Journal of The American Society of Nephrology最新文献

{"title":"Hemodialysis Care: Evolving to Enhance Patient-Level Outcomes.","authors":"Allen R Nissenson, Jörgen Hegbrant, Frank W Maddux, Giovanni F M Strippoli","doi":"10.1681/ASN.0000001286","DOIUrl":"https://doi.org/10.1681/ASN.0000001286","url":null,"abstract":"<p><p>Hemodialysis remains the predominant form of kidney replacement therapy worldwide, yet mortality, hospitalization, symptom burden, and impaired health-related quality of life remain substantial. Historically, dialysis innovation has emphasized surrogate measures such as solute clearance and biochemical targets. Although these advances have improved treatment delivery, gains in patient-important outcomes-including survival, hospitalization, symptoms, and functional status-have been limited, suggesting diminishing returns from further optimization of traditional adequacy targets. Dialysis therapies should therefore be evaluated by their effects on clinical outcomes, patient-reported outcomes, safety, equity, sustainability, and value. This review assesses contemporary extracorporeal modalities and emerging technologies using an outcome-based framework incorporating implementation, health-system implications, and patient priorities. High-flux hemodialysis is the current standard of care but has not consistently been associated with lower all-cause mortality despite achievement of modern adequacy targets. Medium cut-off membranes, adsorption-based approaches, personalized schedules, and portable, wearable, or implantable technologies offer compelling physiologic rationales and may improve selected surrogate measures; however, evidence of meaningful clinical benefit remains limited. Among extracorporeal therapies, online hemodiafiltration has the strongest evidence base. Randomized trials and individual-participant-data meta-analyses indicate better survival with high-volume online hemodiafiltration versus high-flux hemodialysis, with supportive patient-reported and cost-effectiveness evidence. However, CONVINCE patients achieved high convection volumes; benefit is uncertain for those unable to reach these targets, and implementation depends on infrastructure, reimbursement, regulation, and quality assurance. Current evidence supports shifting dialysis innovation from surrogate endpoints toward outcomes that matter to patients. Physiologic plausibility and surrogate improvements alone should not justify widespread adoption. Future progress requires rigorous comparative-effectiveness research, implementation science, real-world evidence, routine integration of standardized patient-reported outcomes, and attention to environmental sustainability and equitable access. Aligning reimbursement, quality metrics, implementation, and policy with patient-level outcomes will be essential to translate technological advances into better care for people with kidney failure.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149025213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hemodiafiltration: Clinical Practice of Today and a Look into the Future.","authors":"Peter J Blankestijn, Sanne Roos, Claudia Barth, Michiel L Bots, Krister Cromm, Andrew Davenport, Jörgen Hegbrant, Giovanni Strippoli, Robin W M Vernooij, Bernard Canaud","doi":"10.1681/ASN.0000001282","DOIUrl":"https://doi.org/10.1681/ASN.0000001282","url":null,"abstract":"<p><p>Hemodiafiltration (HDF) with online production of substitution fluid has emerged as kidney replacement therapy and is increasingly adopted worldwide. Recent randomized controlled trials, individual participant data meta-analyses, and large real-world studies have demonstrated that high-volume HDF improves clinical outcomes compared with conventional high-flux hemodialysis (HD), including reduction in all-cause mortality and hospitalization. Importantly, these benefits appear dose-dependent, with achieved convective volume serving as a modifiable treatment target. Beyond survival, data suggest advantages in patient reported outcomes and evidence for cost-effectiveness. This review provides a practical overview of contemporary HDF delivery, focusing on the prescription variables that determine treatment performance, including vascular access, blood flow rate, filtration fraction, treatment time, dialyzer characteristics, and machine technology. Current evidence suggests that high-volume post-dilution HDF can be achieved safely and reproducibly in routine clinical practice using standard thrice-weekly treatment schedules and contemporary dialysis platforms. Monitoring should extend beyond conventional small-solute clearance metrics to include indicators of middle-molecule removal and patient-centered outcomes. Future developments are expected to move HDF from a uniform prescription strategy towards a more individualized approach. Emerging data support refinement of convection-volume targets according to patient characteristics and treatment response, while incorporation of patient-reported outcomes and predictive models may facilitate precision-based therapy. Advances in automation, digital monitoring, biosensors, and artificial intelligence are most likely to further optimize treatment delivery and personalization. Although implementation requires investment in infrastructure, training, and quality assurance, growing evidence suggests that these costs may be offset by improved clinical outcomes, reduced healthcare utilization, and enhanced sustainability. Collectively, current evidence supports high-volume HDF as among the most effective dialysis modality currently available and it is likely to become the global standard for kidney replacement therapy.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149025246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Translocator Protein and Mitochondrial Dysfunction in Chronic Kidney Disease​.","authors":"Yuchen Feng, Wai Han Yiu, Derek Kong Lam, Jingyuan Ma, Dan Liu, Yuyi Ruan, Xu Luo, Kar Neng Lai, Sydney C W Tang","doi":"10.1681/ASN.0000001262","DOIUrl":"https://doi.org/10.1681/ASN.0000001262","url":null,"abstract":"<p><strong>Background: </strong>Dysregulation of mitochondrial homeostasis is associated with kidney tubular injury and subsequent tubulointerstitial fibrosis, contributing to the development of chronic kidney diseases (CKD). Translocator protein (TSPO), located on the outer mitochondrial membrane, is upregulated in kidney tubules after injury; however, its roles in CKD progression remain unknown.</p><p><strong>Methods: </strong>We investigated the impact of TSPO deficiency on mitochondrial dysfunction, kidney inflammation and fibrosis in mouse models of unilateral ureteral obstruction (UUO) and unilateral ischemia-reperfusion injury (IRI). Tubule-specific TSPO-knockout mice (KspCreERT2; TSPOlox/lox) were used. The role of TSPO in metabolic energy metabolism under hypoxic stress was delineated in TSPO-deficient primary renal proximal tubular epithelial cells (RTECs) from mice and in human proximal tubular epithelial cell line (HK-2 cells). The protective effect of TSPO antagonist PK11195 treatment was evaluated in mice with CKD.</p><p><strong>Results: </strong>TSPO expression was increased in the proximal tubules of patients with CKD, and in UUO- and unilateral IRI-induced mice. Tubule-specific deletion of TSPO and treatment with PK11195 mitigated kidney injury, inflammation and fibrosis in UUO or unilateral IRI mice. Bulk RNA-seq analysis further revealed the enrichment of genes in metabolic pathways with increased oxidative phosphorylation (OXPHOS) and reduced glycolysis in kidneys from TSPO knockout mice. In primary RTECs subjected to hypoxic stress, deletion of TSPO preserved mitochondrial function by enhancing mitochondrial biogenesis and membrane potential, improving OXPHOS and reducing glycolysis, thereby increasing ATP production. Finally, TSPO interacted with the first enzyme of the glycolytic pathway, hexokinase 2 (HK2), on mitochondria, and TSPO knockdown triggered HK2 translocation to the cytosol, thereby decreasing its glycolytic capacity and improving mitochondrial homeostasis.</p><p><strong>Conclusions: </strong>TSPO depletion protected mice from kidney injury and tubulointerstitial fibrosis during CKD progression by disrupting HK2-mediated glycolysis and enhancing mitochondrial energy metabolism.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149017309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Management of IgA Vasculitis Nephritis Beyond Glucocorticoids.","authors":"Vanja Ivković, Giorgio Trivioli, Augusto Vaglio","doi":"10.1681/ASN.0000001283","DOIUrl":"https://doi.org/10.1681/ASN.0000001283","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149002143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glucosuria as a Marker of Adherence to Sodium-Glucose Cotransporter 2 Inhibitors and Clinical Outcomes in Real-World Practice.","authors":"Zongpu Li, Aditya Surapaneni, David M Charytan, Leora Horwitz, Saul Blecker, Jung-Im Shin, Lorna E Thorpe, Michal Melamed, Morgan E Grams","doi":"10.1681/ASN.0000001252","DOIUrl":"10.1681/ASN.0000001252","url":null,"abstract":"<p><strong>Background: </strong>Medication non-adherence contributes to the efficacy-effectiveness gap in real-world practice. Glucosuria, routinely measured on urinalysis, may serve as an objective proxy for assessing medication adherence to sodium-glucose cotransporter 2 (SGLT2) inhibitors, a class of medications that reduce the risks of kidney disease, heart failure, and mortality.</p><p><strong>Methods: </strong>We leveraged two cohorts from the Optum Labs Data Warehouse real-world data (2014-2023): Cohort 1 included 3,987 patients with SGLT2 inhibitor pharmacy claims and a urinalysis performed both before and during active fill periods; cohort 2 included 45,711 patients prescribed SGLT2 inhibitors with urinalysis performed within 6 months after initiation. Glucosuria was defined as urine glucose 2+ or greater. Cohort 2 was followed for a mean of 3.3 years for all-cause mortality, heart failure hospitalization, end-stage kidney disease; fractures were used as a negative control outcome.</p><p><strong>Results: </strong>In cohort 1, SGLT2 inhibitor use (vs. no use) was associated with 18.1-fold higher odds of glucosuria (95% CI, 16.4-20.0), adjusted for diabetes status. In cohort 2, 26,657 (58%) had glucosuria within 6 months of SGLT2 inhibitor initiation, suggesting adherence. After inverse probability of treatment weighting, glucosuria was associated with lower risks of all-cause mortality (HR, 0.78; 95% CI, 0.73-0.83), heart failure hospitalization (HR, 0.87; 95% CI, 0.78-0.98), and end-stage kidney disease (HR, 0.73; 95% CI, 0.58-0.91) compared to no glucosuria. No association was observed with fractures (HR, 1.00; 95% CI, 0.95-1.06).</p><p><strong>Conclusions: </strong>Glucosuria was associated with SGLT2 inhibitor adherence and, among patients prescribed SGLT2 inhibitors, is associated with reductions in risks of all-cause mortality, heart failure, and end-stage kidney disease.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"β-Blockers in Hemodialysis: Does Dialyzability Matter?","authors":"Bróna M Moloney, Finnian R Mc Causland","doi":"10.1681/ASN.0000001253","DOIUrl":"https://doi.org/10.1681/ASN.0000001253","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SLCO4A1 Governs PGE2-Mediated Natriuresis in the Kidney.","authors":"Yanlin Guo, Beibei Ma, Chunxiu Du, Yulong Lin, Bin Li, Jie Sun, Caichao Ye, Taotao Luo, Guixiang Xie, Zaifang Jiang, Ruifen Li, Hui Zhou, Xiaowan Sun, Yingzhi Huang, Jin Zhong, Fang Ye, Hu Xu, Feng Zheng, Lihong Chen, Lei Wang, Yulong Li, Youfei Guan, Xiaoyan Zhang","doi":"10.1681/ASN.0000001258","DOIUrl":"https://doi.org/10.1681/ASN.0000001258","url":null,"abstract":"<p><strong>Background: </strong>Renal sodium retention is a central driver of hypertension and fluid overload. Prostaglandin E2 (PGE2) has long been identified as a potent natriuretic and diuretic factor. However, the mechanisms governing intrarenal PGE2 signaling and tubular sodium transport remain incompletely understood.</p><p><strong>Methods: </strong>Global and renal tubule-specific Slco4a1 knockout mouse, as well as renal tubule-specific Slco4a1 overexpressing mice, were generated to investigate the role of SLCO4A1 in renal sodium and water homeostasis. Computational docking, cellular studies, and in vivo functional analyses were performed to evaluate the role of SLCO4A1in intrarenal distribution of PGE2 and its impact on tubular sodium transport.</p><p><strong>Results: </strong>SLCO4A1 was predominantly localized to the basolateral membrane of multiple renal tubular epithelial cells. Global and renal tubule-specific Slco4a1 gene deletion increased urine output and sodium excretion and reduced sodium reabsorption across multiple nephron segments in mice. This was accompanied by downregulation of key sodium transporters and channels including SGLT2, NHE3, NKCC2, NCC and ENaC. In contrast, renal tubule-specific overexpression of Slco4a1 displayed an opposite effect. Mechanistically, Slco4a1 deficiency led to accumulation of PGE2 in the kidney interstitum, which suppressed the expression of sodium transporter and channels via the EP receptors. Specifically, EP1 mediated the PGE2-induced suppression of NKCC2, α-ENaC, and β-ENaC. EP2 was responsible for the suppression of NCC, while EP3 was involved in suppressing SGLT2, NHE3 and γ-ENaC.</p><p><strong>Conclusions: </strong>Collectively, these findings uncovered a previously unrecognized role of SLCO4A1 in regulating intrarenal PGE2 distribution and identified SLCO4A1-PGE2-EP receptor axis in fine-tuning renal tubular sodium transport.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148977188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Ethics and Logistics of Control Arms in Nephrology Device Trials.","authors":"Raymond R Townsend","doi":"10.1681/ASN.0000001277","DOIUrl":"10.1681/ASN.0000001277","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148969461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatially Patterned Podocyte State Transitions Coordinate Aging of the Glomerulus.","authors":"Christopher Chaney, Jeffrey W Pippin, Uyen Tran, Diana G Eng, Natalya Kaverina, Yuliang Wang, Thomas J Carroll, Stuart J Shankland, Oliver Wessely","doi":"10.1681/ASN.0000001255","DOIUrl":"10.1681/ASN.0000001255","url":null,"abstract":"<p><strong>Background: </strong>Glomerular aging is accompanied by podocyte loss, glomerulosclerosis, and declining kidney function, yet the cellular states and intercellular programs underlying these changes remain incompletely defined. Thus, we tested whether aging produces coordinated, cell type-specific transcriptional changes that differ between outer cortical and juxtamedullary nephrons.</p><p><strong>Methods: </strong>Single-nucleus RNA sequencing was performed in micro-dissected outer cortical and juxtamedullary kidney regions from mice aged 4, 20, and 25 months. Region prediction, lineage-specific sub-clustering, gene-set enrichment, trajectory inference, and ligand-receptor analyses were used to define spatially and age-associated kidney cell states and inferred glomerular communication.</p><p><strong>Results: </strong>Analysis of 860,869 nuclei revealed transcriptional identities linked to anatomical region across multiple cell types, including juxtamedullary enrichment of Napsa. In proximal tubule heterogeneity primarily reflected segment and functional state, without age-dependent redistribution. Conversely, in podocytes, one of the five transcriptionally connected transcriptional states was a stress-adaptive state. It was enriched in the juxtamedullary region and exhibited the greatest aging-, senescence-, and inflammatory gene-set activity. Yet, like parietal epithelial, glomerular endothelial, and mesangial cell states, podocytes showed little compositional remodeling with age. The inferred glomerular communication architecture was largely preserved across age and region, with podocytes having the greatest outgoing and mesangial cells the greatest incoming interaction burden. Aging selectively altered only a limited number of candidate ligand-receptor programs such as juxtamedullary podocyte-to-parietal epithelial cell Egf and Lpl signaling.</p><p><strong>Conclusions: </strong>In healthy mice, anatomical location was a stronger determinant than chronological age. Aging did not produce widespread expansion of discrete aging-associated populations, but instead selectively modified transcriptional and communication programs within an anatomically patterned glomerular landscape. In fact, the juxtamedullary-enriched, stress-associated podocyte state provides a mechanistic explanation for recognized regional-specific glomerular vulnerability.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148969452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CDK4/6 Inhibitor Abemaciclib Arrests and Reverses Kidney Cyst Progression in Preclinical Models of Autosomal Dominant Polycystic Kidney Disease.","authors":"Yingshu Cao, Xiaobo Sun, Yan Huang, Chuan Chen, Biyun Ji, Renee Chen, Yuan Li, Yan Liang, Ariana Aghevli, Nicole Yang, Vishal Patel, Peter Harris, Kun Ling, Jinghua Hu, Kai He","doi":"10.1681/ASN.0000001269","DOIUrl":"10.1681/ASN.0000001269","url":null,"abstract":"<p><strong>Background: </strong>Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited disorder leading to kidney failure. Tolvaptan, the only FDA-approved therapy, modestly slows disease progression but is limited by significant adverse effects, highlighting the need for more effective and better-tolerated treatments. Ciliary polycystins are central to ADPKD pathogenesis. We previously demonstrated that a cilia base-localized pool of CDK6 restricts ciliary polycystin abundance by suppressing axonemal polyglutamylation. However, whether CDK6 inhibition can restore polycystin function and suppress ADPKD progression in vivo remains unknown.</p><p><strong>Methods: </strong>Abemaciclib was tested in in vitro 3D cyst assays and ex vivo metanephric organ cultures. In vivo efficacy of early- and late-stage intervention were assessed in F1(129/B6) Pkd1R3277C/R3277C mice receiving daily abemaciclib. Tolvaptan served as a therapeutic control. Cyst burden, fibrosis in the kidneys, kidney function, and primary cilia of renal epithelial cells were analyzed at study endpoints.</p><p><strong>Results: </strong>CDK6 was prominently upregulated in cyst-lining cells in human and murine PKD kidneys. At doses substantially lower than those used in oncology, abemaciclib robustly suppressed cyst growth in vitro and ex vivo. In vivo, long-term early treatment arrested cyst progression more effectively than tolvaptan without detectable toxicity. Late intervention largely halted cyst growth in females and reversed cyst progression in males. Mechanistically, abemaciclib restored axonemal polyglutamylation and increased ciliary polycystin levels.</p><p><strong>Conclusions: </strong>Abemaciclib has greater therapeutic efficacy and tolerability than tolvaptan in this preclinical model, largely driven by CDK6 inhibition-mediated restoration of axonemal polyglutamylation and increased ciliary polycystin abundance.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148969455","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}