{"title":"The EKFC equation outperforms the CKD-EPI and CKiD equations for GFR estimation in adolescent and young adult kidney transplant patients.","authors":"Chloé Grosyeux, Asma Alla, Françoise Barbé, Laurence Derain Dubourg, Laurence Chardon, Jean-Louis Guéant, Luc Frimat, Abderrahim Oussalah, Isabelle Vrillon","doi":"10.1111/nep.14328","DOIUrl":"10.1111/nep.14328","url":null,"abstract":"<p><strong>Aim: </strong>This study evaluated the bias and accuracy of the CKD-EPI/CKiD and EKFC equations compared with the reference exogenous tracer-based assessment of glomerular filtration rate (GFR) in adult and pediatric patients according to their renal transplant status.</p><p><strong>Methods: </strong>We assessed the bias and P<sub>30</sub> accuracy of the CKD-EPI/CKiD and EKFC equations compared with iohexol-based GFR measurement.</p><p><strong>Results: </strong>In the overall population (n = 59), the median age was 29 years (IQR, 16.0-46.0) and the median measured GFR was 73.9 mL/min/1.73m<sup>2</sup> (IQR, 57.3-84.6). Among non-kidney transplant patients, the median was 77.7 mL/min/1.73m<sup>2</sup> (IQR, 59.3-86.5), while among kidney transplant patients, it was 60.5 mL/min/1.73m<sup>2</sup> (IQR, 54.2-66.8). The bias associated with the EKFC and CKD-EPI/CKiD equations was significantly higher among kidney transplant patients than among non-kidney transplant patients, with a difference between medians (Hodges-Lehmann) of +10.4 mL/min/1.73m<sup>2</sup> (95% CI, 2.2-18.9; p = .02) for the EKFC and +12.1 mL/min/1.73m<sup>2</sup> (95% CI, 4.2-21.4; p = .006) for the CKD-EPI/CKiD equations. In multivariable analysis, kidney transplant status emerged as an independent factor associated with a bias of >3.4 mL/min/1.73m<sup>2</sup> (odds ratio, 7.7; 95% CI, 1.4-43.3; p = .02) for the EKFC equation and a bias of >13.4 mL/min/1.73m<sup>2</sup> (odds ratio, 15.0; 95% CI, 2.6-85.7; p = .002) for the CKD-EPI/CKiD equations.</p><p><strong>Conclusion: </strong>In our study, which included adolescent and young adult kidney transplant patients, both the CKD-EPI/CKiD and EKFC equations tended to overestimate the measured glomerular filtration rate, with the EKFC equation exhibiting less bias. Renal transplant status significantly influenced the degree of estimation bias.</p>","PeriodicalId":19264,"journal":{"name":"Nephrology","volume":" ","pages":"680-687"},"PeriodicalIF":2.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141158951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NephrologyPub Date : 2024-10-01Epub Date: 2024-07-29DOI: 10.1111/nep.14368
Hui Li, Shuaiwei Wang, Shuangshuang An, Biao Gao, Dongdong Wu, Yanzhang Li
{"title":"Hydrogen sulphide reduces renal ischemia-reperfusion injury by enhancing autophagy and reducing oxidative stress.","authors":"Hui Li, Shuaiwei Wang, Shuangshuang An, Biao Gao, Dongdong Wu, Yanzhang Li","doi":"10.1111/nep.14368","DOIUrl":"10.1111/nep.14368","url":null,"abstract":"<p><strong>Aim: </strong>Renal ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury. Hydrogen sulphide (H<sub>2</sub>S) exerts a protective effect in renal IRI. The present study was carried out to investigate the effects of exogenous H<sub>2</sub>S on renal IRI by regulating autophagy in mice.</p><p><strong>Methods: </strong>Mice were randomly assigned to control, IRI and NaHS (an H<sub>2</sub>S donor, 28, 56 and 100 μmol/kg) groups. Renal IRI was induced by clamping the bilateral renal pedicles with non-traumatic arterial clamp for 45 min and then reperfused for 24 h. Mice were administered intraperitoneally with NaHS 20 min prior to renal ischemia. Sham group mice underwent the same procedures without clamping. Serum and kidney tissues were harvested 24 h after reperfusion for functional, histological, oxidative stress, and autophagic determination.</p><p><strong>Results: </strong>Compared with the control group, the concentrations of serum creatinine (Scr), blood urea nitrogen (BUN), and malondialdehyde (MDA), the protein levels of LC3II/I, Beclin-1 and P62, as well as the number of autophagosomes were significantly increased, but the activity of superoxide dismutase (SOD) was decreased after renal IRI. NaHS pre-treatment dramatically attenuated renal IRI-induced renal dysfunction, histological changes, MDA concentration and p62 expression in a dose-dependent manner. However, NaHS increased the SOD activity and the protein levels of LC3II/I and Beclin-1.</p><p><strong>Conclusion: </strong>These results indicate that exogenous H<sub>2</sub>S protects the kidney from IRI through enhancement of autophagy and reduction of oxidative stress. Novel H<sub>2</sub>S donors could be developed in the treatment of renal IRI.</p>","PeriodicalId":19264,"journal":{"name":"Nephrology","volume":" ","pages":"645-654"},"PeriodicalIF":2.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141792979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NephrologyPub Date : 2024-10-01Epub Date: 2024-07-18DOI: 10.1111/nep.14370
Carlos Narváez Mejía, Arshdeep Singh, Florentino Villanego, Javier Naranjo, Juan Manuel Cazorla Lopez, Tomas Daroca Martínez, Marta Alonso Mozo, Jose Manuel Amaro Martín, Manuel Ceballos, Auxiliadora Mazuecos
{"title":"Intracardiac vascular access in haemodialysis: A last resort for exhausted traditional access.","authors":"Carlos Narváez Mejía, Arshdeep Singh, Florentino Villanego, Javier Naranjo, Juan Manuel Cazorla Lopez, Tomas Daroca Martínez, Marta Alonso Mozo, Jose Manuel Amaro Martín, Manuel Ceballos, Auxiliadora Mazuecos","doi":"10.1111/nep.14370","DOIUrl":"10.1111/nep.14370","url":null,"abstract":"<p><p>Depletion of veins for dialysis access is a challenging life threatening situation for patients in need of haemodialysis. The utilisation of intracardiac catheter is a rare procedure with scarce reported experience. We describe the case of a 68-year-old male that contributes to the limited knowledge of performing a life-saving intracardiac catheter placement for emergency haemodialysis in a patient without immediate alternative renal replacement therapy available. We also retrospectively analyse the experience reported so far and summarise complications and outcomes. In our case, the patient was able to pursue haemodialysis after intracardiac catheter placement without any complications. Two weeks later, the patient successfully received a kidney transplant from a deceased donor and has a serum creatinine of 1.7 mg/dL after 2 years of follow-up. There are only four reported cases of kidney transplantation after the procedure, including our own. Intracardiac catheter is an emerging option that could be considered in certain patients as the last resort. Further investigation with regards to patient candidacy and procedure security are necessary.</p>","PeriodicalId":19264,"journal":{"name":"Nephrology","volume":" ","pages":"699-702"},"PeriodicalIF":2.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141634102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NephrologyPub Date : 2024-10-01Epub Date: 2024-07-25DOI: 10.1111/nep.14335
Tao Han, Ye Jiang, Weixing Ge, Yuyu Lu, Rongming Liu, Zunpeng Sun
{"title":"2,5-Dihydroxyacetophenone attenuates acute kidney injury induced by intra-abdominal infection in rats.","authors":"Tao Han, Ye Jiang, Weixing Ge, Yuyu Lu, Rongming Liu, Zunpeng Sun","doi":"10.1111/nep.14335","DOIUrl":"10.1111/nep.14335","url":null,"abstract":"<p><strong>Aims: </strong>As one of the most serious complications of sepsis, acute kidney injury (AKI) is pathologically associated with excessive inflammation. 2,5-Dihydroxyacetophenone (DHAP) is isolated from Radix rehmanniae praeparata and exhibit potent anti-inflammatory property. This research aimed at determining the role of DHAP in sepsis-associated AKI (SA-AKI) and the underlying mechanism.</p><p><strong>Methods: </strong>Plasma creatinine (Cre), blood urea nitrogen (BUN), tumour necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels of SA-AKI patients were detected to evaluate their clinical characteristics. SA-AKI rat models were established by using caecum ligation puncture (CLP) surgery. CLP-induced rats were administered via oral gavage with 20 or 40 mg DHAP after 2 h of CLP surgery. Subsequently, survival rates, serum indexes, histopathological changes, inflammatory factors, renal function indexes and extracellular regulated protein kinases (ERK) and nuclear factor-κB (NF-κB) signalling pathways were detected.</p><p><strong>Results: </strong>SA-AKI patients exhibited markedly higher levels of plasma Cre, BUN, TNF-α and IL-1β than healthy people. Compared with sham rats, CLP-induced septic rats showed significantly decreased survival rate, increased serum lactate dehydrogenase activity and serum lactate level, obvious renal histopathological injury, upregulated TNF-α, IL-1β and TGF-β1 levels, elevated serum creatinine, BUN and serum cystatin C concentrations, serum neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 levels and reduced renal artery blood flow. All the above CLP-induced changes in septic rats were mitigated after DHAP administration. Additionally, CLP-induced elevation in phosphorylated-ERK1/2 and nuclear NF-κB p65 protein levels was inhibited by DHAP treatment.</p><p><strong>Conclusion: </strong>DHAP hinders SA-AKI progression in rat models by inhibiting ERK and NF-κB signalling pathways.</p>","PeriodicalId":19264,"journal":{"name":"Nephrology","volume":" ","pages":"636-644"},"PeriodicalIF":2.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141760086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NephrologyPub Date : 2024-09-18DOI: 10.1111/nep.14393
Bingjie Cheng, Huihui Yang, Lin Huang, Panli Liao, Fei Peng, Xiaowen Wang
{"title":"Nephrotic syndrome in a child with neurofibromatosis type 1: A case report and literature review","authors":"Bingjie Cheng, Huihui Yang, Lin Huang, Panli Liao, Fei Peng, Xiaowen Wang","doi":"10.1111/nep.14393","DOIUrl":"https://doi.org/10.1111/nep.14393","url":null,"abstract":"Neurofibromatosis type 1 (NF1) is an autosomal dominant genetic disorder that caused by <jats:italic>NF1</jats:italic> mutations. <jats:italic>NF1</jats:italic> gene encodes neurofibromin (a GTPase‐activating protein) and plays a regulatory role in many signalling pathway such as the Ras/MAPK pathway, which is important for regulating cell growth, proliferation and neural development. Therefore, <jats:italic>NF1</jats:italic> gene mutations causes the excessive activation of signalling pathways and uncontrolled cell growth. NF1 exhibits complete genetic penetrance and clinical heterogeneity. Glomerular disease has rarely been reported in patients with NF1, especially in children. Currently, the relationship between NF1 and nephrotic syndrome is unclear. Here, we present a case of NF1 with nephrotic syndrome and further explore the association between NF1 and glomerular diseases. It also reminds clinicians that NF1 has complex and highly variable clinical manifestations and that a comprehensive workup is essential for patients.","PeriodicalId":19264,"journal":{"name":"Nephrology","volume":"15 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142258913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A rare multisystemic disorder with chronic kidney disease: Karyomegalic interstitial nephritis due to homozygous FAN1 c.2260C>T variant.","authors":"Merve Guzel Dirim,Ahmet Burak Dirim,Berker Kaya,Naci Senkal,Tugba Kalayci,Ayca Aslanger,Neslihan Berker,Murat Kose,Isin Kilicaslan,Halil Yazici","doi":"10.1111/nep.14394","DOIUrl":"https://doi.org/10.1111/nep.14394","url":null,"abstract":"Karyomegalic interstitial nephritis (KIN) is a rare entity associated with biallelic FAN1 (FANCD2/FANCI-Associated Nuclease 1) gene variants. In FAN1-related KIN, abnormal liver function tests and respiratory involvement are common, in addition to chronic kidney disease. Karyomegalic changes have also been reported in many other organs in patients with FAN1-related KIN in various studies. We report the case of a 35-year-old male with chronic kidney disease of unknown aetiology, concurrent recurrent upper and lower respiratory tract infections, and elevated liver function test results with unidentified aetiology. The patient's family history was remarkable for consanguineous parent marriage and history of kidney transplantation in his aunt. A kidney biopsy was performed, which was consistent with KIN. Clinical exome sequencing revealed a homozygous nonsense variant NM_014967.5 (FAN1): c. 2260C > T (p.Arg754Ter). According to the American College of Medical Genetics (ACMG) criteria, this variant is pathogenic and, to the best of our knowledge, has not been previously reported, homozygously. Therefore, the histopathological and clinical diagnoses of KIN were confirmed by genetic studies in our patient. This case report expands the genetic spectrum of FAN1-related KIN, and briefly reviews the current literature data.","PeriodicalId":19264,"journal":{"name":"Nephrology","volume":"17 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142258911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NephrologyPub Date : 2024-09-18DOI: 10.1111/nep.14392
Kyle C White,Rinaldo Bellomo,Alexis Tabah,Antony G Attokaran,Hayden White,James McCullough,Kiran Shekar,Mahesh Ramanan,Peter Garrett,Philippa McIlroy,Siva Senthuran,Stephen Luke,Ary Serpa-Neto,Tom Larsen,Kevin B Laupland,
{"title":"Sepsis-associated acute kidney injury in patients with chronic kidney disease: Patient characteristics, prevalence, timing, trajectory, treatment and associated outcomes.","authors":"Kyle C White,Rinaldo Bellomo,Alexis Tabah,Antony G Attokaran,Hayden White,James McCullough,Kiran Shekar,Mahesh Ramanan,Peter Garrett,Philippa McIlroy,Siva Senthuran,Stephen Luke,Ary Serpa-Neto,Tom Larsen,Kevin B Laupland,","doi":"10.1111/nep.14392","DOIUrl":"https://doi.org/10.1111/nep.14392","url":null,"abstract":"AIMThe features and outcomes of sepsis-associated acute kidney injury (SA-AKI) may be affected by chronic kidney disease (CKD). Accordingly, we aimed to compare SA-AKI in patients with or without CKD.METHODSRetrospective cohort study in 12 intensive care units (ICU). We studied the prevalence, patient characteristics, timing, trajectory, treatment and outcomes of SA-AKI with and without CKD.RESULTSOf 84 240 admissions, 7255 (8.6%) involved patients with CKD. SA-AKI was more common in patients with CKD (21% vs 14%; p < .001). CKD patients were older (70 vs. 60 years; p < .001), had a higher median Charlson co-morbidity index (5 vs. 3; p < .001) and acute physiology and chronic health evaluation (APACHE) III score (78 vs. 60; p < .001) and were more likely to receive renal replacement therapy (RRT) (25% vs. 17%; p < .001). They had less complete return to baseline function at ICU discharge (48% vs. 60%; p < .001), higher major adverse kidney events at day 30 (MAKE-30) (38% vs. 27%; p < .001), and higher hospital and 90-day mortality (21% vs. 13%; p < .001, and 27% vs. 16%; p < .001, respectively). After adjustment for patient characteristics and severity of illness, however, CKD was not an independent risk factor for increased 90-day mortality (OR 0.88; 95% CI 0.76-1.02; p = .08) or MAKE-30 (OR 0.98; 95% CI 0.80-1.09; p = .4).CONCLUSIONSA-AKI is more common in patients with CKD. Such patients are older, more co-morbid, have higher disease severity, receive different ICU therapies and have different trajectories of renal recovery and greater unadjusted mortality. However, after adjustment day-90 mortality and MAKE-30 risk were not increased by CKD.","PeriodicalId":19264,"journal":{"name":"Nephrology","volume":"75 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142258914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NephrologyPub Date : 2024-09-11DOI: 10.1111/nep.14384
Chih‐Ning Chen, Vin‐Cent Wu
{"title":"Hydrogen sulfide as a therapeutic agent in renal ischemia‐reperfusion injury: Mechanistic insights and clinical potential","authors":"Chih‐Ning Chen, Vin‐Cent Wu","doi":"10.1111/nep.14384","DOIUrl":"https://doi.org/10.1111/nep.14384","url":null,"abstract":"","PeriodicalId":19264,"journal":{"name":"Nephrology","volume":"31 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142222647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Autosomal dominant nephrogenic diabetes insipidus in one family caused by a novel AQP2 mutation","authors":"Hou‐Xuan Huang, Monika Sullivan, Paola Zayas Borges, Sabina Kennedy","doi":"10.1111/nep.14389","DOIUrl":"https://doi.org/10.1111/nep.14389","url":null,"abstract":"A 9‐month‐old male presented with vomiting and dehydration with mild hypernatremia in the context of failure to thrive. He was later diagnosed with nephrogenic diabetes insipidus (NDI) during this hospitalisation and was also found to have eosinophilic esophagitis (EoE). He has since been growing well after EoE and NDI were properly managed. Molecular genetic testing revealed an unreported deletion in <jats:italic>AQP2</jats:italic> which was deemed pathogenic and of autosomal dominant inheritance when correlated with his clinical findings and family history. This case report describes the clinical course of this patient in comparison to his family members and reviews current literature on autosomal dominant NDI caused by <jats:italic>AQP2</jats:italic> mutations.","PeriodicalId":19264,"journal":{"name":"Nephrology","volume":"186 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142222648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"SLC12A1 variant c.1684+1 G>A causes Bartter syndrome type 1 by promoting exon 13 skipping","authors":"Wenke Yang, Yanjun Li, Zhenglong Guo, Yanxin Ren, Jianmei Huang, Huiru Zhao, Shixiu Liao","doi":"10.1111/nep.14390","DOIUrl":"https://doi.org/10.1111/nep.14390","url":null,"abstract":"BackgroundBartter syndrome type 1, an autosomal recessive genetic disorder, is caused by pathogenic loss‐of‐function variants in the <jats:italic>SLC12A1</jats:italic> gene. It is characterized by metabolic alkalosis and prenatal‐onset polyuria leading to polyhydramnios.MethodsWe identified pathogenic gene in a 12‐day‐old newborn boy with Bartter syndrome type 1 using whole‐exome sequencing. Sanger sequencing validated the identified variants. A minigene assay was performed to investigate the effect of a novel splice site variant on pre‐mRNA splicing.ResultsWe found a compound heterozygous variants in the <jats:italic>SLC12A1</jats:italic> gene, consisting of a known pathogenic missense mutation (NM_000338: c.769 G>A; p.Gly257Ser) and a novel splice site variant (c.1684+1 G>A). In silico predictions and an in vitro minigene splicing assay demonstrated that the splicing variant c.1684+1 G>A abolished a consensus splice donor site of <jats:italic>SLC12A1</jats:italic> intron 13, resulting in complete exon 13 skipping, translational frameshift, and premature termination codon, ultimately leading to loss of <jats:italic>SLC12A1</jats:italic> function.ConclusionUsing a cell‐based in vitro assay, we revealed the aberrant effect of the pathogenic splicing variant <jats:italic>SLC12A1</jats:italic> c.1684+1 G>A on pre‐mRNA splicing. Our findings expand the gene mutation spectrum of Bartter syndrome type 1, providing a basis for genetic diagnosis and the development of genetic medicines.<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http://www.w3.org/1999/xlink\" mimetype=\"image/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic/nep14390-gra-0001-m.png\"><jats:alt-text>image</jats:alt-text></jats:graphic></jats:boxed-text>","PeriodicalId":19264,"journal":{"name":"Nephrology","volume":"60 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142222646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}