Nephrology (Carlton, Vic.)最新文献

{"title":"The Janus Effect of Bilirubin After Liver Transplantation: A Retrospective Study of Phase-Dependent Risk and Protection Against Chronic Kidney Disease.","authors":"Lin Lyu, He Dong, Wenli Bi, Lei Lun, Shengnan Dong, Xiaodong Zhang, Aijie Liu, Feng Wang, Qingguo Xu, Jinzhen Cai","doi":"10.1111/nep.70234","DOIUrl":"10.1111/nep.70234","url":null,"abstract":"<p><strong>Aim: </strong>The temporal relationship between post-operative bilirubin dynamics and chronic kidney disease (CKD) following liver transplantation (LT) remains unclear. Given the potential dual (injurious and protective) biological effects of bilirubin, this study aimed to investigate the phase-dependent impact of bilirubin on CKD development.</p><p><strong>Methods: </strong>We retrospectively analysed 552 adult LT recipients (2018-2023) with a 2-year follow-up. Mean total bilirubin (tBil) levels were measured at regular post-operative intervals and stratified into two phases: early (0-3 months) and late (3-24 months). Fine-Grey competing risk models with restricted cubic splines (RCS) evaluated nonlinear associations between tBil and CKD risk. CKD incidence was estimated using cumulative incidence functions. Longitudinal bilirubin trajectories were assessed using linear mixed-effects models (LMM).</p><p><strong>Results: </strong>Early post-operative tBil > 51.30 μmol/L was independently associated with increased CKD risk (adjusted SHR 1.666; 95% CI 1.158-2.397; p = 0.006), with a U-shaped RCS curve. CKD incidence was significantly higher in patients with early tBil > 51.30 μmol/L (44.6%) compared to 25.65-51.30 μmol/L (27.4%, p = 0.006). Late post-operative tBil of 25.65-51.30 μmol/L was protective (adjusted SHR 0.321; 95% CI 0.173-0.594; p < 0.001), and RCS showed a gradual risk reduction with increasing tBil. The lowest CKD incidence (12.2%) occurred in patients with moderate tBil during the late phase (p < 0.001). LMM demonstrated higher sustained tBil from 6 months onward in non-CKD patients (p < 0.001).</p><p><strong>Conclusion: </strong>Post-LT bilirubin exhibits a Janus-like, phase-specific association with CKD: early elevations increase risk, while late moderate levels appear protective. These findings suggest a role for phase-specific bilirubin monitoring and management.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 6","pages":"e70234"},"PeriodicalIF":1.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148140595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined Immunoglobulin Heavy- and Light-Chain Amyloidosis Associated With Waldenström Macroglobulinaemia: A Case Report With Diagnostic Challenges and a Favourable Treatment Outcome.","authors":"Ryo Yamaguchi, Yusuke Murata, Shunsuke Kawamoto, Yurie Akiya, Seiichiro Hemmi, Katsuhiro Miura, Masanori Abe","doi":"10.1111/nep.70235","DOIUrl":"10.1111/nep.70235","url":null,"abstract":"<p><p>Waldenström macroglobulinaemia (WM) is a rare lymphoplasmacytic lymphoma that produces monoclonal IgM, and renal amyloidosis is an uncommon complication. Light-chain amyloidosis occurs more frequently than heavy-chain or combined heavy- and light-chain (AHL) amyloidosis. This report describes a woman with proteinuria in the nephrotic range, elevated IgM, and IgM kappa monoclonal protein in serum and urine. Kidney biopsy revealed AHL amyloidosis with IgM and kappa deposition. Laser microdissection-liquid chromatography-tandem mass spectrometry (LMD-LC-MS/MS) confirmed the presence of peptides from heavy and light chains. WM with renal amyloidosis was diagnosed, and the patient was started on bendamustine and rituximab. She had a significant hematologic response, achieving a very good partial response according to the international criteria. A renal response characterized by a reduction in proteinuria and stabilization of renal function was also observed. The patient remains asymptomatic after 43 months of follow-up. This case of WM with renal AHL amyloidosis highlights the importance of keeping renal amyloidosis in mind in patients with proteinuria. The favourable hematologic and renal response to treatment with bendamustine and rituximab in this case adds valuable data for the management of WM complicated by renal amyloidosis.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 6","pages":"e70235"},"PeriodicalIF":1.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148214228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Late Presentation of de Novo Proliferative Glomerulonephritis With Monoclonal IgG Deposits in a Renal Allograft: A Rare Case With an Unusual Clinical Course.","authors":"Hayley J Duxbury, David A Brown, Adrian Y S Lee, Germaine Wong, Fiona Kwok, Seethalakshmi Viswanathan","doi":"10.1111/nep.70225","DOIUrl":"10.1111/nep.70225","url":null,"abstract":"<p><p>Proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) is a form of monoclonal gammopathy of renal significance (MGRS) in which monoclonal immunoglobulin deposits are found within the glomerulus, without involvement of other renal compartments. This condition can result in kidney dysfunction and ultimately kidney failure. It most commonly presents in the native kidney and has a high risk of recurrence in renal allografts, typically within a few months post-transplantation. PGNMID rarely presents as de novo in a transplanted kidney; if so, it usually manifests within 3 years. Early treatment is required to prevent further deterioration and reduce the risk of allograft loss. We present a case of a patient who presented with progressive kidney function decline 10.5 years after simultaneous pancreas-kidney (SPK) transplantation. The patient had a prior diagnosis of an immune complex-mediated glomerulonephritis on the pre-transplant native renal biopsy. The subsequent allograft biopsy showed electron-dense, glomeruli-limited deposits on electron microscopy, with immunofluorescence showing a nonspecific full-house pattern of staining. Immunofluorescence performed following protease (pronase) digestion on FFPE tissue showed the deposits to be IgG3 lambda light chain restricted, with no plasma cell or lymphoid clone identified in the bone marrow, resulting in a diagnosis of MGRS with a PGNMID pattern in the renal biopsy. This prompted treatment with prednisone and rituximab, with subsequent ongoing improvement in proteinuria and kidney function. To our knowledge, this is the latest presentation of post-transplantation de novo PGNMID with survival reported to date.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 6","pages":"e70225"},"PeriodicalIF":1.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148160399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regional Variation of Aetiologies and Complications in Chronic Kidney Disease From Thailand (THAI-CKD Registry).","authors":"Kavita Jintanapramote, Thatsaphan Srithongkul, Thananda Trakarnvanich, Juthamash Sangsuk, Sirirat Asawamethapant, Jathurong Kittrakulrat, Tossaporn Sapsitthikul, Kajohnsak Noppakun, Narittaya Varothai, Sirirat Anutrakulchai, Chanchana Boonyakrai, Watanyu Parapiboon, Surasak Faisatjatham, Somboon Jeenapongsa, Siriwan Nakwan, Sirimon Hwangkhunnatham, Wisedsin Phannakham, Suri Tangchitthavorngul, Wonngarm Kittanamongkolchai, Phanupong Phutrakool, Talerngsak Kanjanabuch, Vuddhidej Ophascharoensuk, Paweena Susantitaphong","doi":"10.1111/nep.70231","DOIUrl":"10.1111/nep.70231","url":null,"abstract":"<p><strong>Aim: </strong>To investigate regional variations in Chronic Kidney Disease (CKD) aetiologies and complications across KDIGO risk strata in Thailand, aiming to optimise screening and monitoring in resource-constrained settings.</p><p><strong>Methods: </strong>Baseline data from the multicentre THAI-CKD cohort of adults with stages G3-G5 CKD from 41 hospitals were analysed. Demographic, clinical and laboratory data were collected. Causes of kidney disease, including chronic kidney disease of unknown aetiology (CKDu) and metabolic complications were examined across KDIGO glomerular filtration rate and albuminuria (G-A) categories, primary aetiologies, and geographic regions.</p><p><strong>Results: </strong>Among 3371 participants (mean age: 69 ± 12 years; 55% male), stage distribution was G3a 20%, G3b 33%, G4 37% and G5 10%. Diabetic nephropathy (41%) and hypertensive nephrosclerosis (34%) were the most common causes, whereas CKDu accounted for 22% overall and was concentrated in earlier stages with lower albuminuria and in the Central (33%) and Western (24%) regions. Complications showed clear gradients across G-A strata: anaemia and metabolic acidosis increased with lower estimated glomerular filtration rate and higher albuminuria. Secondary hyperparathyroidism occurred across all stages and was most frequent in G5, whereas hyperphosphatemia was mainly observed in G5 and hyperkalaemia remained rare across all categories. The prevalence of complications also varied by primary aetiology and geographic region, and these associations remained significant after multivariable adjustment.</p><p><strong>Conclusion: </strong>This national cohort demonstrated pronounced regional and etiologic heterogeneity in CKD and revealed stage- and albuminuria-dependent patterns of metabolic complications. These findings support the use of KDIGO G-A staging and regional profiles to prioritise etiologic evaluation and tailor laboratory monitoring in low- and middle-income settings.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 6","pages":"e70231"},"PeriodicalIF":1.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148146051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Challenges in the Diagnosis and Management of a Paediatric Patient With Normotensive Pseudohypoaldosteronism Type IID.","authors":"Mohammad Shafi Kuchay, Navein Thomas John, Parjeet Kaur","doi":"10.1111/nep.70211","DOIUrl":"10.1111/nep.70211","url":null,"abstract":"<p><p>Pseudohypoaldosteronism type IID (PHA2D) is a rare genetic disorder caused by mutations in the KLHL3 gene, leading to increased activity of the thiazide-sensitive sodium-chloride cotransporter (NCC) in the kidneys. This overactivity promotes excessive sodium and chloride reabsorption, resulting in hyperkalaemia, hyperchloremic metabolic acidosis, and suppressed renin/aldosterone levels, despite preserved renal function. We report the case of a nine-year-old boy presenting with chronic fatigue, muscle aches, and growth failure. Laboratory evaluation revealed severe hyperkalaemia and hyperchloremic metabolic acidosis with a normal glomerular filtration rate and persistent normotension. Due to an initial clinical suspicion of isolated mineralocorticoid deficiency, a diagnostic trial of fludrocortisone was initiated while awaiting definitive results. Although this trial improved biochemical markers, it was discontinued once suppressed renin and aldosterone levels pointed toward PHA2. Subsequent genetic testing identified a novel homozygous splice-site mutation in the KLHL3, confirming autosomal recessive PHA2D. Following confirmation of the diagnosis, treatment was transitioned to the disease-specific therapy, hydrochlorothiazide (0.5 mg/kg/day). While this regimen normalized serum potassium and acid-base status, it induced symptomatic hypotension. The dosage was ultimately titrated to an alternate-day, low-dose regimen (0.25 mg/kg), which successfully maintained metabolic stability while minimizing adverse effects. This case underscores that normotension in PHA2D may delay diagnosis and that standard thiazide dosing may precipitate hypotension in previously normotensive patients, necessitating highly individualized treatment strategies.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 5","pages":"e70211"},"PeriodicalIF":1.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147795678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Topical Sodium Thiosulfate for the Treatment of Calciphylaxis: Case Report.","authors":"Thiveya Theivendran, Mirna Vucak-Dzumhur, Vincent W Lee, Jennifer Kim, Katrina Chau","doi":"10.1111/nep.70214","DOIUrl":"10.1111/nep.70214","url":null,"abstract":"<p><p>Calciphylaxis is a rare syndrome of microvascular calcification and skin infarction, occurring most commonly in patients with kidney failure. Calciphylaxis carries a poor prognosis, and current treatment involves mitigating risk factors, wound care, and medical therapies such as intravenous sodium thiosulfate for calcium chelation. We present an innovative treatment approach of topical sodium thiosulfate soaked gauze successfully used to treat calciphylaxis of a 58-year-old female with renal transplant. She presented with a tender bruise over the posterior right calf, in the context of good graft function (serum creatinine 88 μmol/L), warfarin use for metallic mitral valve, and total parathyroidectomy. Ultrasound imaging highlighted extensive subcutaneous tissue calcification. A punch biopsy of the lesion confirmed calciphylaxis and revealed acute deep ulceration within necrotic debris and calcium deposits along dermal blood vessels. She was managed with cessation of calcitriol and warfarin (switch to enoxaparin with anti-factor Xa level monitoring), replacement of vitamin K2, analgesia, and diligent wound care and debridement. She had twice-weekly intravenous sodium thiosulfate without any improvement and was suspended at 16 weeks after developing central line bacteraemia. On routine deep tissue debridement, small hard calcium deposits resembling calcinosis were noted to superficialise. The decision was made to commence thrice-weekly applications of topical sodium thiosulfate, prepared as gauze soaked in sodium thiosulfate 25% 15 mL applied for approximately 15 min. The ulcer completely healed, pain resolved, and topical treatment was suspended after a total of 20 weeks. This case demonstrates successful treatment of calciphylaxis using topical gauze soaked in sodium thiosulfate without concurrent intravenous sodium thiosulfate.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 5","pages":"e70214"},"PeriodicalIF":1.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147857991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repeat Kidney Biopsy to Inform Escalation and Discontinuation of Therapy in Light- and Heavy-Chain Deposition Disease.","authors":"Seiji Kakiuchi, Ikumi Takagi, Naru Tomigaki, Akimasa Sakamoto, Shutaro Fujioka, Isamu Harima, Hiroaki Akiyama, Ryotaro Niwa, Yoko Kozuki, Yoshiharu Miyata, Nobuko Iwata, Shigeo Hara, Kodo Tomida","doi":"10.1111/nep.70213","DOIUrl":"10.1111/nep.70213","url":null,"abstract":"<p><p>Persistent renal dysfunction after haematologic remission in monoclonal immunoglobulin deposition disease creates uncertainty regarding treatment intensity when clinical parameters do not distinguish reversible injury from established structural remodelling. We report a 34-year-old man with light- and heavy-chain deposition disease who presented with serum creatinine 1.8 mg/dL and heavy proteinuria (urine protein-to-creatinine ratio 5.0 g/gCr). After cyclophosphamide, bortezomib and dexamethasone therapy, haematologic parameters improved and proteinuria decreased; however, renal function continued to worsen, and serum creatinine increased to 4.1 mg/dL before autologous stem cell transplantation. Despite a deep haematologic response after transplantation, serum creatinine remained elevated at 2.7 mg/dL. A second kidney biopsy demonstrated persistent proliferative glomerular lesions with limited global sclerosis (1/56 glomeruli). Minimal residual disease remained detectable at 0.0029%, supporting additional clone-directed therapy. Following CD38-directed treatment, proteinuria resolved and minimal residual disease became undetectable, yet serum creatinine remained approximately 1.9 mg/dL with persistent microscopic haematuria. Because laboratory findings could not determine whether residual dysfunction reflected ongoing activity or fixed chronic change, a third kidney biopsy was performed. This biopsy revealed resolution of active glomerular lesions with predominance of chronic remodelling (5/32 globally sclerotic glomeruli). Therapy was discontinued, and renal function subsequently improved gradually to 1.1 mg/dL, remaining stable for more than 5 years without further therapy. Serial kidney biopsies informed two distinct therapeutic decisions-treatment escalation and subsequent discontinuation-when clinical parameters alone were insufficient to guide management.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 5","pages":"e70213"},"PeriodicalIF":1.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147944518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biallelic NPHP3 Variants Causing Late Onset Chronic Kidney Insufficiency in Nephronophthisis: A Case Report.","authors":"Yu Wu, Mengshi Li, Lei Jiang, Xujie Zhou, Yilun Zhou","doi":"10.1111/nep.70226","DOIUrl":"10.1111/nep.70226","url":null,"abstract":"<p><p>Emerging evidence suggests that the overall prevalence of nephronophthisis (NPHP) in adult-onset end-stage kidney disease (ESKD) is very likely underestimated. Thus, a comprehensive understanding of the genetic basis and clinicopathologic features of adult-onset NPHP is essential. In this case, we report a 38-year-old woman who exhibited no growth disorders or urinary abnormalities in prior physical examinations. However, at 38 years of age, she presented with renal dysfunction (eGFR 29.5 mL/min/1.73 m²). Urine tests revealed a low specific gravity of urine, but no proteinuria or microscopic hematuria, while urinary (α1-MG) was elevated (137 mg/L). Extrarenal phenotypes were absent. For a definitive diagnosis, a renal biopsy was conducted. Light microscopic findings showed established irregular microcystic dilatation in the tubules, irregular focal lamellation of the tubular basement membrane and moderate fibrosis in the interstitial area. Genetic analysis identified biallelic NPHP3 variants in trans: c.1047C>A (p.Tyr349Ter) non-sense variant and c.3725A>G (p.Tyr1242Cys) missense variant., leading to a definitive diagnosis of NPHP. This case highlights NPHP3 as an appreciable genetic cause for adult-onset nonsyndromic NPHP. Further studies are required to clarify the genotype-phenotype correlations of NPHP in adults.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 5","pages":"e70226"},"PeriodicalIF":1.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147990810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Double Whammy for a Child: Unusual Association of Nephrotic Syndrome With Duchenne Muscle Dystrophy.","authors":"Suprita Kalra, Aradhana Dwivedi, Balmukund, Harini Sri","doi":"10.1111/nep.70212","DOIUrl":"10.1111/nep.70212","url":null,"abstract":"","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 5","pages":"e70212"},"PeriodicalIF":1.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147937278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Discordant ANCA Positivity in Immune Complex Glomerulonephritis Secondary to Bartonella henselae Prosthetic Valve Endocarditis.","authors":"Boris Long Hei Yow, Reina Carlin Kittaka, Ching Shan Jason Yeung","doi":"10.1111/nep.70224","DOIUrl":"10.1111/nep.70224","url":null,"abstract":"<p><p>Bartonella henselae is an intracellular bacterium which classically causes cat scratch disease as well as culture-negative endocarditis. We report a man in his 60s, with a mechanical aortic valve replacement who presented with a 6-month fever of unknown origin (FUO), splenomegaly and acute kidney injury. Investigations showed discordant ANCA serologies, screening anti-MPO positivity followed by confirmatory anti-PR3 positivity, raising concern for ANCA-associated vasculitis (AAV). However, renal biopsy demonstrated immune complex deposition, inconsistent with the pauci-immune glomerulonephritis typical of AAV. Subsequent investigations revealed positive Bartonella serology and PCR. Transoesophageal echocardiography confirmed the diagnosis of B. henselae prosthetic valve endocarditis. He was treated with a prolonged course of rifampicin and doxycycline which led to clinical improvement. This case illustrates how B. henselae can mimic AAV, with discordant ANCA results contributing to diagnostic uncertainty, and reinforces the need to consider alternative causes of ANCA positivity.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 5","pages":"e70224"},"PeriodicalIF":1.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147990843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}