{"title":"Osmotic Demyelination Syndrome in a High-Risk Patient Despite Cautious Correction of Hyponatremia.","authors":"Cheolgu Hwang","doi":"10.5049/EBP.2023.21.2.61","DOIUrl":"10.5049/EBP.2023.21.2.61","url":null,"abstract":"<p><p>Hyponatremia is a common electrolyte disorder requiring careful management to prevent severe complications. Osmotic demyelination syndrome (ODS) is a serious neurological disorder that can develop from rapid correction of hyponatremia. Herein, is a description of the case of a 61-year-old man with multiple risk factors, including alcoholism, hypokalemia, malnutrition, and alcoholic liver cirrhosis, who developed ODS despite adherence to the recommended correction rate for hyponatremia. The patient presented to the emergency department with generalized weakness, gait disturbance, and decreased muscle strength. Initial laboratory investigations revealed severe hyponatremia, hypokalemia, and dehydration. The patient was treated with cautious correction of the hyponatremia below 8 mmol/L per day. However, on the seventh hospital day, he developed tremors, rigidity, and decreased consciousness and was diagnosed with osmotic demyelination syndrome. Despite receiving general supportive care, desmopressin, and dextrose 5% in water to reduce the serum sodium levels, the patient did not show significant improvement and was transferred to a nursing home for long-term conservative care on day 35 of hospitalization. This case report highlights the challenges associated with the diagnosis and management of osmotic demyelination syndrome and the importance of identifying patients at high risk of developing this neurological disorder.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"21 2","pages":"61-65"},"PeriodicalIF":0.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10751207/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139049451","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}
Seung Heon Lee, Sukyung Lee, Hyunsung Kim, Gheun-Ho Kim
{"title":"Pseudo-Gitelman Syndrome Presenting with Hypokalemic Metabolic Alkalosis and Hypocalciuria.","authors":"Seung Heon Lee, Sukyung Lee, Hyunsung Kim, Gheun-Ho Kim","doi":"10.5049/EBP.2023.21.2.72","DOIUrl":"10.5049/EBP.2023.21.2.72","url":null,"abstract":"<p><p>Pseudo-Bartter syndrome is a well-known differential diagnosis that needs to be excluded in cases of normotensive hypokalemic metabolic alkalosis. Pseudo-Bartter syndrome and pseudo-Gitelman syndrome are often collectively referred to as pseudo-Bartter/Gitelman syndrome; however, pseudo-Gitelman syndrome should be considered as a separate entity because Gitelman syndrome is characterized by hypocalciuria and hypomagnesemia, while Bartter syndrome is usually associated with hypercalciuria. Herein, we report the cases of two young adult female patients who presented with severe hypokalemic metabolic alkalosis, hypocalciuria, and hypomagnesemia. Diuretic or laxative abuse and self-induced vomiting were absent, and a chloride deficit and remarkable bicarbonaturia were observed. Initial sequencing studies for <i>SLC12A3</i>, <i>CLCKNB</i>, and <i>KCNJ10</i> revealed no mutations, and whole-exome sequencing revealed no pathogenic variants. The metabolic alkalosis was saline-responsive in one case, and steroid therapy was necessary in the other to relieve chronic tubulointerstitial nephritis, which was diagnosed with kidney biopsy. A new category of pseudo-Gitelman syndrome should be defined, and various etiologies should be investigated.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"21 2","pages":"72-76"},"PeriodicalIF":0.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10751206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139049452","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}
Yeonhee Lee, Kyung Don Yoo, Seon Ha Baek, Yang Gyun Kim, Hyo Jin Kim, Ji Young Ryu, Jin Hyuk Paek, Sang Heon Suh, Se Won Oh, Jeonghwan Lee, Jong Hyun Jhee, Jin-Soon Suh, Eun Mi Yang, Young Ho Park, Yae Lim Kim, Miyoung Choi, Kook-Hwan Oh, Sejoong Kim
{"title":"Korean Society of Nephrology 2022 Recommendations on Controversial Issues in Diagnosis and Management of Hyponatremia.","authors":"Yeonhee Lee, Kyung Don Yoo, Seon Ha Baek, Yang Gyun Kim, Hyo Jin Kim, Ji Young Ryu, Jin Hyuk Paek, Sang Heon Suh, Se Won Oh, Jeonghwan Lee, Jong Hyun Jhee, Jin-Soon Suh, Eun Mi Yang, Young Ho Park, Yae Lim Kim, Miyoung Choi, Kook-Hwan Oh, Sejoong Kim","doi":"10.5049/EBP.2022.20.1.21","DOIUrl":"https://doi.org/10.5049/EBP.2022.20.1.21","url":null,"abstract":"<p><p>The Korean Society for Electrolyte and Blood Pressure Research, in collaboration with the Korean Society of Nephrology, has published a clinical practice guideline (CPG) document for hyponatremia treatment. The document is based on an extensive evidence-based review of the diagnosis, evaluation, and treatment of hyponatremia with the multidisciplinary participation of representative experts in hyponatremia with methodologist support for guideline development. This CPG consists of 12 recommendations (two for diagnosis, eight for treatment, and two for special situations) based on eight detailed topics and nine key questions. Each recommendation begins with statements graded by the strength of the recommendations and the quality of the evidence. Each statement is followed by rationale supporting the recommendations. The committee issued conditional recommendations in favor of rapid intermittent bolus administration of hypertonic saline in severe hyponatremia, the use of vasopressin receptor antagonists in heart failure with hypervolemic hyponatremia, and syndrome of inappropriate antidiuresis with moderate to severe hyponatremia, the individualization of desmopressin use, and strong recommendation on the administration of isotonic fluids as maintenance fluid therapy in hospitalized pediatric patients. We hope that this CPG will provide useful recommendations in practice, with the aim of providing clinical support for shared decision-making to improve patient outcomes.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"20 1","pages":"21-38"},"PeriodicalIF":0.0,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/90/ae/ebp-20-21.PMC9685326.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40711516","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":"Practical Issues in the Management of Polycystic Kidney Disease: Blood Pressure and Water Balance.","authors":"Hayne Cho Park, Yun Kyu Oh","doi":"10.5049/EBP.2022.20.1.10","DOIUrl":"https://doi.org/10.5049/EBP.2022.20.1.10","url":null,"abstract":"<p><p>Autosomal dominant polycystic kidney disease is the most common hereditary renal disease affecting more than 13 million people worldwide. Renal function deteriorates as the cysts in both kidneys increase in number and size, which eventually results in end-stage kidney failure. Until recently, conservative management for chronic kidney disease such as blood pressure control, low sodium diet, adequate water intake, and weight control were known for the only treatment of polycystic kidney disease. However, the introduction of disease-modifying drug has led to the new paradigm shift in the management of polycystic kidney disease. Tolvaptan, the vasopressin V2 receptor antagonist, has been introduced to the patients with large kidneys since it can inhibit cyclic adenosine monophosphate, attenuates cyst growth, and delays renal failure. This article reviews the two important practical issues in the management of polycystic kidney disease: blood pressure and water balance. Firstly, the article will review the pathogenesis of high blood pressure in polycystic kidney disease and will demonstrate the current up-to-date management plan for blood pressure control. Secondly, this article will explain the mechanism of Tolvaptan on the treatment of polycystic kidney disease and its possible adverse effect on water and sodium balance.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"20 1","pages":"10-16"},"PeriodicalIF":0.0,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fd/91/ebp-20-10.PMC9685325.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40711514","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}
Ji-Eun Kim, Seun Deuk Hwang, Seoung Woo Lee, Joon Ho Song, Kipyo Kim
{"title":"Potassium Channel Syndrome Caused by Nicorandil in Chronic Kidney Disease: A Case Report and Literature Review.","authors":"Ji-Eun Kim, Seun Deuk Hwang, Seoung Woo Lee, Joon Ho Song, Kipyo Kim","doi":"10.5049/EBP.2022.20.1.17","DOIUrl":"https://doi.org/10.5049/EBP.2022.20.1.17","url":null,"abstract":"<p><p>Nicorandil is an anti-anginal drug that is commonly used in the treatment of ischemic heart disease. Nicorandil acts as a nitrate donor and ATP-sensitive potassium channel agonist, inducing coronary artery vasodilation. Potassium efflux through ATP-sensitive potassium channels activated by nicorandil can cause refractory hyperkalemia, particularly in patients with chronic kidney disease (CKD). Here, we report the case of an 85-year-old man who presented with severe refractory hyperkalemia, despite proper medical management. His serum potassium level increased from 4.96 to 7.21 mEq/L 7 days after restarting nicorandil. Hyperkalemia resolved shortly after discontinuation of nicorandil, which was presumed to be the offending drug. Previously, a few cases reported nicorandil-induced hyperkalemia called potassium channel syndrome in patients with CKD, and hyperkalemia can be reversed by ceasing nicorandil or using sulfonyl urea drugs. Given that CKD patients may have several contributing factors to this adverse event, clinicians should be aware of the risk of nicorandil-induced hyperkalemia, and medication review and drug discontinuation should be considered.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"20 1","pages":"17-20"},"PeriodicalIF":0.0,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/48/76/ebp-20-17.PMC9685324.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40711515","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}
Jong Hyun Jhee, Hyeong Cheon Park, Hoon Young Choi
{"title":"Skin Sodium and Blood Pressure Regulation.","authors":"Jong Hyun Jhee, Hyeong Cheon Park, Hoon Young Choi","doi":"10.5049/EBP.2022.20.1.1","DOIUrl":"https://doi.org/10.5049/EBP.2022.20.1.1","url":null,"abstract":"<p><p>Hypertension is a major public health concern due to its high prevalence and increased risk of cardiovascular disease and mortality. Complex traits resulting from both genetic and environmental factors affect the development of hypertension. Among environmental factors, a high salt diet is an important cause for hypertension. Humans show a heterogeneous blood pressure (BP) response to sodium intake. Although the precise mechanisms for the association between salt sensitivity and hypertension have not been fully elucidated, renal sodium handling has been considered to play a pivotal role. However, this conventional view has recently been challenged in that a third compartment, namely, skin may have a role in the regulation of sodium homeostasis. Skin is comprised of a significant portion of interstitium, which is a major extracellular fluid compartment, and its complex capillary network regulates body temperature and skin perfusion. Growing evidence indicates that local regulatory action of cutaneous blood flow as well as salt and water metabolism is associated with systemic BP control. Previous experimental studies have shown that dietary salt loading resulted in nonosmotic sodium accumulation via glycosaminoglycans and lymphatics embedded in the skin that were mediated by several endogenous factors and attenuated an increase in BP. Studies in humans have also suggested that the skin serves as a buffer system for sodium storage and that skin sodium contributes to salt sensitivity and hypertension. Thus, skin sodium storage provides the possibility of being an additional buffering system in response to salt loading and concomitant BP changes in humans.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"20 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/92/40/ebp-20-1.PMC9685327.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40711517","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}
Won Ki Kim, Taeho Lee, Ae Jin Kim, Han Ro, Jae Hyun Chang, Hyun Hee Lee, Wookyung Chung, Ji Yong Jung
{"title":"Adipsic Hypernatremia after Clipping of a Ruptured Aneurysm in the Anterior Communicating Artery: A Case Report.","authors":"Won Ki Kim, Taeho Lee, Ae Jin Kim, Han Ro, Jae Hyun Chang, Hyun Hee Lee, Wookyung Chung, Ji Yong Jung","doi":"10.5049/EBP.2021.19.2.56","DOIUrl":"https://doi.org/10.5049/EBP.2021.19.2.56","url":null,"abstract":"<p><p>Adipsia is a rare disorder that occurs due to damage to the osmoreceptor and not feeling thirst despite hyperosmolality. Adipsic hypernatremia can occur when there is damage to the anterior communicating artery that supplies blood to osmoreceptors, and the level of arginine vasopressin secretion varies widely. A 37-year-old woman, suffering from severe headache, was consulted to the nephrology department for hypernatremia and polyuria after clipping of a ruptured aneurysm in the anterior communicating artery. Despite her hypernatremic hyperosmolar state, she denied thirst and did not drink spontaneously. She was diagnosed adipsic hypernatremia by evaluating the osmoregulatory and baroregulatory function tests. Because adipsic hypernatremia is caused by not enough drinking water even for hyperosmolality due to the lack of thirst stimulus, the strategies of treatment are that setting the target body weight when serum osmolality is normal and have the patient drink water until patient reach the target body weight. Adipsic hypernatremia should be considered to be a rare complication of subarachnoid hemorrhage associated with an anterior communicating artery aneurysm.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"19 2","pages":"56-60"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2f/18/ebp-19-56.PMC8715226.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39800584","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":"Current Understanding of Pressure Natriuresis.","authors":"Eun Ji Baek, Sejoong Kim","doi":"10.5049/EBP.2021.19.2.38","DOIUrl":"https://doi.org/10.5049/EBP.2021.19.2.38","url":null,"abstract":"<p><p>Pressure natriuresis refers to the concept that increased renal perfusion pressure leads to a decrease in tubular reabsorption of sodium and an increased sodium excretion. The set point of blood pressure is the point at which pressure natriuresis and extracellular fluid volume are in equilibrium. The term \"abnormal pressure natriuresis\" usually refers to the expected abnormal effect of a certain level of blood pressure on sodium excretion. Factors that cause abnormal pressure natriuresis are known. Sympathetic nerve system, genetic factors, and dietary factors may affect an increase in renal perfusion pressure. An increase in renal perfusion pressure increases renal interstitial hydrostatic pressure (RIHP). Increased RIHP affects tubular reabsorption through alterations in tight junctional permeability to sodium in proximal tubules, redistribution of apical sodium transporters, and/or release of renal autacoids. Renal autocoids such as nitric oxide, prostaglandin E2, kinins, and angiotensin II may also regulate pressure natriuresis by acting directly on renal tubule sodium transport. In addition, inflammation and reactive oxygen species may mediate pressure natriuresis. Recently, the use of new drugs associated with pressure natriuretic mechanisms, such as angiotensin receptor neprilysin inhibitor and sodium glucose co-transporter 2 inhibitors, has been consistently demonstrated to reduce mortality and hypertension-related complications. Therefore, the understanding of pressure natriuresis is gaining attention as an antihypertensive strategy. In this review, we provide a basic overview of pressure natriuresis to the target audience of nephrologists.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"19 2","pages":"38-45"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e6/4d/ebp-19-38.PMC8715224.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39800581","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":"Metabolic Acidosis in Chronic Kidney Disease: Pathogenesis, Clinical Consequences, and Treatment.","authors":"Hyo Jin Kim","doi":"10.5049/EBP.2021.19.2.29","DOIUrl":"https://doi.org/10.5049/EBP.2021.19.2.29","url":null,"abstract":"<p><p>The kidneys play an important role in regulating the acid-base balance. Metabolic acidosis is common in chronic kidney disease (CKD) patients and can lead to poor outcomes, such as bone demineralization, muscle mass loss, and worsening of renal function. Metabolic acidosis is usually approached with evaluating the serum bicarbonate levels but should be assessed by counting blood pH. Current guidelines recommend oral bicarbonate supplementation to maintain the serum bicarbonate levels within the normal range. However, a slow decline in the glomerular filtration rate might occur, even though the serum bicarbonate levels were in the normal range. Because the serum bicarbonate levels decrease when metabolic acidosis advances, other biomarkers are necessary to indicate acid retention for early diagnosis of metabolic acidosis. For this, urine citrate and ammonium excretion may be used to follow the course of CKD patients. Metabolic acidosis can be treated with an increased fruit and vegetable intake and oral alkali supplementation. Previous studies have suggested that administration of oral sodium bicarbonate may preserve kidney function without significant increases in blood pressure and body weight. Veverimer, a non-absorbed, counterion-free, polymeric drug, is emerging to treat metabolic acidosis, but further researches are awaited. Further studies are also needed to clarify the target therapeutic range of serum bicarbonate and the drugs used for metabolic acidosis.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"19 2","pages":"29-37"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b7/23/ebp-19-29.PMC8715222.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39913672","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":"Venetoclax with Azacitidine Induced Tumor Lysis Syndrome in an Elderly Patient with Acute Myeloid Leukemia: A Case Report.","authors":"Mihee Kim, Hyun-Jin Bang, Ga-Young Song, Seo-Yeon Ahn, Sung-Hoon Jung, Yong-Su Song, Jae-Sook Ahn","doi":"10.5049/EBP.2021.19.2.46","DOIUrl":"https://doi.org/10.5049/EBP.2021.19.2.46","url":null,"abstract":"<p><p>Combination treatment with hypomethylating agents (HMAs) and venetoclax is being used increasingly in elderly patients with acute myeloid leukemia (AML). Venetoclax with HMAs has been reported to be associated with tumor lysis syndrome (TLS) in AML patients with high leukemic burden. We present a case of an elderly AML patient with low leukemic burden who developed TLS while receiving venetoclax and azacitidine (AZA). A 74-year-old man with newly diagnosed AML with NPM1 mutation received combination therapy with venetoclax and AZA in an outpatient clinic. Within 12 hours after starting venetoclax and AZA, the patient was admitted to the emergency room with fever, general weakness, and laboratory findings consistent with TLS. Based on our results, we recommend monitoring at the start of the treatment with venetoclax and HMAs to prevent and control TLS regardless of the leukemic burden and favorable genetic risk.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"19 2","pages":"46-50"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ad/0e/ebp-19-46.PMC8715223.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39800582","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}