Case Reports in Nephrology最新文献

{"title":"Severe Hypokalemia Associated With Piperacillin-Tazobactam Use.","authors":"Angelina Kravcik, Jason Zelt, Stephen Kravcik","doi":"10.1155/crin/1957735","DOIUrl":"https://doi.org/10.1155/crin/1957735","url":null,"abstract":"<p><p>Piperacillin-tazobactam is a generally well-tolerated broad-spectrum antibacterial. Mild hypokalemia may occur with piperacillin-tazobactam therapy as a result of increased renal potassium losses. Severe hypokalemia is rare. We report here a case of very severe hypokalemia during piperacillin-tazobactam therapy, refractory to aggressive potassium replacement.</p>","PeriodicalId":9604,"journal":{"name":"Case Reports in Nephrology","volume":"2026 ","pages":"1957735"},"PeriodicalIF":0.0,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13542582/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896558","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":"Primary Hyperoxaluria Type 1 Diagnosed After Kidney Transplantation in the Absence of Classical Features.","authors":"Rawh Sultan, Zein A Alsayed-Ahmad, Ahmad Ryyan Shheibar, Rawda Shawwa, Karam Albitar, Sami Albitar","doi":"10.1155/crin/4378614","DOIUrl":"10.1155/crin/4378614","url":null,"abstract":"<p><strong>Background: </strong>Primary hyperoxaluria Type 1 is a rare inherited metabolic disorder caused by pathogenic variants in the AGXT gene. Because the disorder leads to excessive internal oxalate formation, progressive end-stage kidney disease (ESKD) may occur. While most affected individuals present during childhood, a subset is diagnosed only later in adult life, frequently after substantial renal deterioration. Delayed diagnosis increases the risk of recurrent oxalate nephropathy and graft dysfunction following kidney transplantation.</p><p><strong>Case presentation: </strong>We report a 30-year-old woman with ESKD of unknown aetiology who underwent living-donor kidney transplantation. One year later, during a subsequent pregnancy, she developed progressive graft dysfunction. Kidney biopsy demonstrated extensive calcium oxalate crystal deposition, raising suspicion for an underlying metabolic disorder. Genetic testing subsequently confirmed a pathogenic AGXT mutation, establishing the diagnosis of adult-onset PH1. Urinary oxalate concentrations were within normal limits before and after transplantation, emphasizing the diagnostic challenge.</p><p><strong>Conclusion: </strong>This case highlights the importance of considering PH1 in adults with unexplained chronic or ESKD, even in the absence of classical features or elevated urinary oxalate excretion. Early genetic testing and careful assessment of family history are essential for timely diagnosis, enabling appropriate transplant planning, disease-specific therapy, and genetic counselling.</p>","PeriodicalId":9604,"journal":{"name":"Case Reports in Nephrology","volume":"2026 ","pages":"4378614"},"PeriodicalIF":0.0,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13526188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863756","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 Nephritis Exhibiting a Membranoproliferative Pattern in Primary Myelofibrosis: A Diagnostic Challenge of Occult SLE.","authors":"Alaa Alem, Raghad Altayyar, Fadyah Alradaddi, Rayan Alahmadi","doi":"10.1155/crin/2339466","DOIUrl":"10.1155/crin/2339466","url":null,"abstract":"<p><p>Lupus nephritis (LN) with a membranoproliferative pattern is an uncommon but recognized renal manifestation of systemic lupus erythematosus (SLE). While autoimmune myelofibrosis (AMF) has been described in association with SLE, the coexistence of primary myelofibrosis (PMF) with this pattern of LN has not been previously documented. We report a 50-year-old man with JAK2-positive PMF, undifferentiated connective tissue disease (UCTD), and Stage 3b chronic kidney disease who developed nephrotic syndrome and worsening kidney function. Initial serologic evaluation revealed positive antinuclear antibody (ANA), low serum complement C3, and negative antidouble-stranded DNA (anti-dsDNA) antibodies. Kidney biopsy demonstrated a membranoproliferative pattern of injury with mesangial and subendothelial immune complex deposits staining for IgM and C1q. Subsequent testing revealed high-titer anticardiolipin IgM antibodies. The patient met the 2019 EULAR/ACR classification criteria for SLE. Induction therapy with high-dose prednisone and mycophenolate mofetil resulted in a partial remission, with stabilization of renal function on follow-up. To our knowledge, this is the first reported case of LN with a membranoproliferative pattern of injury in a patient with PMF. The case underscores the diagnostic value of kidney biopsy in uncovering occult systemic autoimmune disease in patients with myeloproliferative neoplasms (MPNs), particularly when the clinical and demographic profile is atypical for SLE.</p>","PeriodicalId":9604,"journal":{"name":"Case Reports in Nephrology","volume":"2026 ","pages":"2339466"},"PeriodicalIF":0.0,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13501890/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148812056","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":"Relapse of Steroid-Dependent Nephrotic Syndrome Despite Long-Term Ciclosporin Therapy in an 11-Year-Old Child: A Case Report and Review on the Management of Nephrotic Syndrome in Children.","authors":"Abdullah Faiz Zaihan, Nurdiana Jamil, Chia Siang Kow","doi":"10.1155/crin/1396986","DOIUrl":"https://doi.org/10.1155/crin/1396986","url":null,"abstract":"<p><strong>Background: </strong>Frequently relapsing nephrotic syndrome (FRNS) and steroid-dependent nephrotic syndrome (SDNS) are distinct phenotypes defined by relapse frequency and the temporal relationship of relapse to prednisolone therapy, respectively. Both remain therapeutic challenges despite the use of corticosteroid-sparing agents. Relapses may be triggered by intercurrent infections and can be complicated by significant edema, hypoalbuminemia, and infection risk, requiring prompt optimization of immunosuppressive and supportive therapy.</p><p><strong>Case presentation: </strong>An 11-year-old boy with SDNS presented with a two-day history of bilateral periorbital swelling and facial puffiness following fever, rhinorrhea, and productive cough. He had experienced 11 previous relapses and was receiving ciclosporin 50 mg twice daily and enalapril 5 mg once daily with good adherence. Previous kidney biopsy showed minor glomerular change, and ciclosporin trough concentration was therapeutic. On admission, he was febrile (38.3°C) with leukocytosis, neutrophilia, thrombocytosis, marked hypoalbuminemia, significant proteinuria, and hematuria. Penicillin V was initiated for spontaneous bacterial peritonitis prophylaxis. Prednisolone was optimized from 40 mg once daily to 30 mg twice daily based on a body surface area of 1.17 m². Progressive edema and weight gain required escalation to intravenous frusemide with 20% human albumin, resulting in marked clinical improvement. Proteinuria, hematuria, and ascites resolved, and he was discharged clinically stable with minimal residual edema.</p><p><strong>Conclusion: </strong>This case highlights several important therapeutic considerations in relapsing childhood nephrotic syndrome: recognition of SDNS as a subgroup of SSNS, accurate prednisolone dosing during relapse, careful assessment of edema and intravascular volume status before diuretic therapy, and individualized use of steroid-sparing agents and antimicrobial prophylaxis. In children receiving prolonged ciclosporin therapy, treatment should be regularly reviewed with blood pressure, renal function, and therapeutic drug monitoring in view of potential calcineurin inhibitor toxicity, and alternative steroid-sparing options such as levamisole may be considered where clinically appropriate.</p>","PeriodicalId":9604,"journal":{"name":"Case Reports in Nephrology","volume":"2026 ","pages":"1396986"},"PeriodicalIF":0.0,"publicationDate":"2026-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13478731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788537","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 Classic and Unusual Presentation of Atheroembolic Renal Disease: Report of Two Cases.","authors":"Kai Zong Teo, Angela Bayly, Surjit Tarafdar, Lisa Phipps, Jian Cheng, Seethalakshmi Viswanathan","doi":"10.1155/crin/9627594","DOIUrl":"10.1155/crin/9627594","url":null,"abstract":"<p><p>Atheroembolic renal disease (AERD) is an underdiagnosed condition with diverse clinical presentations that can mimic various renal pathologies. Most cases follow intravascular procedures or anticoagulation, while only rare case reports of spontaneous AERD have been described. We present two contrasting cases of AERD with markedly different presentations. The first patient was a 74-year-old male who presented with worsening dyspnoea, acute renal failure and skin changes following coronary bypass surgery, typical of AERD. The second patient was a 70-year-old male who presented with symptomatic hypertension and acute-on-chronic kidney injury without identifiable precipitating factors, initially suspected to be rapidly progressive glomerulonephritis. Renal biopsies revealed cholesterol emboli within arteries, characterised by needle-shaped clefts surrounded by foreign body giant cells, with background interstitial fibrosis and tubular atrophy confirming the diagnosis. These contrasting cases demonstrate the diagnostic challenges of AERD and highlight the importance of renal biopsy for accurate diagnosis in both classic and atypical presentations.</p>","PeriodicalId":9604,"journal":{"name":"Case Reports in Nephrology","volume":"2026 ","pages":"9627594"},"PeriodicalIF":0.0,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13455123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705572","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":"Favorable Outcome With Eculizumab in Hemolytic Uremic Syndrome Presenting With Severe Neurological Complications: A Case Report.","authors":"Maryam Zaitoun, Abdulkarim Alanazi, Tasneem Kattash, Abdullah Wali, Amna Abdelbagi, Sawsan Al Batati, Hassan Faqeehi, Saeed Al Zabali","doi":"10.1155/crin/8844271","DOIUrl":"10.1155/crin/8844271","url":null,"abstract":"<p><strong>Introduction: </strong>Thrombotic microangiopathies (TMAs) are a group of rare, life-threatening disorders characterized by a classic triad of MAHA, severe thrombocytopenia, and ischemic tissue injury. Thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) are the main types of TMAs. Based on the cause, HUS can be classified as typical or atypical.</p><p><strong>Case presentation: </strong>We present the case of a 4-year-old child referred to King Fahad Medical City in Riyadh, Saudi Arabia, with complaints of bloody diarrhea, vomiting, and fever. The condition progressed to altered consciousness, seizures, and quadriparesis.</p><p><strong>Result: </strong>Upon admission, the patient received plasma infusion and underwent peritoneal dialysis. Eculizumab therapy was initiated 1 week after the presentation. Hematological and renal parameters improved rapidly, but neurological recovery was gradual, with significant progress observed over 6 years of follow-up.</p><p><strong>Conclusion: </strong>This case highlights that severe neurological manifestations can be an initial feature of HUS, not just TTP. Eculizumab was effective and life-saving in pediatric patients with TMA and severe neurological involvement, though CNS recovery may take years.</p>","PeriodicalId":9604,"journal":{"name":"Case Reports in Nephrology","volume":"2026 ","pages":"8844271"},"PeriodicalIF":0.0,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13434026/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673011","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 Rare Diagnostic Dilemma of P-ANCA/MPO Positive Crescentic Glomerulonephritis in an Immunosuppressed Lupus Patient.","authors":"Omar Elrefy, Sweta Carpenter, Manu Saini, Manjula Balasubramanian, Daranee Chewaproug","doi":"10.1155/crin/1850355","DOIUrl":"10.1155/crin/1850355","url":null,"abstract":"<p><p>Perinuclear antineutrophil cytoplasmic antibodies (P-ANCAs) and myeloperoxidase (MPO) antibodies are detected in 15%-25% of lupus nephritis patients, but systemic lupus erythematosus (SLE)/ANCA-associated vasculitis (AAV) overlap syndrome is rare, occurring in approximately 2% of cases. We present a 57-year-old woman with SLE and antiphospholipid syndrome (APS) on belimumab, hydroxychloroquine, and prednisone, who presented with acute ischemic stroke requiring thrombectomy and rapidly progressive renal failure (creatinine rising from 1.1 to 5.2 mg/dL) with nephrotic-range proteinuria (8.6 g/g). P-ANCA titer was > 1:640 with MPO positivity, while anti-dsDNA, C3, and C4 were normal. Kidney biopsy revealed crescentic glomerulonephritis with neutrophil-rich infiltrates and immune complex deposits on electron microscopy but without \"full house\" immunofluorescence, favoring SLE/AAV overlap rather than isolated lupus nephritis flare. Treatment with methylprednisolone, rituximab, and anticoagulation resulted in significant renal recovery (creatinine 1.7 mg/dL, proteinuria 4.4 g/g). This case highlights the importance of ANCA testing in SLE patients with unexplained rapidly progressive glomerulonephritis, as early recognition of overlap syndrome carries distinct therapeutic implications, including the use of rituximab-based regimens targeting both disease processes.</p>","PeriodicalId":9604,"journal":{"name":"Case Reports in Nephrology","volume":"2026 ","pages":"1850355"},"PeriodicalIF":0.0,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13373297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148469238","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 Common Collagen of Alport Syndrome and Arthritis: A Case Report and Review of Pathophysiology.","authors":"Craig A Mendonca, Lalarukh Haider, Anusha Attre, Eric M Mortensen, Narinder Maheshwari","doi":"10.1155/crin/9705418","DOIUrl":"10.1155/crin/9705418","url":null,"abstract":"<p><strong>Aim: </strong>Through the lens of a clinical case, we explore the overlap in pathophysiology between Alport syndrome and seronegative inflammatory arthritis, focusing on the collagen structural changes that can occur in Alport syndrome.</p><p><strong>Results: </strong>Genetic variant information was obtained for a patient diagnosed with Alport syndrome. Few cases of Alport syndrome associated with inflammatory arthritis have been reported in the literature so far. The genes encoding collagen fibrils affected in Alport syndrome are also expressed in hyaline cartilage. The inflammatory response triggered by these misfolded, truncated, or missing proteins may contribute to inflammatory pathways present in arthritis through compromised collagen structures.</p><p><strong>Clinical takeaway: </strong>Evaluation of hematuria and concomitant inflammatory arthritis should include consideration of hereditary connective tissue disorders, such as Alport syndrome.</p>","PeriodicalId":9604,"journal":{"name":"Case Reports in Nephrology","volume":"2026 ","pages":"9705418"},"PeriodicalIF":0.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13319906/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148366972","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":"Exercise-Induced Rhabdomyolysis With Markedly Elevated Creatine Kinase and Preserved Renal Function.","authors":"Navuddh Oam, Sophareine Samphon, Pisey Say, Samith Sourn","doi":"10.1155/crin/3900923","DOIUrl":"10.1155/crin/3900923","url":null,"abstract":"<p><strong>Background: </strong>Exercise-induced rhabdomyolysis results from skeletal muscle injury after strenuous or unaccustomed exertion. Acute kidney injury is a feared complication, but creatine kinase magnitude alone is an imperfect predictor of kidney injury.</p><p><strong>Case presentation: </strong>A 24-year-old previously healthy male presented with dark urine after one week of high-intensity resistance and eccentric exercise as a novice participant in structured high-intensity training. He reported daily oral hydration of more than 2.5 L and denied creatine monohydrate use. Initial tests showed creatine kinase of 79,038 U/L, creatinine of 1.3 mg/dL, estimated glomerular filtration rate of approximately 79 mL/min/1.73 m² by the 2021 CKD-EPI creatinine equation, aspartate aminotransferase (AST) of 507 U/L, and urine dipstick blood of 3+ with few red blood cells. Urea, potassium, calcium, magnesium, and phosphorus were within reference ranges, and urinalysis showed only trace protein without leukocytes or nitrites. He received isotonic intravenous fluids without bicarbonate, diuretics, or renal replacement therapy. Creatinine decreased to 0.6 mg/dL within 24 h and remained stable; urine dipstick blood became negative by Day 2; creatine kinase declined to 722 U/L by Day 10 and 287 U/L by Day 16, while creatinine remained normal at 0.7 mg/dL and aminotransferases improved to AST of 25 U/L and ALT of 42 U/L.</p><p><strong>Conclusion: </strong>This case is best interpreted as severe exertional rhabdomyolysis with pigmenturia and preserved renal function, rather than confirmed intrinsic acute kidney injury. The report highlights the need to avoid creatine kinase-centric risk assessment and to interpret a mildly elevated admission creatinine in context, especially when rapid normalization follows fluid resuscitation.</p>","PeriodicalId":9604,"journal":{"name":"Case Reports in Nephrology","volume":"2026 ","pages":"3900923"},"PeriodicalIF":0.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148374629","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":"Liddle Syndrome Presenting as Hypertensive Crisis and Myocardial Injury in a Young Male: A Case Report.","authors":"Abbas Khan, Alina Batool, Askar Nisar, Jaweria Farman, Okasha Tahir, Muhammad Hassaan Javaid, Raghabendra Kumar Mahato, Tayyeb Ali","doi":"10.1155/crin/7218869","DOIUrl":"10.1155/crin/7218869","url":null,"abstract":"<p><strong>Introduction: </strong>Liddle's syndrome is a rare inherited disorder associated with early-onset and resistant hypertension due to hyperactivity of epithelial sodium channels (ENaCs). The condition is caused by mutations in the genes SCNN1A, SCNN1B, and SCNN1G. Liddle's syndrome leads to hypertension, hypokalemia, and metabolic alkalosis.</p><p><strong>Case presentation: </strong>A previously healthy 21-year-old male patient complained of severe central chest pain radiating to both arms and had a hypertensive emergency with a BP reading of 267/170 mmHg. The patient had marked elevation in troponin I (13.9 ng/mL), hypokalemia (2.8 mmol/L), and metabolic alkalosis. The electrocardiogram showed left ventricular hypertrophy with a strain pattern and QTc prolongation due to hypokalemia. Coronary angiography ruled out the possibility of primary acute coronary syndrome by revealing normal coronary arteries. Echocardiogram showed concentric left ventricular hypertrophy with normal ejection fraction and no wall motion abnormalities. In search of the secondary cause of hypertension, renal Doppler ultrasonography and aldosterone-to-renin ratio were normal, thus ruling out primary hyperaldosteronism. About the typical clinical and biochemical presentation, a clinical diagnosis of Liddle syndrome was highly likely. Genetic tests were not performed owing to financial constraints. However, treatment with amiloride brought about remarkable improvement in the control of hypertension and normalization of potassium levels.</p><p><strong>Conclusion: </strong>Liddle's syndrome should be suspected in cases where there are young individuals who have severe hypertension, hypokalaemia, and an aldosterone-to-renin ratio that is normal or low. The diagnosis must be made promptly because delay may lead to complications. In instances where molecular testing is impractical, treatment with ENaC inhibition using amiloride is diagnostic and potentially life-saving.</p>","PeriodicalId":9604,"journal":{"name":"Case Reports in Nephrology","volume":"2026 ","pages":"7218869"},"PeriodicalIF":0.0,"publicationDate":"2026-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13310365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148343972","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}