Pub Date : 2025-02-01DOI: 10.1016/j.xkme.2024.100943
Porntep Amornritvanich , Thunyarat Anothaisintawee , John Attia , Gareth J. McKay , Ammarin Thakkinstian
<div><h3>Rationale & Objective</h3><div>To comprehensively summarize the efficacy of mineralocorticoid receptor antagonists (MRAs) to improve kidney and cardiovascular (CV) outcomes in patients with chronic kidney disease (CKD).</div></div><div><h3>Study Design</h3><div>Relevant studies were identified from Medline and Scopus databases from their inception up to August 2023.</div></div><div><h3>Setting & Study Populations</h3><div>Patients with nondialysis or dialysis CKD.</div></div><div><h3>Selection Criteria for Studies</h3><div>Systematic reviews and meta-analyses (SR-MAs) of randomized controlled trials (RCTs) that investigated the efficacy of MRAs on kidney and CV outcomes in patients with nondialysis or dialysis CKD were included in this study.</div></div><div><h3>Data Extraction</h3><div>Characteristics of studies and participants, and treatment effects were extracted.</div></div><div><h3>Analytic Approach</h3><div>Efficacy of MRAs was qualitatively summarized according to types of patients and MRAs.</div></div><div><h3>Results</h3><div>Forty SR-MAs were included. When compared with placebo/usual care, steroidal MRAs (sMRAs) provided significant benefit in decreasing all-cause (pooled RRs of 0.38 [0.22-0.65] to 0.87 [0.77-0.98]) and CV mortality (pooled RRs of 0.34 [0.15-0.75] to 0.46 [0.28-0.76]) only in patients treated with dialysis, when compared with placebo. Nonsteroidal MRAs (nsMRAs) significantly lowered composite CV events in both nondialysis CKD (pooled RRs of 0.86 [0.79-0.94] to 0.92 [0.85-0.99]) and patients with diabetic kidney disease (DKD) (pooled RRs of 0.86 [0.78-0.95] to 0.88 [0.81-0.96]). In addition, nsMRAs showed significant benefit in reducing composite kidney outcomes in patients with either nondialysis CKD or DKD when compared with placebo. However, this efficacy was lower than sodium-glucose cotransporter-2 inhibitors (SGLT2i) in patients with DKD. Moreover, both sMRAs and nsMRAs significantly increased the risk of hyperkalemia in patients with nondialysis CKD and DKD.</div></div><div><h3>Limitations</h3><div>The comparison between nsMRAs and SGLT2i is based on network meta-analyses. Consequently, additional head-to-head RCTs are necessary to confirm the advantages of SGLT2i over nsMRAs.</div></div><div><h3>Conclusions</h3><div>sMRAs offer benefits in reducing all-cause and cardiovascular mortality and composite CV events in patients treated with dialysis. nsMRAs improve kidney outcomes in patients with nondialysis CKD and DKD but increase hyperkalemia risk.</div></div><div><h3>Plain Language Summary</h3><div>Chronic kidney disease (CKD) can increase the risk of severe kidney problems and heart disease. A key factor in kidney decline and heart disease risk is the overactivation of mineralocorticoid receptors (MR). Medications called MR antagonists (MRAs) may lower heart disease risk. We performed a thorough review of all existing studies on both steroidal MRAs (sMRAs) and nonsteroidal MR antagonists (nsMRA
{"title":"Efficacy of Mineralocorticoid Receptor Antagonists on Kidney and Cardiovascular Outcomes in Patients With Chronic Kidney Disease: An Umbrella Review","authors":"Porntep Amornritvanich , Thunyarat Anothaisintawee , John Attia , Gareth J. McKay , Ammarin Thakkinstian","doi":"10.1016/j.xkme.2024.100943","DOIUrl":"10.1016/j.xkme.2024.100943","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>To comprehensively summarize the efficacy of mineralocorticoid receptor antagonists (MRAs) to improve kidney and cardiovascular (CV) outcomes in patients with chronic kidney disease (CKD).</div></div><div><h3>Study Design</h3><div>Relevant studies were identified from Medline and Scopus databases from their inception up to August 2023.</div></div><div><h3>Setting & Study Populations</h3><div>Patients with nondialysis or dialysis CKD.</div></div><div><h3>Selection Criteria for Studies</h3><div>Systematic reviews and meta-analyses (SR-MAs) of randomized controlled trials (RCTs) that investigated the efficacy of MRAs on kidney and CV outcomes in patients with nondialysis or dialysis CKD were included in this study.</div></div><div><h3>Data Extraction</h3><div>Characteristics of studies and participants, and treatment effects were extracted.</div></div><div><h3>Analytic Approach</h3><div>Efficacy of MRAs was qualitatively summarized according to types of patients and MRAs.</div></div><div><h3>Results</h3><div>Forty SR-MAs were included. When compared with placebo/usual care, steroidal MRAs (sMRAs) provided significant benefit in decreasing all-cause (pooled RRs of 0.38 [0.22-0.65] to 0.87 [0.77-0.98]) and CV mortality (pooled RRs of 0.34 [0.15-0.75] to 0.46 [0.28-0.76]) only in patients treated with dialysis, when compared with placebo. Nonsteroidal MRAs (nsMRAs) significantly lowered composite CV events in both nondialysis CKD (pooled RRs of 0.86 [0.79-0.94] to 0.92 [0.85-0.99]) and patients with diabetic kidney disease (DKD) (pooled RRs of 0.86 [0.78-0.95] to 0.88 [0.81-0.96]). In addition, nsMRAs showed significant benefit in reducing composite kidney outcomes in patients with either nondialysis CKD or DKD when compared with placebo. However, this efficacy was lower than sodium-glucose cotransporter-2 inhibitors (SGLT2i) in patients with DKD. Moreover, both sMRAs and nsMRAs significantly increased the risk of hyperkalemia in patients with nondialysis CKD and DKD.</div></div><div><h3>Limitations</h3><div>The comparison between nsMRAs and SGLT2i is based on network meta-analyses. Consequently, additional head-to-head RCTs are necessary to confirm the advantages of SGLT2i over nsMRAs.</div></div><div><h3>Conclusions</h3><div>sMRAs offer benefits in reducing all-cause and cardiovascular mortality and composite CV events in patients treated with dialysis. nsMRAs improve kidney outcomes in patients with nondialysis CKD and DKD but increase hyperkalemia risk.</div></div><div><h3>Plain Language Summary</h3><div>Chronic kidney disease (CKD) can increase the risk of severe kidney problems and heart disease. A key factor in kidney decline and heart disease risk is the overactivation of mineralocorticoid receptors (MR). Medications called MR antagonists (MRAs) may lower heart disease risk. We performed a thorough review of all existing studies on both steroidal MRAs (sMRAs) and nonsteroidal MR antagonists (nsMRA","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 2","pages":"Article 100943"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143179058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.xkme.2024.100929
Laurene M. Asare MD , Dia R. Waguespack MD , Jose J. Perez MD , Jade M. Teakell MD, PhD
{"title":"Home Dialysis for Undocumented Individuals: A Five-Year Single Center Experience","authors":"Laurene M. Asare MD , Dia R. Waguespack MD , Jose J. Perez MD , Jade M. Teakell MD, PhD","doi":"10.1016/j.xkme.2024.100929","DOIUrl":"10.1016/j.xkme.2024.100929","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 2","pages":"Article 100929"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11731473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143007953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.xkme.2024.100948
Rajesh Gupta , Michelle M. Estrella , Rebecca Scherzer , Pamela S. Brewster , Lance D. Dworkin , Hanh T. Nguyen , Yanmei Xie , Joachim H. Ix , Michael G. Shlipak , Timothy P. Murphy , Donald E. Cutlip , Eldrin F. Lewis , Christopher J. Cooper
Rationale & Objective
Although renal artery stenosis (RAS) and heart failure (HF) have been linked, the incidence and predictors of HF among patients with RAS are not well described.
Study Design
Post hoc analysis of the Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL) multicenter, open-label, randomized controlled trial (RCT).
Settings and Participants
Patients with atherosclerotic RAS and elevated blood pressure, chronic kidney disease, or both, and without a history of HF at enrollment.
Intervention
Medical therapy alone versus medical therapy plus renal artery stenting.
Outcomes
Incident HF events.
Results
This analysis included 808 participants enrolled in the CORAL trial without evidence of baseline HF. During a median follow-up of 4.8 years, 54 participants (6.7%) developed incident HF. HF incidence rates did not differ by randomized intervention (HR, 0.84; 95% confidence interval [CI], 0.49-1.43 for stent arm with medical arm as reference). Baseline diabetes (subdistribution hazard ratio (sHR), 2.07; 95% CI, 1.20-3.58), albuminuria (sHR, 1.12 per doubling of urinary albumin-creatinine ratio, 95% CI, 1.02-1.24), lower eGFR (sHR, 0.78 per 10 mL/min/1.73 m2 estimated glomerular filtration rate calculated with cystatin C and creatinine, 95% CI, 0.69-0.88), and peripheral vascular disease (PVD) (sHR, 2.18, 95% CI, 1.21-3.91) were independent predictors of incident HF. Participants who experienced incident HF had greater kidney function decline before HF events.
Limitations
This is a post hoc analysis of a RCT. The number of HF events is small.
Conclusions
In patients with RAS, rates of incident HF did not differ between participants randomized to optimal medical therapy alone versus optimal medical therapy plus renal artery stenting. The presence of diabetes, PVD, and worse kidney health at baseline were associated with future HF events.
Plain-Language Summary
Renal artery stenosis has been linked with heart failure. The CORAL randomized controlled trial has the largest study population of participants with renal artery stenosis. In this analysis, we assessed the incidence and predictors of heart failure in CORAL. We found similar rates of incident heart failure among participants randomized to medical therapy alone vs. medical therapy plus renal artery stent. We identified independent predictors of incident heart failure among people with renal artery stenosis include PAD, diabetes, albuminuria, and lower baseline eGFR. In addition, eGFR declined prior to heart failure events.
{"title":"Incident Heart Failure in Atherosclerotic Renal Artery Stenosis: A Post Hoc Analysis of the CORAL Trial","authors":"Rajesh Gupta , Michelle M. Estrella , Rebecca Scherzer , Pamela S. Brewster , Lance D. Dworkin , Hanh T. Nguyen , Yanmei Xie , Joachim H. Ix , Michael G. Shlipak , Timothy P. Murphy , Donald E. Cutlip , Eldrin F. Lewis , Christopher J. Cooper","doi":"10.1016/j.xkme.2024.100948","DOIUrl":"10.1016/j.xkme.2024.100948","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Although renal artery stenosis (RAS) and heart failure (HF) have been linked, the incidence and predictors of HF among patients with RAS are not well described.</div></div><div><h3>Study Design</h3><div>Post hoc analysis of the Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL) multicenter, open-label, randomized controlled trial (RCT).</div></div><div><h3>Settings and Participants</h3><div>Patients with atherosclerotic RAS and elevated blood pressure, chronic kidney disease, or both, and without a history of HF at enrollment.</div></div><div><h3>Intervention</h3><div>Medical therapy alone versus medical therapy plus renal artery stenting.</div></div><div><h3>Outcomes</h3><div>Incident HF events.</div></div><div><h3>Results</h3><div>This analysis included 808 participants enrolled in the CORAL trial without evidence of baseline HF. During a median follow-up of 4.8 years, 54 participants (6.7%) developed incident HF. HF incidence rates did not differ by randomized intervention (HR, 0.84; 95% confidence interval [CI], 0.49-1.43 for stent arm with medical arm as reference). Baseline diabetes (subdistribution hazard ratio (sHR), 2.07; 95% CI, 1.20-3.58), albuminuria (sHR, 1.12 per doubling of urinary albumin-creatinine ratio, 95% CI, 1.02-1.24), lower eGFR (sHR, 0.78 per 10<!--> <!-->mL/min/1.73<!--> <!-->m<sup>2</sup> estimated glomerular filtration rate calculated with cystatin C and creatinine, 95% CI, 0.69-0.88), and peripheral vascular disease (PVD) (sHR, 2.18, 95% CI, 1.21-3.91) were independent predictors of incident HF. Participants who experienced incident HF had greater kidney function decline before HF events.</div></div><div><h3>Limitations</h3><div>This is a post hoc analysis of a RCT. The number of HF events is small.</div></div><div><h3>Conclusions</h3><div>In patients with RAS, rates of incident HF did not differ between participants randomized to optimal medical therapy alone versus optimal medical therapy plus renal artery stenting. The presence of diabetes, PVD, and worse kidney health at baseline were associated with future HF events.</div></div><div><h3>Plain-Language Summary</h3><div>Renal artery stenosis has been linked with heart failure. The CORAL randomized controlled trial has the largest study population of participants with renal artery stenosis. In this analysis, we assessed the incidence and predictors of heart failure in CORAL. We found similar rates of incident heart failure among participants randomized to medical therapy alone vs. medical therapy plus renal artery stent. We identified independent predictors of incident heart failure among people with renal artery stenosis include PAD, diabetes, albuminuria, and lower baseline eGFR. In addition, eGFR declined prior to heart failure events.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 2","pages":"Article 100948"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787008/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-15DOI: 10.1016/j.xkme.2025.100965
Ayub Akbari , Sriram Sriperumbuduri , Shreepryia Mangalgi , Vijay Joshi , Manish Sood , Amos Buh , Mohan Biyani , Christopher McCudden , Gregory L. Hundemer , Pierre Antoine Brown
<div><h3>Rationale & Objective</h3><div>Arginine vasopressin (AVP) is an established driver of cyst growth in autosomal dominant polycystic kidney disease (ADPKD). Urine osmolality (osm) measures are surrogate markers of AVP activity. Both 24-hour and spot urine samples are used as indicators of AVP suppression. The agreement between these 2 measurements remains unclear.</div></div><div><h3>Study Design</h3><div>A retrospective cohort study.</div></div><div><h3>Setting & Study Population</h3><div>Three hundred and forty-nine patients with ADPKD with 839 urine samples from a tertiary care center.</div></div><div><h3>Selection Criteria for Study</h3><div>Patients with ADPKD with records of spot and 24-hour urine measurements.</div></div><div><h3>Data Extraction</h3><div>Consecutive patients’ data from January 2018 to March 2023 were extracted from the quality assurance database of The Ottawa Hospital Cystic Kidney Disease Clinic.</div></div><div><h3>Analytical Approach</h3><div>Discordance assessed at target urine osmolality of 250 and 270<!--> <!-->mmol/kg. Agreement assessed by Bland-Altman plots. The percentage of patients with difference in osmolality between the 2 measures for cutoff points of<!--> <!-->><!--> <!-->50,<!--> <!-->><!--> <!-->100,<!--> <!-->>150, and<!--> <!-->><!--> <!-->200<!--> <!-->mmol/kg was calculated.</div></div><div><h3>Results</h3><div>The mean 24-hour urine osm was 364<!--> <!-->mmol/kg, and the mean spot urine osm was 424 mosm/kg. Mean age of 46 years, 52% females, and 47 (13.5%) were on tolvaptan. Overall, in comparing spot urine osm to 24-hour urine osm, the discordance at 250 and 270<!--> <!-->mmol/kg was 24% with poor agreement on Bland-Altman plots. The differences between the 2 measures at varying cutoff points were 53.9% at 50<!--> <!-->mmol/kg, 35.8% at 100<!--> <!-->mmol/kg, 24.1% at 150<!--> <!-->mmol/kg, and 16.1% at 200<!--> <!-->mmol/kg. Results were similar when only a single measurement from each patient was used for analysis.</div></div><div><h3>Limitations</h3><div>Total of 29% of patients did not have concurrent spot urine osmolality and 24-hour urine osmolality. The study was conducted at a single center. Limited number of patients were on tolvaptan.</div></div><div><h3>Conclusions</h3><div>In adults with ADPKD, important differences exist between the 24-hour urine osmolality and spot urine osmolality that preclude interchangeable use. The method employed may impact clinical decision-making. More research is needed to determine, which urine osm should be used when assessing AVP suppression.</div></div><div><h3>Plain Language Summary</h3><div>Urine osmolality measures are used clinically to dose tolvaptan in patients with adult polycystic kidney disease. We compared urine osmolality from 24-hour and spot urine samples. We found out that important differences exist between 24-hour and spot urine samples’ osmolality. The method employed to determine urine osmolality may impact clin
{"title":"Spot Versus 24-Hour Urine Osmolality Measurement in Autosomal Dominant Polycystic Kidney Disease: A Diagnostic Test Study","authors":"Ayub Akbari , Sriram Sriperumbuduri , Shreepryia Mangalgi , Vijay Joshi , Manish Sood , Amos Buh , Mohan Biyani , Christopher McCudden , Gregory L. Hundemer , Pierre Antoine Brown","doi":"10.1016/j.xkme.2025.100965","DOIUrl":"10.1016/j.xkme.2025.100965","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Arginine vasopressin (AVP) is an established driver of cyst growth in autosomal dominant polycystic kidney disease (ADPKD). Urine osmolality (osm) measures are surrogate markers of AVP activity. Both 24-hour and spot urine samples are used as indicators of AVP suppression. The agreement between these 2 measurements remains unclear.</div></div><div><h3>Study Design</h3><div>A retrospective cohort study.</div></div><div><h3>Setting & Study Population</h3><div>Three hundred and forty-nine patients with ADPKD with 839 urine samples from a tertiary care center.</div></div><div><h3>Selection Criteria for Study</h3><div>Patients with ADPKD with records of spot and 24-hour urine measurements.</div></div><div><h3>Data Extraction</h3><div>Consecutive patients’ data from January 2018 to March 2023 were extracted from the quality assurance database of The Ottawa Hospital Cystic Kidney Disease Clinic.</div></div><div><h3>Analytical Approach</h3><div>Discordance assessed at target urine osmolality of 250 and 270<!--> <!-->mmol/kg. Agreement assessed by Bland-Altman plots. The percentage of patients with difference in osmolality between the 2 measures for cutoff points of<!--> <!-->><!--> <!-->50,<!--> <!-->><!--> <!-->100,<!--> <!-->>150, and<!--> <!-->><!--> <!-->200<!--> <!-->mmol/kg was calculated.</div></div><div><h3>Results</h3><div>The mean 24-hour urine osm was 364<!--> <!-->mmol/kg, and the mean spot urine osm was 424 mosm/kg. Mean age of 46 years, 52% females, and 47 (13.5%) were on tolvaptan. Overall, in comparing spot urine osm to 24-hour urine osm, the discordance at 250 and 270<!--> <!-->mmol/kg was 24% with poor agreement on Bland-Altman plots. The differences between the 2 measures at varying cutoff points were 53.9% at 50<!--> <!-->mmol/kg, 35.8% at 100<!--> <!-->mmol/kg, 24.1% at 150<!--> <!-->mmol/kg, and 16.1% at 200<!--> <!-->mmol/kg. Results were similar when only a single measurement from each patient was used for analysis.</div></div><div><h3>Limitations</h3><div>Total of 29% of patients did not have concurrent spot urine osmolality and 24-hour urine osmolality. The study was conducted at a single center. Limited number of patients were on tolvaptan.</div></div><div><h3>Conclusions</h3><div>In adults with ADPKD, important differences exist between the 24-hour urine osmolality and spot urine osmolality that preclude interchangeable use. The method employed may impact clinical decision-making. More research is needed to determine, which urine osm should be used when assessing AVP suppression.</div></div><div><h3>Plain Language Summary</h3><div>Urine osmolality measures are used clinically to dose tolvaptan in patients with adult polycystic kidney disease. We compared urine osmolality from 24-hour and spot urine samples. We found out that important differences exist between 24-hour and spot urine samples’ osmolality. The method employed to determine urine osmolality may impact clin","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 3","pages":"Article 100965"},"PeriodicalIF":3.2,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143131171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-04DOI: 10.1016/j.xkme.2024.100960
Alisha Puri , Anita M. Lloyd , Aminu K. Bello , Marcello Tonelli , Sandra M. Campbell , Karthik Tennankore , Sara N. Davison , Stephanie Thompson
<div><h3>Rationale & Objective</h3><div>Frailty represents a loss of physiologic reserve across multiple biological systems, confers a higher risk of adverse health outcomes, and is highly prevalent among people with chronic kidney disease (CKD). We evaluated the measurement properties of frailty tools used in CKD and summarized the association of frailty with death and hospitalization.</div></div><div><h3>Study Design</h3><div>Systematic review and meta-analysis.</div></div><div><h3>Setting & Study Populations</h3><div>Studies assessing multidimensional frailty tools in adults at any stage of CKD and evaluating a measurement property of interest as per the Consensus-based Standards for the Selection of Health Measurement Instruments taxonomy.</div></div><div><h3>Selection Criteria for Studies</h3><div>Observational studies and randomized trials.</div></div><div><h3>Data Extraction</h3><div>Risk and precision measurements; measurement properties.</div></div><div><h3>Analytical Approach</h3><div>The Comprehensive Geriatric Assessment was the clinical standard for frailty identification. We pooled data using random effects models or summarized with narrative synthesis when data were too heterogenous to pool.</div></div><div><h3>Results</h3><div>We included 105 studies with data for at least one of the following: discriminative (n<!--> <!-->=<!--> <!-->84; 80%), convergent (n<!--> <!-->=<!--> <!-->20; 19%), and criterion validity (n<!--> <!-->=<!--> <!-->2; 2%); responsiveness (n<!--> <!-->=<!--> <!-->9; 9%) and reliability (n<!--> <!-->=<!--> <!-->1; 0.1%). For the Fried Frailty Phenotype (FFP), the pooled adjusted HR (aHR) for mortality was 2.01 (95% confidence intervals [CI], 1.35-2.98; <em>P</em> <!-->=<!--> <!-->0.001; <em>I</em><sup>2</sup> <!-->=<!--> <!-->58%) and 1.89 (95% CI, 1.25-2.85; <em>P</em> <!-->=<!--> <!-->0.002; <em>I</em><sup>2</sup> <!-->=<!--> <!-->0%) for hospitalization in kidney failure (KF) populations. The pooled aHR for the Clinical Frailty Scale for mortality in pre-frail versus non-frail was 1.75 (95% CI, 1.17-2.60; <em>I</em><sup>2</sup> <!-->=<!--> <!-->26%) and 2.20 (95% CI, 1.00-4.80; <em>I</em><sup>2</sup> <!-->=<!--> <!-->66%) in frail versus non-frail. The Fatigue, Resistance, Ambulation, Illness, and Loss of weight scale showed consistent discriminative validity for higher mortality in non-dialysis CKD. The modified FFP (self-reported) showed acceptable discriminative validity and agreement with the FFP in patients with KF. In CKD and KF populations, agreement between clinicians’ subjective impression of frailty and frailty tools was low.</div></div><div><h3>Limitations</h3><div>Few studies compared the accuracy of frailty tools to the Comprehensive Geriatric Assessment. Only 1 study reported reliability. Studies were of overall low-moderate quality.</div></div><div><h3>Conclusions</h3><div>The FFP and Clinical Frailty Scale showed acceptable discriminant validity for clinical outcomes, and the modified
{"title":"Frailty Assessment Tools in Chronic Kidney Disease: A Systematic Review and Meta-analysis","authors":"Alisha Puri , Anita M. Lloyd , Aminu K. Bello , Marcello Tonelli , Sandra M. Campbell , Karthik Tennankore , Sara N. Davison , Stephanie Thompson","doi":"10.1016/j.xkme.2024.100960","DOIUrl":"10.1016/j.xkme.2024.100960","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Frailty represents a loss of physiologic reserve across multiple biological systems, confers a higher risk of adverse health outcomes, and is highly prevalent among people with chronic kidney disease (CKD). We evaluated the measurement properties of frailty tools used in CKD and summarized the association of frailty with death and hospitalization.</div></div><div><h3>Study Design</h3><div>Systematic review and meta-analysis.</div></div><div><h3>Setting & Study Populations</h3><div>Studies assessing multidimensional frailty tools in adults at any stage of CKD and evaluating a measurement property of interest as per the Consensus-based Standards for the Selection of Health Measurement Instruments taxonomy.</div></div><div><h3>Selection Criteria for Studies</h3><div>Observational studies and randomized trials.</div></div><div><h3>Data Extraction</h3><div>Risk and precision measurements; measurement properties.</div></div><div><h3>Analytical Approach</h3><div>The Comprehensive Geriatric Assessment was the clinical standard for frailty identification. We pooled data using random effects models or summarized with narrative synthesis when data were too heterogenous to pool.</div></div><div><h3>Results</h3><div>We included 105 studies with data for at least one of the following: discriminative (n<!--> <!-->=<!--> <!-->84; 80%), convergent (n<!--> <!-->=<!--> <!-->20; 19%), and criterion validity (n<!--> <!-->=<!--> <!-->2; 2%); responsiveness (n<!--> <!-->=<!--> <!-->9; 9%) and reliability (n<!--> <!-->=<!--> <!-->1; 0.1%). For the Fried Frailty Phenotype (FFP), the pooled adjusted HR (aHR) for mortality was 2.01 (95% confidence intervals [CI], 1.35-2.98; <em>P</em> <!-->=<!--> <!-->0.001; <em>I</em><sup>2</sup> <!-->=<!--> <!-->58%) and 1.89 (95% CI, 1.25-2.85; <em>P</em> <!-->=<!--> <!-->0.002; <em>I</em><sup>2</sup> <!-->=<!--> <!-->0%) for hospitalization in kidney failure (KF) populations. The pooled aHR for the Clinical Frailty Scale for mortality in pre-frail versus non-frail was 1.75 (95% CI, 1.17-2.60; <em>I</em><sup>2</sup> <!-->=<!--> <!-->26%) and 2.20 (95% CI, 1.00-4.80; <em>I</em><sup>2</sup> <!-->=<!--> <!-->66%) in frail versus non-frail. The Fatigue, Resistance, Ambulation, Illness, and Loss of weight scale showed consistent discriminative validity for higher mortality in non-dialysis CKD. The modified FFP (self-reported) showed acceptable discriminative validity and agreement with the FFP in patients with KF. In CKD and KF populations, agreement between clinicians’ subjective impression of frailty and frailty tools was low.</div></div><div><h3>Limitations</h3><div>Few studies compared the accuracy of frailty tools to the Comprehensive Geriatric Assessment. Only 1 study reported reliability. Studies were of overall low-moderate quality.</div></div><div><h3>Conclusions</h3><div>The FFP and Clinical Frailty Scale showed acceptable discriminant validity for clinical outcomes, and the modified ","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 3","pages":"Article 100960"},"PeriodicalIF":3.2,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143131343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.xkme.2024.100937
Nicholas L.S. Roberts , Salama Fadhil , Megan Willkens , Grace Ruselu , Bernard Desderius , Said Kanenda , Ladius Rudovick , Bazil B. Kavishe , Serena P. Koenig , Sri Lekha Tummalapalli , Myung Hee Lee , Robert N. Peck
<div><h3>Rationale & Objective</h3><div>Longitudinal research on chronic kidney disease (CKD) in sub-Saharan Africa is sparse, especially among people living with HIV (PLWH). We evaluated the incidence of CKD among PLWH compared with HIV-uninfected controls in Tanzania.</div></div><div><h3>Study Design</h3><div>Prospective cohort study.</div></div><div><h3>Setting & Participants</h3><div>A total of 495 newly diagnosed PLWH who initiated antiretroviral therapy (ART) and 505 HIV-uninfected adults enrolled from public HIV clinics and followed from 2016-2021. The control group was recruited from HIV treatment partners from the same HIV clinics.</div></div><div><h3>Exposures</h3><div>Untreated HIV (at baseline), ART, sociodemographic information, health behaviors, hypertension, and diabetes.</div></div><div><h3>Outcomes</h3><div>Incident CKD, defined as a follow-up estimated glomerular filtration rate (eGFR) of<!--> <!--><60<!--> <!-->mL/min/1.73<!--> <!-->m<sup>2</sup> with<!--> <!-->≥25% reduction from baseline; annual eGFR change; incident albuminuria; 3-year all-cause mortality.</div></div><div><h3>Analytical Approach</h3><div>Multivariable Poisson and linear regression determined the association between HIV and other factors with a baseline prevalent reduced eGFR and albuminuria, incident CKD and albuminuria, and annual eGFR change. Cox hazard regression assessed the association between baseline CKD and mortality.</div></div><div><h3>Results</h3><div>Median age was 35 years and 67.5% were women. There were 101 incident CKD cases, 71 among PLWH and 30 among HIV-uninfected participants, equivalent to a CKD incidence of 57.9 per 1,000 person-years (95% CI, 44.4-71.4) and 26.2 per 1,000 person-years (95% CI, 16.8-35.5), respectively. PLWH had a more rapid eGFR decline (−6.65 vs<!--> <!-->−2.61<!--> <!-->mL/min/1.73<!--> <!-->m<sup>2</sup> per year). Female sex and older age were positively associated with incident CKD. Albuminuria incidence did not differ by HIV status. PLWH with albuminuria at baseline had higher mortality (HR, 2.13; 95% CI, 1.08-4.21).</div></div><div><h3>Limitations</h3><div>As an observational cohort study, there was no comparison group of HIV-positive participants on a nontenofovir disoproxil fumarate–based ART regimen.</div></div><div><h3>Conclusions</h3><div>PLWH receiving tenofovir disoproxil fumarate–based ART had a very high incidence of CKD and rapid eGFR decline. Conversely, albuminuria stabilized with ART use. Expanding access to less-nephrotoxic ART, such as tenofovir alafenamide, is urgently needed throughout sub-Saharan Africa.</div></div><div><h3>Plain-Language Summary</h3><div>Managing chronic kidney disease (CKD) among people living with HIV (PLWH) in sub-Saharan Africa is complex owing to resource constraints and sparse longitudinal data. Using a prospective cohort of 495 newly diagnosed PLWH who initiated tenofovir disoproxil fumarate–based antiretroviral therapy (ART) and 505 HIV-uninfected controls i
{"title":"HIV and CKD in the Tenofovir Era: A Prospective Parallel-Group Cohort Study From Tanzania","authors":"Nicholas L.S. Roberts , Salama Fadhil , Megan Willkens , Grace Ruselu , Bernard Desderius , Said Kanenda , Ladius Rudovick , Bazil B. Kavishe , Serena P. Koenig , Sri Lekha Tummalapalli , Myung Hee Lee , Robert N. Peck","doi":"10.1016/j.xkme.2024.100937","DOIUrl":"10.1016/j.xkme.2024.100937","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Longitudinal research on chronic kidney disease (CKD) in sub-Saharan Africa is sparse, especially among people living with HIV (PLWH). We evaluated the incidence of CKD among PLWH compared with HIV-uninfected controls in Tanzania.</div></div><div><h3>Study Design</h3><div>Prospective cohort study.</div></div><div><h3>Setting & Participants</h3><div>A total of 495 newly diagnosed PLWH who initiated antiretroviral therapy (ART) and 505 HIV-uninfected adults enrolled from public HIV clinics and followed from 2016-2021. The control group was recruited from HIV treatment partners from the same HIV clinics.</div></div><div><h3>Exposures</h3><div>Untreated HIV (at baseline), ART, sociodemographic information, health behaviors, hypertension, and diabetes.</div></div><div><h3>Outcomes</h3><div>Incident CKD, defined as a follow-up estimated glomerular filtration rate (eGFR) of<!--> <!--><60<!--> <!-->mL/min/1.73<!--> <!-->m<sup>2</sup> with<!--> <!-->≥25% reduction from baseline; annual eGFR change; incident albuminuria; 3-year all-cause mortality.</div></div><div><h3>Analytical Approach</h3><div>Multivariable Poisson and linear regression determined the association between HIV and other factors with a baseline prevalent reduced eGFR and albuminuria, incident CKD and albuminuria, and annual eGFR change. Cox hazard regression assessed the association between baseline CKD and mortality.</div></div><div><h3>Results</h3><div>Median age was 35 years and 67.5% were women. There were 101 incident CKD cases, 71 among PLWH and 30 among HIV-uninfected participants, equivalent to a CKD incidence of 57.9 per 1,000 person-years (95% CI, 44.4-71.4) and 26.2 per 1,000 person-years (95% CI, 16.8-35.5), respectively. PLWH had a more rapid eGFR decline (−6.65 vs<!--> <!-->−2.61<!--> <!-->mL/min/1.73<!--> <!-->m<sup>2</sup> per year). Female sex and older age were positively associated with incident CKD. Albuminuria incidence did not differ by HIV status. PLWH with albuminuria at baseline had higher mortality (HR, 2.13; 95% CI, 1.08-4.21).</div></div><div><h3>Limitations</h3><div>As an observational cohort study, there was no comparison group of HIV-positive participants on a nontenofovir disoproxil fumarate–based ART regimen.</div></div><div><h3>Conclusions</h3><div>PLWH receiving tenofovir disoproxil fumarate–based ART had a very high incidence of CKD and rapid eGFR decline. Conversely, albuminuria stabilized with ART use. Expanding access to less-nephrotoxic ART, such as tenofovir alafenamide, is urgently needed throughout sub-Saharan Africa.</div></div><div><h3>Plain-Language Summary</h3><div>Managing chronic kidney disease (CKD) among people living with HIV (PLWH) in sub-Saharan Africa is complex owing to resource constraints and sparse longitudinal data. Using a prospective cohort of 495 newly diagnosed PLWH who initiated tenofovir disoproxil fumarate–based antiretroviral therapy (ART) and 505 HIV-uninfected controls i","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 1","pages":"Article 100937"},"PeriodicalIF":3.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11714399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142950837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.xkme.2024.100928
Anuja Java , Lindsey Fuller
Complement 3 glomerulopathy (C3G) is an ultra-rare glomerulonephritis caused by dysregulation of the alternative complement pathway. C3G has an estimated incidence of 1-3 cases per million people in the United States. Diagnosing C3G based solely on clinical and laboratory features is challenging because it mimics several other glomerular diseases; therefore, diagnosis requires a kidney biopsy. In the absence of disease-modifying therapies and optimal patient management strategies, C3G poses a significant physical and emotional burden on patients and caregivers. Common symptoms of glomerulonephritis include fatigue, edema, anxiety, and/or depression, which have profound effects on patients’ daily lives. Approximately half of all patients progress to kidney failure within 10 years of diagnosis. Encouragingly, the treatment landscape in C3G is poised to change, with several targeted complement inhibitors in late-stage development. This perspectives article explores a patient’s journey in C3G and discusses the current and future status of clinical outcomes and patient management from the viewpoints of a practicing nephrologist and a patient.
{"title":"Establishing the Future Direction of Clinical Outcomes in C3 Glomerulopathy: Perspectives From a Patient and a Physician","authors":"Anuja Java , Lindsey Fuller","doi":"10.1016/j.xkme.2024.100928","DOIUrl":"10.1016/j.xkme.2024.100928","url":null,"abstract":"<div><div>Complement 3 glomerulopathy (C3G) is an ultra-rare glomerulonephritis caused by dysregulation of the alternative complement pathway. C3G has an estimated incidence of 1-3 cases per million people in the United States. Diagnosing C3G based solely on clinical and laboratory features is challenging because it mimics several other glomerular diseases; therefore, diagnosis requires a kidney biopsy. In the absence of disease-modifying therapies and optimal patient management strategies, C3G poses a significant physical and emotional burden on patients and caregivers. Common symptoms of glomerulonephritis include fatigue, edema, anxiety, and/or depression, which have profound effects on patients’ daily lives. Approximately half of all patients progress to kidney failure within 10 years of diagnosis. Encouragingly, the treatment landscape in C3G is poised to change, with several targeted complement inhibitors in late-stage development. This perspectives article explores a patient’s journey in C3G and discusses the current and future status of clinical outcomes and patient management from the viewpoints of a practicing nephrologist and a patient.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 1","pages":"Article 100928"},"PeriodicalIF":3.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699595/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.xkme.2024.100931
Christopher Knapp MD, MPH , Shuling Li PhD , Chuanyu Kou MS , James B. Wetmore MD , Kirsten L. Johansen MD
{"title":"Peritoneal Dialysis-Associated Peritonitis Rates in the Outpatient and Hospital Setting Among Incident Dialysis Patients With Medicare, 2009–2018","authors":"Christopher Knapp MD, MPH , Shuling Li PhD , Chuanyu Kou MS , James B. Wetmore MD , Kirsten L. Johansen MD","doi":"10.1016/j.xkme.2024.100931","DOIUrl":"10.1016/j.xkme.2024.100931","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 1","pages":"Article 100931"},"PeriodicalIF":3.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11697115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.xkme.2024.100935
Fouad T. Chebib , Neera Dahl , Xiaolei Zhou , Diana Garbinsky , Jinyi Wang , Sasikiran Nunna , Dorothee Oberdhan , Ancilla W. Fernandes
<div><h3>Rational & Objective</h3><div>Data are limited regarding the long-term efficacy of tolvaptan in adults aged 18-35 years with autosomal dominant polycystic kidney disease (ADPKD) at increased risk of rapid progression. We assessed the effects of tolvaptan within a larger population of younger adults and over longer follow-up than individual clinical trials could provide.</div></div><div><h3>Study Design</h3><div>Pooled database study.</div></div><div><h3>Setting & Study Populations</h3><div>A consolidated clinical study database with ADPKD patients aged 18-35 years.</div></div><div><h3>Selection Criteria for Studies</h3><div>Studies that enrolled patients who received either tolvaptan or standard-of-care treatment not including tolvaptan.</div></div><div><h3>Data Extraction</h3><div>Annual rate of change in estimated glomerular filtration rate (eGFR) and time to kidney failure.</div></div><div><h3>Analytical Approach</h3><div>For individuals participating in multiple studies, their data were longitudinally linked to extend the follow-up period. We matched tolvaptan-treated patients with controls based on age, sex, chronic kidney disease stage, eGFR, and, where possible, Mayo Imaging Classification. We compared eGFR decline between groups using mixed-effects modeling.</div></div><div><h3>Results</h3><div>The matched analysis set encompassed 204 tolvaptan-treated individuals and 204 controls. Median follow-up was 4.6 years for the tolvaptan group and 1.7 years for controls. In the mixed-effects model, the eGFR decline rate (in mL/min/1.73<!--> <!-->m<sup>2</sup>/year) was –2.58 for the tolvaptan cohort and -4.28 for controls. This indicates reduction in the eGFR decline rate by 1.69<!--> <!-->mL/min/1.73<!--> <!-->m<sup>2</sup>/year (95% confidence interval: 0.87-2.52; <em>P</em> <!--><<!--> <!-->0.001) with tolvaptan, a 40% improvement. Extrapolating eGFR over 35 years, tolvaptan could delay kidney failure onset by approximately 11 years.</div></div><div><h3>Limitations</h3><div>Median follow-up was shorter in the control cohort than the tolvaptan cohort. The projection of time to kidney failure assumed a linear model of eGFR decline.</div></div><div><h3>Conclusions</h3><div>This analysis offers insights into the anticipated treatment benefits of tolvaptan for young adults with ADPKD. These findings are crucial for weighing treatment benefits against any associated risks.</div></div><div><h3>Plain-Language Summary</h3><div>Tolvaptan is the only approved treatment for delaying kidney function decline in patients with autosomal dominant polycystic kidney disease (ADPKD) at high risk of rapid progression. Clinical trials have included few patients aged 18-35 years, a group potentially benefiting significantly from early tolvaptan initiation. We pooled clinical study data, matching tolvaptan-treated patients with untreated controls by baseline characteristics. The results showed a statistically significant reduction in kidney functi
{"title":"Tolvaptan and Autosomal Dominant Polycystic Kidney Disease Progression in Individuals Aged 18-35 Years: A Pooled Database Analysis","authors":"Fouad T. Chebib , Neera Dahl , Xiaolei Zhou , Diana Garbinsky , Jinyi Wang , Sasikiran Nunna , Dorothee Oberdhan , Ancilla W. Fernandes","doi":"10.1016/j.xkme.2024.100935","DOIUrl":"10.1016/j.xkme.2024.100935","url":null,"abstract":"<div><h3>Rational & Objective</h3><div>Data are limited regarding the long-term efficacy of tolvaptan in adults aged 18-35 years with autosomal dominant polycystic kidney disease (ADPKD) at increased risk of rapid progression. We assessed the effects of tolvaptan within a larger population of younger adults and over longer follow-up than individual clinical trials could provide.</div></div><div><h3>Study Design</h3><div>Pooled database study.</div></div><div><h3>Setting & Study Populations</h3><div>A consolidated clinical study database with ADPKD patients aged 18-35 years.</div></div><div><h3>Selection Criteria for Studies</h3><div>Studies that enrolled patients who received either tolvaptan or standard-of-care treatment not including tolvaptan.</div></div><div><h3>Data Extraction</h3><div>Annual rate of change in estimated glomerular filtration rate (eGFR) and time to kidney failure.</div></div><div><h3>Analytical Approach</h3><div>For individuals participating in multiple studies, their data were longitudinally linked to extend the follow-up period. We matched tolvaptan-treated patients with controls based on age, sex, chronic kidney disease stage, eGFR, and, where possible, Mayo Imaging Classification. We compared eGFR decline between groups using mixed-effects modeling.</div></div><div><h3>Results</h3><div>The matched analysis set encompassed 204 tolvaptan-treated individuals and 204 controls. Median follow-up was 4.6 years for the tolvaptan group and 1.7 years for controls. In the mixed-effects model, the eGFR decline rate (in mL/min/1.73<!--> <!-->m<sup>2</sup>/year) was –2.58 for the tolvaptan cohort and -4.28 for controls. This indicates reduction in the eGFR decline rate by 1.69<!--> <!-->mL/min/1.73<!--> <!-->m<sup>2</sup>/year (95% confidence interval: 0.87-2.52; <em>P</em> <!--><<!--> <!-->0.001) with tolvaptan, a 40% improvement. Extrapolating eGFR over 35 years, tolvaptan could delay kidney failure onset by approximately 11 years.</div></div><div><h3>Limitations</h3><div>Median follow-up was shorter in the control cohort than the tolvaptan cohort. The projection of time to kidney failure assumed a linear model of eGFR decline.</div></div><div><h3>Conclusions</h3><div>This analysis offers insights into the anticipated treatment benefits of tolvaptan for young adults with ADPKD. These findings are crucial for weighing treatment benefits against any associated risks.</div></div><div><h3>Plain-Language Summary</h3><div>Tolvaptan is the only approved treatment for delaying kidney function decline in patients with autosomal dominant polycystic kidney disease (ADPKD) at high risk of rapid progression. Clinical trials have included few patients aged 18-35 years, a group potentially benefiting significantly from early tolvaptan initiation. We pooled clinical study data, matching tolvaptan-treated patients with untreated controls by baseline characteristics. The results showed a statistically significant reduction in kidney functi","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 1","pages":"Article 100935"},"PeriodicalIF":3.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11731472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142983910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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