CEN Case Reports最新文献

{"title":"Clinicopathological features of familial fibronectin glomerulopathy caused by a splice site variant in the Fibronectin 1 gene: a case report.","authors":"Yoshikuni Nagayama, Masako Otani, Mariko Hashimoto, Ayana Ichikura-Iida, Takashi Inoue","doi":"10.1007/s13730-025-00987-2","DOIUrl":"10.1007/s13730-025-00987-2","url":null,"abstract":"<p><p>Fibronectin glomerulopathy (FNG) is a rare autosomal dominant inherited disease characterized by extensive deposits of fibronectin in the mesangium and subendothelial space of the glomeruli with membranoproliferative glomerulonephritis (MPGN)-like pattern. Currently, ten exonic and one intronic pathogenic variants in the fibronectin 1 gene have been identified; however, genotype-phenotype correlation data are lacking. We herein report a familial FNG caused by a splice site variant in intron 36 (c.5888-2A > G). The gene mutation was recently found, but to our knowledge, this is the first case report of a familial FNG with the intronic variant that describes the clinicopathological characteristics. In the current study, Case 1 is a previously healthy 29-year-old woman with nephrotic syndrome. Treatment with glucocorticoids, combined with the immunosuppressant mizoribine and an angiotensin II receptor blocker (ARB), resulted in an incomplete remission of nephrotic syndrome; however, renal function has been preserved. Case 2, the mother of Case 1, is a 49-year-old woman with vasculo-Behçet's disease with mild proteinuria and renal dysfunction. Due to the administration of azathioprine, aspirin, and ARB, renal function and proteinuria have been stable over 10 years. The kidney biopsy revealed MPGN-like histological features in both the mother and the daughter; however, the mesangial area exhibited a milder expansion in the mother than in the daughter. Accumulating genotype-phenotype correlation data will be essential for managing FNG.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"351-357"},"PeriodicalIF":1.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691275","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":"The natural history of untreated X-linked nephrogenic diabetes insipidus with mutation in the vasopressin V2 receptor gene.","authors":"Giusy Capasso, Stefano Guarino, Anna Di Sessa, Margherita Luciano, Emanuele Miraglia Del Giudice, Francesco Trepiccione, Pierluigi Marzuillo","doi":"10.1007/s13730-024-00954-3","DOIUrl":"10.1007/s13730-024-00954-3","url":null,"abstract":"<p><p>Nephrogenic diabetes insipidus (NDI) results from the kidneys' inability to concentrate urine. We describe a 6-month-old male with a history of poor weight gain who presented with an incidental finding of hypernatremia (155 mEq/L) during an episode of acute gastroenteritis. The arginine vasopressin (AVP) test, along with molecular analysis revealing the M272R mutation in the AVP receptor 2 (AVPR2) gene, confirmed the diagnosis of congenital NDI. Interestingly, this mutation was also identified in the patient's maternal grandfather, who had never been diagnosed or treated for NDI despite a history of polydipsia, polyuria, and evidence of chronic kidney disease (CKD), severe bilateral hydronephrosis, hypertension, and severe bladder dysfunction. Early intervention with hydrochlorothiazide in the infant resulted in a significant reduction in urinary output and improved growth. The untreated grandfather's case highlights the potential severity of untreated NDI and the benefits of timely therapeutic intervention. This report contributes to the limited long-term data on congenital NDI, emphasizing the critical role of early detection and consistent management in preventing severe complications such as CKD, hydronephrosis, and bladder dysfunction. Regular follow-up, including renal ultrasound and monitoring of renal function, is essential for effectively managing NDI and improving patient outcomes.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"306-311"},"PeriodicalIF":1.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791173","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":"Early administration of caplacizumab combined with plasma exchange for thrombotic microangiopathy due to malignant hypertension: a case report.","authors":"Hiroyuki Okawa, Yukihiro Wada, Kazuhiro Takeuchi, Tomomi Motohashi, Tetsuya Abe, Ryota Uchitsubo, Naohiro Kawamura, Sayumi Kawamura, Shun Sakurabayashi, Kosuke Honda, Masamitsu Morishita, Shokichi Naito, Togo Aoyama, Yasuo Takeuchi","doi":"10.1007/s13730-025-00978-3","DOIUrl":"10.1007/s13730-025-00978-3","url":null,"abstract":"<p><p>Both thrombotic thrombocytopenic purpura (TTP) and malignant hypertension (MHT) present with thrombotic microangiopathy (TMA). Combination therapy with caplacizumab, anti-von Willebrand factor (VWF) A1 domain antibody, and plasma exchange (PE) has recently been highlighted as a novel therapeutic option for TTP. We treated a 51-year-old woman who showed severe hypertension, retinopathy, and acute kidney injury. Level of consciousness was clear on admission, but low-grade fever was observed. Laboratory tests showed normocytic anemia, thrombocytopenia, renal dysfunction, and a slight decrease in haptoglobin. Neither disseminated intravascular coagulation nor leukemia was diagnosed. The patient emergently received intravenous antihypertensive therapy, continuous hemodiafiltration, and sufficient blood transfusion. However, thrombocytopenia and oliguria remained despite control of blood pressure. On hospital day 8, administration of caplacizumab combined with PE was initiated before receiving results for a disintegrin-like and metalloprotease with thrombospondin type 1 motifs 13 (ADAMTS13) activity and inhibitor levels. We then administered caplacizumab for 5 days and performed 2 sessions of PE until confirming ADAMTS13 activity of 42% and absence of its inhibitor, contributing to increased serum hemoglobin and platelet levels with cessation of dialysis. Renal biopsy findings on hospital day 20 showed arteriolar nephrosclerosis and intimal hyperplasia in small arteries. To the best of our knowledge, this represents the first description of MHT-induced TMA treated with caplacizumab. MHT-induced TMA exhibiting symptoms of TTP tends to show poor renal prognosis, so early administration of caplacizumab with PE before receiving results for ADAMTS13 might prove beneficial for cases in which MHT complicated with TTP is suspected.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"442-449"},"PeriodicalIF":1.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540370","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":"Case of maternal uniparental isodisomy with autosomal recessive Alport syndrome combined with congenital myasthenia and Oguchi disease.","authors":"Misaki Akiyama, Keiko Matsubara, Hiroshi Terashima, Yuichi Abe, Kinji Ohno, Koichi Kamei","doi":"10.1007/s13730-025-00972-9","DOIUrl":"10.1007/s13730-025-00972-9","url":null,"abstract":"<p><p>Uniparental isodisomy (UPiD) is a genetic condition in which an individual inherits two identical copies of a chromosome, or part of a chromosome, from one parent. UPiD can result in the development of autosomal recessive disorders if the chromosome inherited from one parent has a pathogenic variant. Herein, we present a 20 year-old female patient who had no significant family history including kidney, muscular, or ocular diseases. She had muscle weakness since infancy and was suspected with congenital myasthenia. She was diagnosed with Oguchi disease, a congenital condition characterized by night blindness, by an ophthalmologist. At 3 years of age, hematuria was noted, and gross hematuria was occasionally observed thereafter. Exome analysis revealed homozygous variants in the COL4A4, CHRND, and SAG genes on chromosome 2, which are the causative genes of Alport syndrome, congenital myasthenic syndrome, and Oguchi disease, respectively. Array comparative genomic hybridization analysis and microsatellite analysis revealed maternal UPiD. At approximately 18 years of age, she presented with proteinuria with mild kidney impairment, and kidney biopsy was performed at 20 years of age. Type IV collagen α5 chain staining showed a weak but positive image in the glomerular basement membrane. However, thinning and irregular thickening of the glomerular basement membrane and reticular changes in the dense layer were observed, which were consistent with Alport syndrome. Angiotensin II receptor blocker (candesartan) was administered, and her urinary protein levels decreased. She had a homozygous missense variant, positive α5 chain staining, and a mild phenotype.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"396-401"},"PeriodicalIF":1.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254676","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":"From diagnosis to treatment of minimal change disease in pregnancy.","authors":"Petra Bolt, Iana Adamović, Matija Horaček, Ivana Vuković Brinar, Tonko Gulin","doi":"10.1007/s13730-025-00996-1","DOIUrl":"10.1007/s13730-025-00996-1","url":null,"abstract":"<p><p>Preeclampsia accounts for the majority of nephrotic syndrome in pregnancy. However, primary renal diseases, although not as common, can also be the cause. The authors report a case of a 33-year-old pregnant woman at 22 weeks of gestation who presented with significant proteinuria, hypoalbuminemia, hyperlipidemia and discrete pitting edema. After the initial workup, a kidney biopsy was performed to diagnose minimal change disease (MCD), which revealed extensive podocyte foot process effacement. Treatment with IV methylprednisolone followed by oral prednisone led to remission, but a relapse occurred at 37 weeks of gestation. Labor was induced due to oligohydramnios with fetal growth restriction and a female hypotrophic neonate was delivered. Later on, the neonate developed sepsis and was successfully treated. Postpartum, the mother acquired a steroid resistance, and tacrolimus was used to achieve complete remission. In this case report, we emphasize the importance of kidney biopsy in adequately diagnosing primary renal diseases, even in pregnancy. This greatly helps clinicians in choosing the appropriate therapy for the patient, leading to disease remission.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"374-380"},"PeriodicalIF":1.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967115","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":"An educational case of toluene intoxication: importance of kidney function and timing in diagnosis.","authors":"Masatomo Ogata, Naoto Tominaga, Satoru Morikubo, Tomohiko Inoue, Yugo Shibagaki, Masahiko Yazawa","doi":"10.1007/s13730-025-00964-9","DOIUrl":"10.1007/s13730-025-00964-9","url":null,"abstract":"<p><p>Metabolic acidosis (MA) is common in daily clinical settings and requires evaluation not only by serum anion gap (AG) but also by urine AG (UAG) and urine osmolal gap (UOG) to investigate potential causes and determine appropriate treatment. Herein, we report an educational case of non-gap (normal AG) MA (pH 7.16, HCO₃^- 8.4, AG 11.6) with nausea and fatigue. The patient had three episodes of hospital admission with MA in the previous three months. Although serum lactate and ketone levels were negative, the AG levels were notably inconsistent (elevated or not) each time. Nevertheless, the patient was suspected to have toluene intoxication because of low UAG and high UOG levels in the non-gap acidosis phase. Eventually, he was diagnosed with toluene intoxication due to a significantly elevated urinary hippurate level (28.7 g/L) despite never admitting to using toluene. Additionally, he had a high AG only in the presence of significant kidney dysfunction, which suggests that the high AG was either due to kidney dysfunction or accumulated hippurate in the blood (when UOG was high). Thus, it should be noted that the use of serum AG alone may lead to incorrect determination of cause(s) of MA when kidney dysfunction coexists, and that UAG and UOG, in addition to AG, are necessary to determine correct diagnosis.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"390-395"},"PeriodicalIF":1.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022241","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":"A case of renal infiltration by Bence Jones protein kappa-producing lymphoplasmacytic lymphoma.","authors":"Kazuhiro Sonomura, Hozue Ehara, Hiroya Adachi, Yusuke Yamane, Eri Kawata, Yasukiyo Mori","doi":"10.1007/s13730-025-00977-4","DOIUrl":"10.1007/s13730-025-00977-4","url":null,"abstract":"<p><p>Lymphoplasmacytic lymphoma (LPL) is a type of low-grade B-cell lymphoma, with 90-95% of cases associated with Waldenström macroglobulinemia, characterized by the presence of IgM-type M-protein. We report, for the first time, a case of LPL-producing Bence Jones (BJ) protein kappa. The patient was a 78-year-old woman admitted to our department due to general fatigue and proteinuria that had persisted for 2 months. No M-protein was detected by blood immunofixation, but kappa-type BJ protein was detected in the urine. Light microscopy of a kidney biopsy sample revealed infiltration of lymphocytes and plasma cells into the perirenal adipose tissue and renal interstitium. The infiltrating cells exhibited kappa light chain restriction. Bone marrow examination revealed clusters of immature plasmacytoid lymphocytes that were CD20 positive, CD5 negative, and exhibited light chain restriction. Genetic analysis detected a MYD88 mutation, leading to the diagnosis of LPL in the patient. Six months after starting treatment with tirabrutinib, urinary protein levels improved to 0.2 g/gCr. Renal infiltration was identified due to urinary protein, and currently, no extramedullary lesions outside the kidneys are observed. Tirabrutinib has been extremely effective, but careful follow-up is still required.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"428-433"},"PeriodicalIF":1.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143406081","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":"Edoxaban-induced acute interstitial nephritis.","authors":"Shiko Gen, Ririko Higashi, Natsuki Nagae, Ryuta Kigure, Yuta Kamikubo, Kanako Nobe, Naofumi Ikeda","doi":"10.1007/s13730-025-00974-7","DOIUrl":"10.1007/s13730-025-00974-7","url":null,"abstract":"<p><p>A 76 year-old man with no specific medical history was diagnosed with atrial fibrillation and was started on edoxaban. Seven days after starting edoxaban, renal dysfunction was observed. He was suspected of having anticoagulant-related nephropathy due to acute kidney injury that occurred after starting edoxaban, and a renal biopsy was performed on day 5 of the illness to confirm the diagnosis. The renal biopsy results showed no red blood cell casts in the renal tubules, and inflammatory cell infiltration of lymphocytes and plasma cells was found in the interstitium, leading to a diagnosis of acute interstitial nephritis. There were no findings suggestive of autoimmune disease, and a drug-induced lymphocyte stimulation test to edoxaban was positive, leading to a diagnosis of edoxaban-induced acute interstitial nephritis. In addition to anticoagulant-related nephropathy, drug-induced interstitial nephritis should be considered as a cause of acute kidney injury after initiation of anticoagulant drugs.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"301-305"},"PeriodicalIF":1.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413577","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":"Systemic AA amyloidosis with amyloid deposition in the peritoneum at the time of initiating peritoneal dialysis.","authors":"Masato Habuka, Chihiro Sakurazawa, Yuichi Sakamaki, Asa Ogawa, Suguru Yamamoto, Ichiei Narita","doi":"10.1007/s13730-025-00981-8","DOIUrl":"10.1007/s13730-025-00981-8","url":null,"abstract":"<p><p>Amyloidosis is characterized by the deposition of insoluble amyloid fibrils formed by disease-specific precursor proteins in the extracellular interstitium of various organs throughout the body, resulting in organ damage. Patients with amyloidosis often develop end-stage kidney disease (ESKD), which can be managed with dialysis or kidney transplantation. Peritoneal dialysis (PD) is advantageous over hemodialysis (HD) in managing the circulatory dynamics and removing the precursor proteins of amyloid fibrils. However, the clinical course of PD using an amyloid-deposited peritoneum has not been reported. In this paper, we describe a rare case of systemic AA amyloidosis with amyloid deposition in the peritoneum at the beginning of PD. The peritoneal equilibrium test (PET) at PD initiation revealed a high transport rate. The dialysis solution was temporarily changed to a high-glucose concentration peritoneal dialysate, and a weekly extracorporeal ultrafiltration method was added. The patient continued with PD treatment without any complications. The PET category changed from \"high\" to \"high average\" during the subsequent PD treatment course. The serum amyloid A levels improved post-nephrectomy and remained in the normal range. Amyloid A was not detected in the dialysate drainage. In conclusion, the amyloid-deposited peritoneum has no uniform effect on the clinical course of PD. Moreover, amyloidosis therapy can alter the peritoneal function with amyloid deposition. However, future studies should investigate the exact mechanism of the alteration of peritoneal function with amyloidosis therapy.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"408-412"},"PeriodicalIF":1.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539430","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":"Tubular damage and SGLT2 expression in a patient with Beni-koji tablet-associated acute kidney injury and Fanconi syndrome.","authors":"Ayaka Kamada, Takuo Hirose, Hideaki Hashimoto, Yukari Konya, Fumiya Sato, Katsuya Ishiyama, Kensuke Joh, Wako Yumura, Takefumi Mori","doi":"10.1007/s13730-025-00984-5","DOIUrl":"10.1007/s13730-025-00984-5","url":null,"abstract":"<p><p>Since March 2024, many cases of renal dysfunction have been reported in Japan among individuals taking a supplement containing red yeast rice. We present the case of a 51-year-old woman who developed renal dysfunction and Fanconi syndrome after taking the supplement. The patient was referred to our hospital with hypouricemia, hypokalemia, hypophosphatemia, and glucosuria. Following a renal biopsy broadcast reports of kidney damage caused by the red yeast rice supplement and the patient's declaration of taking this supplement, we diagnosed her with supplement-induced acute kidney injury and Fanconi syndrome. Renal pathological findings revealed acute tubular necrosis, including brush border loss and mitochondrial fragmentation in the proximal tubular cells. These were consistent with the clinical and pathological findings of previous cases involving the red yeast rice supplement. Additionally, a reduction in sodium-glucose co-transporter 2 (SGLT2) expression was observed in the proximal tubules, supporting that the red yeast rice supplement damaged the proximal tubular cells. The reduction of SGLT2 protein expression may be linked to supplement-induced glucosuria. After supplement intake was ceased, renal function recovered and laboratory findings including glucosuria returned to normal within 6 months. The loss of glucosuria suggests that SGLT2 protein expression may be reversible. In consideration of our case and previous cases, it is probable that the nephrotoxicity of red yeast rice supplement is primarily affecting the proximal tubules, particularly the S1 and S2 segments.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"358-365"},"PeriodicalIF":1.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699735","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}