates of adverse outcomes; single-center design.CONCLUSIONSA clinic SBP goal of <120 mmHg is feasible to achieve with the help of real-time home BP monitoring and appears to be safe in this study population with advanced CKD. Larger trials to determine optimal BP targets in advanced CKD and the risks and benefits associated with more intensive BP control are warranted.
{"title":"Intensive Home Blood Pressure Lowering in Patients with Advanced CKD.","authors":"Elaine Ku,Timothy P Copeland,Charles E McCulloch,Divya Seth,Christopher A Carlos,Kerry Cho,Anna Malkina,Lowell J Lo,Raymond K Hsu","doi":"10.1053/j.ajkd.2024.08.010","DOIUrl":"https://doi.org/10.1053/j.ajkd.2024.08.010","url":null,"abstract":"RATIONALE & OBJECTIVEOptimal blood pressure (BP) targets in advanced CKD are controversial. More intensive BP lowering in the setting of advanced CKD is thought to be associated with risk of acute kidney injury, hyperkalemia, and ESKD. We aimed to conduct a pilot trial of intensive BP control to determine if lower SBP targets can be safely achieved for patients with CKD through titration of BP medications using in-home measured BP.STUDY DESIGNNon-blinded randomized controlled trial.SETTINGS & PARTICIPANTS108 patients with advanced CKD (eGFR ≤30 mL/min/1.73 m2) and hypertension.INTERVENTIONSParticipants were randomized either to a target home SBP goal of <120 mmHg (N=66) or a less intensive SBP goal (N=42). Antihypertensive medications were titrated to achieve the target home SBP range in the first 4 months of the study and maintained until the end of the study. Home BP was measured using a wireless Bluetooth-enabled monitor that transmitted readings to providers in real-time.OUTCOMESThe primary efficacy outcome was the difference in achieved clinic SBP between the two study arms from months 4-12. Safety outcomes included hyperkalemia, a composite outcome of falls or syncope, and onset of need for dialysis or kidney transplantation.RESULTSThe mean clinic SBP at month 12 was 124.7 mmHg in the intensive SBP group vs. 138.2 mmHg in the less intensive SBP group. Averaged over months 4-12, the achieved mean clinic SBP in the intensive SBP arm was 11.7 mmHg (95% CI 7.5 to 16 mmHg, p<0.001) lower than the mean SBP achieved in the less intensive SBP arm. Primary safety outcomes were not statistically significantly different between the two arms (all p>0.05).LIMITATIONSSmall sample size which may limit our ability to detect clinically significant differences in rates of adverse outcomes; single-center design.CONCLUSIONSA clinic SBP goal of <120 mmHg is feasible to achieve with the help of real-time home BP monitoring and appears to be safe in this study population with advanced CKD. Larger trials to determine optimal BP targets in advanced CKD and the risks and benefits associated with more intensive BP control are warranted.","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"124 1","pages":""},"PeriodicalIF":13.2,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142486321","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}
Japan has recently faced a public health crisis owing to "Beni Koji Choleste Help," a product marketed as a dietary supplement. It is made from red yeast rice and has cholesterol-lowering effects. Following the identification of the first case of acute kidney injury (AKI) caused by the product, 76 possibly related deaths and 492 hospitalizations have been reported in Japan. We herein demonstrate three cases of AKI with renal tubular acidosis and Fanconi syndrome following consumption of the product for 2 weeks to 7 months. Kidney biopsy revealed diffuse tubular injury, tubular cell flattening, loss of brush border, sparse debris, and cast formation containing periodic acid-Schiff- and silver stain-positive fluffy material in the tubular lumens with interstitial cell infiltration, together with mild fibrosis. Electron microscopy revealed fluffy materials in the tubular lumen surrounded by necrotic tubular cell debris and intracellular contents. Discontinuation of the supplement and the treatment with prednisolone improved kidney function and Fanconi syndrome. Longitudinal monitoring and surveys are required to detect and prevent the progression to chronic kidney disease in people who have consumed "Beni Koji Choleste Help."
由于 "Beni Koji Choleste Help "这种作为膳食补充剂销售的产品，日本最近面临着一场公共卫生危机。该产品由红曲米制成，具有降低胆固醇的功效。在发现首例由该产品引起的急性肾损伤（AKI）病例后，日本已报告了 76 例可能与之相关的死亡病例和 492 例住院病例。我们在此展示了三例在服用该产品 2 周至 7 个月后出现肾小管酸中毒和范可尼综合征的急性肾损伤病例。肾活检显示肾小管弥漫性损伤、肾小管细胞扁平化、刷状缘消失、碎屑稀疏、肾小管管腔内含有周期性酸-施氏银染色阳性绒毛状物质的铸型形成，并伴有间质细胞浸润和轻度纤维化。电子显微镜检查发现，肾小管管腔内的绒毛状物质被坏死的肾小管细胞碎片和细胞内内容物包围。停用补充剂并用泼尼松龙治疗后，肾功能和范可尼综合征得到改善。需要进行纵向监测和调查，以发现和预防服用 "贝尼小儿胆汁帮助 "的人发展为慢性肾病。
{"title":"Three Cases of Red Yeast Rice-Containing Supplement-Induced Acute Kidney Injury and Fanconi Syndrome.","authors":"Ayako Chikasue,Kensei Taguchi,Ryuji Iwatani,Koki Kimura,Seiya Okuda,Noriko Uesugi,Kei Fukami","doi":"10.1053/j.ajkd.2024.08.007","DOIUrl":"https://doi.org/10.1053/j.ajkd.2024.08.007","url":null,"abstract":"Japan has recently faced a public health crisis owing to \"Beni Koji Choleste Help,\" a product marketed as a dietary supplement. It is made from red yeast rice and has cholesterol-lowering effects. Following the identification of the first case of acute kidney injury (AKI) caused by the product, 76 possibly related deaths and 492 hospitalizations have been reported in Japan. We herein demonstrate three cases of AKI with renal tubular acidosis and Fanconi syndrome following consumption of the product for 2 weeks to 7 months. Kidney biopsy revealed diffuse tubular injury, tubular cell flattening, loss of brush border, sparse debris, and cast formation containing periodic acid-Schiff- and silver stain-positive fluffy material in the tubular lumens with interstitial cell infiltration, together with mild fibrosis. Electron microscopy revealed fluffy materials in the tubular lumen surrounded by necrotic tubular cell debris and intracellular contents. Discontinuation of the supplement and the treatment with prednisolone improved kidney function and Fanconi syndrome. Longitudinal monitoring and surveys are required to detect and prevent the progression to chronic kidney disease in people who have consumed \"Beni Koji Choleste Help.\"","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"13 1","pages":""},"PeriodicalIF":13.2,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142451443","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 : 2024-10-16DOI: 10.1053/j.ajkd.2024.08.008
Sara S Jdiaa,Reem A Mustafa,Alan S L Yu
Autosomal dominant polycystic kidney disease (ADPKD) is a chronic systemic disease that affects all races and ethnicities. It is the fourth leading cause of end-stage kidney disease, and it has a heterogenous phenotype ranging from mild to severe disease. Identifying patients with ADPKD who are at risk of rapid progression can guide therapeutic decisions. Several tools to predict disease severity are available, based on features such as total kidney volume from magnetic resonance imaging, PKD genotype, eGFR trajectory, and the occurrence of hypertension and urologic complications early in life. Over the past decade, more evidence has emerged regarding optimal ADPKD management. The HALT PKD trial supported intensive blood pressure control in patients younger than 50 years of age with preserved kidney function. A healthy lifestyle, including maintaining a healthy weight, salt restriction and smoking cessation, is likely to be beneficial. Tolvaptan, the only disease-modifying agent for ADPKD patients that are at risk of rapid progression, is gaining wider use, but is still limited by its side-effects. This is an exciting time for the ADPKD community as multiple promising interventions are in the pipeline and being investigated.
{"title":"Treatment of Autosomal Dominant Polycystic Kidney Disease.","authors":"Sara S Jdiaa,Reem A Mustafa,Alan S L Yu","doi":"10.1053/j.ajkd.2024.08.008","DOIUrl":"https://doi.org/10.1053/j.ajkd.2024.08.008","url":null,"abstract":"Autosomal dominant polycystic kidney disease (ADPKD) is a chronic systemic disease that affects all races and ethnicities. It is the fourth leading cause of end-stage kidney disease, and it has a heterogenous phenotype ranging from mild to severe disease. Identifying patients with ADPKD who are at risk of rapid progression can guide therapeutic decisions. Several tools to predict disease severity are available, based on features such as total kidney volume from magnetic resonance imaging, PKD genotype, eGFR trajectory, and the occurrence of hypertension and urologic complications early in life. Over the past decade, more evidence has emerged regarding optimal ADPKD management. The HALT PKD trial supported intensive blood pressure control in patients younger than 50 years of age with preserved kidney function. A healthy lifestyle, including maintaining a healthy weight, salt restriction and smoking cessation, is likely to be beneficial. Tolvaptan, the only disease-modifying agent for ADPKD patients that are at risk of rapid progression, is gaining wider use, but is still limited by its side-effects. This is an exciting time for the ADPKD community as multiple promising interventions are in the pipeline and being investigated.","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"2 1","pages":""},"PeriodicalIF":13.2,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142451444","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 : 2024-10-16DOI: 10.1053/j.ajkd.2024.07.018
Scott G. Westphal , Roslyn B. Mannon
Alloimmune injury is a major cause of long-term kidney allograft failure whether due to functionally stable (subclinical) or overt clinical rejection. These episodes may be mediated by immune cells (cellular rejection) or alloantibody (antibody-mediated rejection). Early recognition of immune injury is needed for timely appropriate intervention to maintain graft functional viability. However, the conventional measure of kidney function (ie, serum creatinine) is insufficient for immune monitoring due to limited sensitivity and specificity for rejection. As a result, there is need for biomarkers that more sensitively detect the immune response to the kidney allograft. Recently, several biomarkers have been clinically implemented into the care of kidney transplant recipients. These biomarkers attempt to achieve multiple goals including (1) more sensitive detection of clinical and subclinical rejection, (2) predicting impending rejection, (3) monitoring for the adequacy of treatment response, and (4) facilitating personalized immunosuppression. In this review, we summarize the findings to date in commercially available biomarkers, along with biomarkers approaching clinical implementation. While we discuss the analytical and clinical validity of these biomarkers, we identify the challenges and limitations to widespread biomarker use, including the need for biomarker-guided prospective studies to establish evidence of clinical utility of these new assays.
{"title":"Biomarkers of Rejection in Kidney Transplantation","authors":"Scott G. Westphal , Roslyn B. Mannon","doi":"10.1053/j.ajkd.2024.07.018","DOIUrl":"10.1053/j.ajkd.2024.07.018","url":null,"abstract":"<div><div>Alloimmune injury is a major cause of long-term kidney allograft failure whether due to functionally stable (subclinical) or overt clinical rejection. These episodes may be mediated by immune cells (cellular rejection) or alloantibody (antibody-mediated rejection). Early recognition of immune injury is needed for timely appropriate intervention to maintain graft functional viability. However, the conventional measure of kidney function (ie, serum creatinine) is insufficient for immune monitoring due to limited sensitivity and specificity for rejection. As a result, there is need for biomarkers that more sensitively detect the immune response to the kidney allograft. Recently, several biomarkers have been clinically implemented into the care of kidney transplant recipients. These biomarkers attempt to achieve multiple goals including (1) more sensitive detection of clinical and subclinical rejection, (2) predicting impending rejection, (3) monitoring for the adequacy of treatment response, and (4) facilitating personalized immunosuppression. In this review, we summarize the findings to date in commercially available biomarkers, along with biomarkers approaching clinical implementation. While we discuss the analytical and clinical validity of these biomarkers, we identify the challenges and limitations to widespread biomarker use, including the need for biomarker-guided prospective studies to establish evidence of clinical utility of these new assays.</div></div>","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":"85 3","pages":"Pages 364-374"},"PeriodicalIF":9.4,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142449332","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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