J. Kopeć, M. Krzanowski, J. Królczyk, J. Jaworek-Troć, K. Krzanowska, W. Sułowicz
{"title":"慢性肾脏疾病患者的先天性门静脉缺失I型畸形。","authors":"J. Kopeć, M. Krzanowski, J. Królczyk, J. Jaworek-Troć, K. Krzanowska, W. Sułowicz","doi":"10.20452/pamw.3729","DOIUrl":null,"url":null,"abstract":"1012 as well as immunological markers were negative. On the basis of electroencephalography and head computed tomography (CT), the patient was di‐ agnosed with nonconvulsive epilepsy (treated with valproic acid). An abdominal CT scan re‐ vealed polysplenia (FIGURE 1A) and the absence of the portal vein (FIGURE 1B). It also showed that the splenic and intestinal venous blood flowed via the splenic and mesenteric veins to the in‐ ferior vena cava and to the left renal vein with‐ out passing through the liver (FIGURE 1C). On por‐ tovenography with the occlusion test (FIGURE 1D), the liver was not perfused with portal blood and the superior mesenteric vein and splenic vein did not join to form confluence (abernethy malfor‐ mation type IB). A 31 ‐year ‐old male patient with chronic membra‐ noproliferative glomerulonephritis (confirmed by biopsy) treated with immunosuppression (steroids, cyclosporine, mycophenolate mofetil) was admitted to the hospital due to nephrotic syndrome with chronic kidney disease stage 3 and coma (rigid pupils with bilateral Babinski sign). Blood tests revealed elevated concentra‐ tions of ammonia (288 μmol/l), serum creati‐ nine (258 μmol/l), urea (31.2 mmol/l), serum albumin (27 g/l), alanine aminotransferase (37 U/l), aspartate aminotransferase (30 U/l), biliru‐ bin (24 μmol/l), γ‐glutamyltranspeptidase (138 U/l), cholinesterase (3678 U/l), ceruloplasmin (0.26 g/l), and alkaline phosphatase (205 U/l). Se‐ rological markers for hepatitis A, B, C, G viruses, CLINICAL IMAGE","PeriodicalId":20343,"journal":{"name":"Polskie Archiwum Medycyny Wewnetrznej","volume":"21 1","pages":"1012-1013"},"PeriodicalIF":0.0000,"publicationDate":"2016-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"Abernethy malformation type I (congenital absence of the portal vein) in a patient with chronic kidney disease.\",\"authors\":\"J. Kopeć, M. Krzanowski, J. Królczyk, J. Jaworek-Troć, K. Krzanowska, W. Sułowicz\",\"doi\":\"10.20452/pamw.3729\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"1012 as well as immunological markers were negative. On the basis of electroencephalography and head computed tomography (CT), the patient was di‐ agnosed with nonconvulsive epilepsy (treated with valproic acid). An abdominal CT scan re‐ vealed polysplenia (FIGURE 1A) and the absence of the portal vein (FIGURE 1B). It also showed that the splenic and intestinal venous blood flowed via the splenic and mesenteric veins to the in‐ ferior vena cava and to the left renal vein with‐ out passing through the liver (FIGURE 1C). On por‐ tovenography with the occlusion test (FIGURE 1D), the liver was not perfused with portal blood and the superior mesenteric vein and splenic vein did not join to form confluence (abernethy malfor‐ mation type IB). A 31 ‐year ‐old male patient with chronic membra‐ noproliferative glomerulonephritis (confirmed by biopsy) treated with immunosuppression (steroids, cyclosporine, mycophenolate mofetil) was admitted to the hospital due to nephrotic syndrome with chronic kidney disease stage 3 and coma (rigid pupils with bilateral Babinski sign). Blood tests revealed elevated concentra‐ tions of ammonia (288 μmol/l), serum creati‐ nine (258 μmol/l), urea (31.2 mmol/l), serum albumin (27 g/l), alanine aminotransferase (37 U/l), aspartate aminotransferase (30 U/l), biliru‐ bin (24 μmol/l), γ‐glutamyltranspeptidase (138 U/l), cholinesterase (3678 U/l), ceruloplasmin (0.26 g/l), and alkaline phosphatase (205 U/l). Se‐ rological markers for hepatitis A, B, C, G viruses, CLINICAL IMAGE\",\"PeriodicalId\":20343,\"journal\":{\"name\":\"Polskie Archiwum Medycyny Wewnetrznej\",\"volume\":\"21 1\",\"pages\":\"1012-1013\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2016-12-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Polskie Archiwum Medycyny Wewnetrznej\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.20452/pamw.3729\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Polskie Archiwum Medycyny Wewnetrznej","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.20452/pamw.3729","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Abernethy malformation type I (congenital absence of the portal vein) in a patient with chronic kidney disease.
1012 as well as immunological markers were negative. On the basis of electroencephalography and head computed tomography (CT), the patient was di‐ agnosed with nonconvulsive epilepsy (treated with valproic acid). An abdominal CT scan re‐ vealed polysplenia (FIGURE 1A) and the absence of the portal vein (FIGURE 1B). It also showed that the splenic and intestinal venous blood flowed via the splenic and mesenteric veins to the in‐ ferior vena cava and to the left renal vein with‐ out passing through the liver (FIGURE 1C). On por‐ tovenography with the occlusion test (FIGURE 1D), the liver was not perfused with portal blood and the superior mesenteric vein and splenic vein did not join to form confluence (abernethy malfor‐ mation type IB). A 31 ‐year ‐old male patient with chronic membra‐ noproliferative glomerulonephritis (confirmed by biopsy) treated with immunosuppression (steroids, cyclosporine, mycophenolate mofetil) was admitted to the hospital due to nephrotic syndrome with chronic kidney disease stage 3 and coma (rigid pupils with bilateral Babinski sign). Blood tests revealed elevated concentra‐ tions of ammonia (288 μmol/l), serum creati‐ nine (258 μmol/l), urea (31.2 mmol/l), serum albumin (27 g/l), alanine aminotransferase (37 U/l), aspartate aminotransferase (30 U/l), biliru‐ bin (24 μmol/l), γ‐glutamyltranspeptidase (138 U/l), cholinesterase (3678 U/l), ceruloplasmin (0.26 g/l), and alkaline phosphatase (205 U/l). Se‐ rological markers for hepatitis A, B, C, G viruses, CLINICAL IMAGE