CEN Case Reports最新文献

{"title":"Macroscopic hematuria-associated severe acute kidney injury triggered by kidney stone formation in a patient with thin basement membrane and no history of microscopic hematuria.","authors":"Shuzo Kaneko, Ririko Murata, Ainori Hoshimoto, Rina Hisada, Makiko Harano, Emi Anno, So Hagiwara, Eri Imai, Michio Nagata","doi":"10.1007/s13730-024-00942-7","DOIUrl":"https://doi.org/10.1007/s13730-024-00942-7","url":null,"abstract":"<p><p>Macroscopic hematuria (MH)-associated acute kidney injury (AKI) is a rare condition that causes acute tubular damage due to severe glomerular bleeding with MH. A 66-year-old Japanese woman with no significant past medical history was referred for severe kidney injury with oliguric MH. Her prior medical checkup results showed no occult blood in her urine. Seven days earlier, she had experienced transient severe acute right lumbar back pain. On admission, her serum urea nitrogen was 147 mg/dL, serum creatinine (sCr) 18.3 mg/dL, urinary red blood cells (RBCs) > 100/hpf, urinary protein 28.8 g/gCr, with no hydronephrosis in either kidney, but two stones were found in the right kidney and right ureteropelvic junction. At the start of her hemodialysis, the patient was treated with high-dose steroids because of suspected rapidly progressive glomerulonephritis. A renal biopsy of the left kidney showed acute tubular injury with massive RBC casts filling the tubular lumen. Glomerulitis was not detected, but electron microscopy revealed diffuse glomerular thin basement membrane (TBM). Despite immediate steroid discontinuation, the patient's renal function and MH improved, and she was weaned from hemodialysis. The stones resolved 2 months after onset, but microscopic hematuria persisted for 7 months post-onset. The sCr level was fixed at 1.1 mg/dL 20 months post-onset. This is the first report of MH-AKI in a TBM without the risk of MH-AKI development, such as bleeding tendency or iron overload. In this TBM, a colic attack of the renal urinary tract induced glomerular bleeding, and intolerance to hematuria may have caused severe tubular damage.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":""},"PeriodicalIF":1.0,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459021","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":"Unusual late presentation of cryptococcal meningitis with simultaneous CMV antigenemia in a kidney transplant recipient.","authors":"Tsz Hing Mok, Li Man Maggie Lam, Chi Yuen Cheung","doi":"10.1007/s13730-024-00939-2","DOIUrl":"https://doi.org/10.1007/s13730-024-00939-2","url":null,"abstract":"<p><p>Cryptococcosis is the third most common invasive fungal infection in solid-organ transplant (SOT) recipients after candidiasis and aspergillosis. These patients are at risk of disseminated cryptococcosis because of immuosuppressive therapy. The median time to disease onset after kidney transplantation is approximately 35 months and it rarely occurs more than 10 years after transplantation. Herein, we report a case of 64-year-old kidney transplant recipient suffering from coexisting disseminated cryptococcosis with brain and skin involvement, together with cytomegalovirus (CMV) antigenemia more than 20 years after transplant. She presented with frontal headache and bilateral hand tremor, in addition to multiple nodular lesions over bilateral lower limbs. The diagnosis was made after lumbar puncture and skin biopsy. She was successfully treated with a course of anti-fungal and anti-CMV regimen without any relapse of central nervous system infection. Our case illustrates that disseminated cryptococcosis can occur very late after organ transplant. It is thus important to watch out for late-onset opportunistic infections and strike the balance between risks of infections and rejections in SOT patients.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":""},"PeriodicalIF":1.0,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459022","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":"A case of de novo glomerulonephritis following COVID-19 in a patient with preexistent IgA vasculitis.","authors":"Daigo Kobayashi, Jun Yoshino, Maki Hanada, Masafumi Ohba, Tomohiro Oka, Kenichi Itoga, Daisuke Niino, Takeshi Kanda","doi":"10.1007/s13730-024-00940-9","DOIUrl":"https://doi.org/10.1007/s13730-024-00940-9","url":null,"abstract":"<p><p>During the unprecedented COVID-19 outbreak, new-onset or relapsing glomerulonephritis, such as ANCA-associated glomerulonephritis and Immunoglobulin A (IgA) nephropathy, following COVID-19 has been reported. However, to date, the association of COVID-19 with preexistent IgA vasculitis (IgAV) remains unclear. Here, we present the case of a 20-something old Japanese woman with preexistent IgAV who newly developed glomerulonephritis following COVID-19. At the diagnosis of IgAV, she had cutaneous purpura, joint pains, and gastrointestinal symptoms, but no signs of kidney involvement. Three months ago, she was tested positive for COVID-19 and subsequently developed hematuria and proteinuria. She was then admitted to our hospital and renal biopsy showed glomerular mesangial expansion and hypercellularity and cellular and fibrocellular crescents, accompanied by diffuse IgA and C3 deposits. With the diagnosis of de novo IgAV nephritis, the patient was treated with intravenous methylprednisolone followed by oral prednisolone. She had favorable responses to this treatment and has achieved and maintained the remission of hematuria and proteinuria after initiation of glucocorticoid therapy. Our case highlights that immune response to SARS-CoV-2 infection could trigger the onset of glomerulonephritis in the IgAV patients who have no renal involvement.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":""},"PeriodicalIF":1.0,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459018","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":"Case of successful treatment with glucocorticoid for isolated anti-centromere antibody-positive acute interstitial nephritis.","authors":"Chisa Takata, Akihiro Kuma, Atsuko Suwabe, Takahide Iwasaki, Takahiro Kuragano","doi":"10.1007/s13730-024-00937-4","DOIUrl":"https://doi.org/10.1007/s13730-024-00937-4","url":null,"abstract":"<p><p>Acute interstitial nephritis (AIN) is known to cause acute kidney injury and is characterized by immunocyte infiltration and interstitial fibrosis. Primary etiologies include drugs, infections, and autoimmune disorders. Herein, we presented the case of a 78-year-old woman patient with AIN with anti-centromere antibody (ACA) positivity, secondary to an idiopathic immune system disorder. Her serum creatinine (sCr) was 0.67 mg/dL 2 months prior to consulting us, which increased to 2.79 mg/dL. The renal biopsy revealed an AIN comprising interstitial infiltration with immunocytes and CD138 + cells. Furthermore, all other antibodies tested negative using immunofluorescence on both glomeruli and tubulointerstitial lesions. The ACA was elevated to a level of ≥ 500 U/mL. The ACA positive has been known to be accompanied by worsening kidney function in patients with systemic sclerosis and primary biliary cholangitis. However, any autoimmune disease were not diagnosed. Successful treatment with an initial dose of 30 mg/day of glucocorticoids tapered to 25 mg/day resulted in a decrease in the sCr to 1.53 mg/dL 4 weeks later. Nine months later, glucocorticoids was tapered, based on the threshold of a sCr of 1.03 mg/dL and the titer of ACA of 291 U/mL. In this case, glucocorticoid treatment remarkably improved renal function in AIN containing CD138 + cells accompanied by a reduction of ACA titer. The etiology of ACA-positive AIN was unknown; however, the incidence of ACA-positive AIN should always be deliberated.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":""},"PeriodicalIF":1.0,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459019","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":"Chronic kidney disease associated with extremely premature birth and extremely low birth weight may progress through the burden of growth.","authors":"Chinatsu Onodera, Ken Ishikawa, Hiroshi Sugawara, Saeko Nishimi, Hiromi Furukawa, Akira Takada, Manami Akasaka, Megumi Kobayashi","doi":"10.1007/s13730-024-00931-w","DOIUrl":"https://doi.org/10.1007/s13730-024-00931-w","url":null,"abstract":"<p><p>Chronic kidney disease associated with low birth weight and/or premature birth (L/P-CKD) in infants may result from a decreased number of nephrons at birth. These infants may develop acute kidney injury due to exposure to nephrotoxic substances or other events during nephrogenesis in early infancy. Nonetheless, L/P-CKD progression remains unclear. We present three cases of L/P-CKD diagnosed after neonatal intensive care unit (NICU) discharge. Three patients were born extremely prematurely (gestational age, 24-26 weeks) with extremely low birth weight (606-906 g). They were admitted to the NICU (117-311 days) anad received several nephrotoxic medications during the early postnatal period. They showed elevated serum creatinine levels at 4 weeks after birth, which decreased to normal levels at NICU discharge. Proteinuria was first detected during adolescence (10-15 years) on annual school urine screening, with a remarkable increase in their height (18 - 50.8 cm), without known episodes of urinary tract infection, dehydration, lifestyle-related issues, such as excessive salt/protein intake, and extreme lack of exercise that might have caused kidney damage. Their kidneys were smaller than normal on renal ultrasonography. Open renal biopsy findings indicated glomerulomegaly and perihilar glomerulosclerosis in two of the three patients, suggesting glomerular hypertension. The remarkable differences between the body height before CKD and the timing of diagnosis of CKD could contribute to the progress of CKD. Long-term follow-up of low birth weight and extremely premature infants, from NICU discharge until adulthood, should be established.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":""},"PeriodicalIF":1.0,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379133","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":"Immunoglobulin A-dominant membranoproliferative glomerulonephritis-like pattern of injury as a possible paraneoplastic nephropathy in a breast cancer patient.","authors":"Shuntaro Taira, Mika Kawagoe, Hitoshi Anzai, Minoru Yasukawa, Shinichiro Asakawa, Shigeyuki Arai, Osamu Yamazaki, Yoshifuru Tamura, Yasutoshi Oshima, Satoe Numakura, Ryuji Ohashi, Shigeru Shibata, Yoshihide Fujigaki","doi":"10.1007/s13730-024-00936-5","DOIUrl":"https://doi.org/10.1007/s13730-024-00936-5","url":null,"abstract":"<p><p>A middle-aged woman was found to have proteinuria during a health check-up. About sixteen months later, she was diagnosed with stage IIA invasive ductal carcinoma of the right breast. Her proteinuria progressed to nephrotic syndrome with significant hematuria. Hormone therapy was initiated for her estrogen and progesterone receptor-positive breast cancer. A kidney biopsy performed 47 days after starting the therapy revealed an IgA-dominant membranoproliferative glomerulonephritis-like pattern of injury. Electron microscopy showed subendothelial-dominant electron-dense deposits (EDD), with small amounts of mesangial EDD and a single occurrence of subepithelial hump-like EDD, along with occasional mesangial interpositions. Similar pathology can be caused by IgA vasculitis with nephritis, IgA-dominant infection-associated glomerulonephritis, and liver disease-associated glomerulopathy, but all of these were ruled out. The deposited IgA was found to be galactose-deficient IgA1. Thus, IgA nephropathy with glomerular capillary IgA deposition was considered. She underwent a right partial mastectomy and sentinel lymph node biopsy in the right axilla 75 days after starting hormone therapy, followed by adjuvant radiation. Proteinuria and hematuria tended to decrease after the treatment, and this trend continued even after corticosteroid therapy for glomerulonephritis, which was administered 156 days after starting hormone therapy. Approximately 15 months after starting hormone therapy, her proteinuria had reduced to around 1.0 g/g of creatinine, and her hematuria was negative. IgA nephropathy with glomerular capillary IgA deposition is known to be resistant to corticosteroid therapy. The favorable clinical course of the rare glomerulopathy following breast cancer treatment suggested a diagnosis of paraneoplastic glomerulopathy secondary to breast cancer in our patient.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":""},"PeriodicalIF":1.0,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371064","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":"A novel homozygous SLC12A3 mutation causing Gitelman syndrome with co-existent autoimmune thyroiditis: a case report and review of the literature.","authors":"Oguzhan Koca, Mustafa Tarık Alay, Ahmet Murt, Aysel Kalayci Yigin, Mehmet Seven, Isil Bavunoglu","doi":"10.1007/s13730-023-00845-z","DOIUrl":"10.1007/s13730-023-00845-z","url":null,"abstract":"<p><p>Gitelman syndrome is a rare, autosomal recessively inherited tubulopathy manifesting with hypokalemia, hypomagnesemia, hypocalciuria, and metabolic alkalosis. Common symptoms include fatigue, myalgia, reduced performance capacity, tetany, paresthesia, and delayed growth. However, as reported in the literature, diagnosis in some patients is prompted by an incidental finding of hypokalemia. GS develops due to mutations in the SLC12A3 gene, which encodes the thiazide-sensitive Na-Cl cotransporter. Many variants in the SLC12A3 gene causing GS have been reported in literature. A new pathogenic homozygous mutation (c.2612G > T), absence of hypomagnesemia, and accompanying autoimmune thyroiditis are remarkable in our patient. There are a few Gitelman syndrome cases that are complicated with autoimmune thyroiditis in the literature. In this study, we present a case of Gitelman syndrome with a novel homozygous mutation and accompanying autoimmune thyroiditis and review of the literature.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"330-338"},"PeriodicalIF":1.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11442957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139680722","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}

{"title":"Additional renoprotective effect of the SGLT2 inhibitor dapagliflozin in a patient with ADPKD receiving tolvaptan treatment.","authors":"Shun Minatoguchi, Hiroki Hayashi, Ryosuke Umeda, Shigehisa Koide, Midori Hasegawa, Naotake Tsuboi","doi":"10.1007/s13730-024-00859-1","DOIUrl":"10.1007/s13730-024-00859-1","url":null,"abstract":"<p><p>Autosomal dominant polycystic kidney disease (ADPKD) is a major cause of end-stage kidney disease (ESKD). Vasopressin plays a pivotal role in ADPKD progression; therefore, the selective vasopressin V2 receptor antagonist tolvaptan is used as a key drug in the management of ADPKD. On the other hand, sodium-glucose cotransporter-2 inhibitors (SGLT2i), which may possibly stimulate vasopressin secretion due to the diuretic effect of the drug, have been shown to have both renal and cardioprotective effects in various populations, including those with non-diabetic chronic kidney disease. However, the effect of SGLT2i in patients with ADPKD have not been fully elucidated. Herein, we report the case of a patient with ADPKD on tolvaptan who was administered the SGLT2i dapagliflozin. The patient was a Japanese woman diagnosed with ADPKD at age 30. Despite the treatment with tolvaptan, eGFR was gradually declined from 79.8 to 50 ml/min/1.73 m² in almost 5 years and 10 mg of dapagliflozin was initiated in the hope of renoprotective effects. Although a small increase in vasopressin levels was observed, eGFR decline rate was moderated after dapagliflozin initiation. This case suggested an additional renoprotective effect of dapagliflozin in patient with ADPKD receiving tolvaptan. Although there is no evidence about the renal protective effect of SGLT2i in patients with ADPKD, we hereby report a case successfully treated with dapagliflozin for approximately 2 years. Further research, including clinical trials, is needed to evaluate whether SGLT2i are effective in patients with ADPKD.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"419-424"},"PeriodicalIF":1.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11444039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140142835","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}

{"title":"Lupus-like membranous nephropathy during the postpartum period expressing glomerular antigens exostosin 1/exostosin 2 and phospholipase A2 receptor: a case report.","authors":"Ryoma Miyasaka, Yukihiro Wada, Kazuhiro Takeuchi, Tetsuya Abe, Ryota Uchitsubo, Sayumi Kawamura, Shun Sakurabayashi, Shokichi Naito, Togo Aoyama, Akira Shimizu, Yasuo Takeuchi","doi":"10.1007/s13730-023-00848-w","DOIUrl":"10.1007/s13730-023-00848-w","url":null,"abstract":"<p><p>Recently, several target antigens of membranous nephropathy (MN), such as phospholipase A2 receptor (PLA2R) and exostosin 1/exostosin 2 (EXT1/2), have been discovered. A 30-year-old woman was referred to our hospital with nephrotic range proteinuria and microscopic hematuria. She was first noted to have proteinuria before pregnancy, and her proteinuria worsened in the postpartum period. A renal biopsy showed MN. Immunofluorescence microscopy showed IgG, IgA, IgM, C3, C4, and C1q depositions in the mesangial area and glomerular capillary walls (GCWs). Regarding the IgG subclass, IgG1 and IgG3 were detected on glomeruli. Electron microscopy showed subepithelial electron-dense deposits (EDDs). EDDs were also detected in paramesangial and subendothelial areas. The diagnosis of membranous lupus nephritis (MLN) was suspected, but she did not fulfill the criteria for systemic lupus erythematosus. Neither anti-nuclear antibody nor hypocomplementemia were detected. We further evaluated glomerular EXT1/2 expressions, which were evident on GCWs. In addition, PLA2R was also detected on GCWs, although serum antibody for PLA2R was negative. She responded to immunosuppressive therapy with decreased proteinuria. In the present case, glomerular PLA2R expression implied the possibility of primary MN. However, pathological findings with a full-house staining pattern and glomerular EXT1/2 expressions were very similar to those of lupus-associated MN. Glomerular PLA2R expression appeared not to reflect immunocomplexes of PLA2R and autoantibody when considering the results for glomerular IgG subclass and the absence of serum anti-PLA2R antibody. Collectively, it is plausible that this was a case of a relatively young postpartum female who developed latent MLN rather than primary MN.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"318-325"},"PeriodicalIF":1.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11442721/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139569163","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}

{"title":"Two acute kidney injury episodes after ICI therapy: a case report.","authors":"Kohei Ishiga, Ryu Kobayashi, Tomohiko Kanaoka, Jotaro Harada, Ikuma Kato, Satoshi Fujii, Hiromichi Wakui, Yoshiyuki Toya, Kouichi Tamura","doi":"10.1007/s13730-024-00855-5","DOIUrl":"10.1007/s13730-024-00855-5","url":null,"abstract":"<p><p>A 74-year-old Japanese male with lung squamous cell carcinoma received his first dose of immune checkpoint inhibitors (ICIs): ipilimumab and nivolumab. He developed acute kidney injury (AKI) and was admitted to our department. We diagnosed kidney immune-related adverse effects (irAE), and a kidney biopsy revealed acute tubulointerstitial nephritis. We started oral prednisolone (PSL) and his AKI immediately improved. The patient maintained stable findings after PSL was tapered off. However, seven months after the ICI administration, he developed rapid progressive glomerular nephritis and was admitted to our department again. The second kidney biopsy showed findings consistent with anti-glomerular basement membrane glomerulonephritis. Although the patient was treated with pulse methylprednisolone followed by oral PSL and plasma exchange, he became dependent on maintenance hemodialysis. To our knowledge, no case report has described two different types of biopsy-proven nephritis. In cases of suspected relapsing kidney irAEs, both a relapse of previous nephritis and the development of another type of nephritis should be considered.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"408-415"},"PeriodicalIF":1.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11444024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140058692","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}