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In terms of personal background&#44; he was a smoker of 50 pack-years and had dyslipidaemia and arterial hypertension of several months&#8217; evolution&#46; His daily treatment included enalapril 20<span class="elsevierStyleHsp" style=""></span>mg&#44; atorvastatin 80<span class="elsevierStyleHsp" style=""></span>mg&#44; acetylsalicylic acid 100<span class="elsevierStyleHsp" style=""></span>mg and furosemide 60<span class="elsevierStyleHsp" style=""></span>mg&#46; The following results were obtained in the physical exploration&#58; blood pressure 120&#47;73<span class="elsevierStyleHsp" style=""></span>mmHg&#44; oxygen saturation 97&#37;&#44; pitting oedema as far as the knee&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">The analytical results were normal haemogram&#44; fibrinogen 706<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; D-dimer 1&#46;7 microg&#47;mL &#40;nv &#91;normal value&#93;&#58; 0&#46;3&#8211;0&#46;5&#41;&#44; rest of coagulation normal&#59; creatinine 1&#46;1<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; urea 39<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; albumin 2<span class="elsevierStyleHsp" style=""></span>g&#47;dL&#44; cholesterol 191<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; triglycerides 80<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; ions normal&#46; IgG 389<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; the other immunoglobulins were normal with no monoclonal component&#59; complements&#44; autoimmunity including anti-PLA2R&#44; thyroid hormones&#44; prostate-specific antigen &#40;PSA&#41;&#44; hepatitis markers&#44; human immunodeficiency virus &#40;HIV&#41; and normal or negative lues serology&#46; Proteinuria 6&#46;59<span class="elsevierStyleHsp" style=""></span>g&#47;24<span class="elsevierStyleHsp" style=""></span>h without a monoclonal component&#59; sediment with one to three red blood cells per field&#46; The electrocardiogram &#40;ECG&#41; and the echocardiogram were normal&#46; The computed tomography angiography &#40;CTA&#41; of the pulmonary arteries&#47;computed tomography &#40;CT&#41; of the chest showed a defect in the lateral segmental artery of the right basal pyramid consistent with pulmonary thromboembolism&#44; whereby anticoagulation was initiated &#40;suspended transiently as necessary&#41;&#59; a nodular opacity of 10<span class="elsevierStyleHsp" style=""></span>mm was also identified in the left upper lobe&#46; The lower extremity &#40;LE&#41; Doppler ultrasound identified an aneurysm of the left femoral&#47;popliteal arteries 2<span class="elsevierStyleHsp" style=""></span>cm in diameter&#44; partially thrombosed but no signs of deep vein thrombosis&#46; The renal artery abdominal ultrasound&#47;Doppler ultrasound showed no pathological findings in the renal echostructure&#44; nor renal artery thrombosis&#46; The thoracic-abdominal CT scan showed a 6-mm-thick mural thrombus in the infrarenal segment of the aorta &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; Ten glomeruli were identified by renal biopsy&#59; by optical microscopy and immunofluorescence lesions were compatible with membranous glomerulonephritis&#46; The gastroscopy was normal&#59; adenomas with low-grade dysplasia were identified in the colonoscopy and were resected&#46; A polypectomy of several low-grade dysplasia adenomas was performed&#46; In the thrombophilia study&#44; the results for anticardiolipin antibodies &#40;Ab&#41;&#44; lupus anticoagulant&#44; Factor V Leiden&#44; protein C and S and the prothrombin gene were negative or normal&#44; while antithrombin was 66&#37; &#40;NV 80&#37;&#8211;100&#37;&#41;&#44; and the ACII &#40;A384S&#41; heterozygous mutation was identified by means of the allele-specific polymerase chain reaction assay followed by restriction analysis&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">The pulmonary nodule was removed&#44; and the histological study showed an <span class="elsevierStyleItalic">in situ</span> bronchogenic carcinoma&#46; At discharge&#44; anticoagulation with low molecular weight heparin was maintained&#59; factor Xa levels showed adequate anticoagulation&#46; After one year of follow-up&#44; proteinuria of 6&#46;5<span class="elsevierStyleHsp" style=""></span>g in 24<span class="elsevierStyleHsp" style=""></span>h persisted&#44; with hypoalbuminaemia and preserved renal function&#44; negative anti-PLA2R&#44; with no tumour recurrence data&#44; and rituximab 1<span class="elsevierStyleHsp" style=""></span>g<span class="elsevierStyleHsp" style=""></span>&#215;<span class="elsevierStyleHsp" style=""></span>2 was subsequently given&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Antithrombin is the body&#8217;s most important physiological anticoagulant factor with a molecular weight similar to that of albumin and both levels are correlated in NS&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#8211;5</span></a> Antithrombin deficiency is present in 70&#37; of cases of NS<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> and promotes the multifactorial hypercoagulability status of this syndrome &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41; which usually induces venous thrombosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;7</span></a> On the other hand&#44; in NS&#44; AT is described in children and is usually in the lower extremities and coronary location&#59; aortic involvement is very rare and potentially catastrophic&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">8&#44;9</span></a> Some authors point to severe hypoalbuminaemia &#40;1&#46;6<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#41; and the use of diuretics and corticosteroids as risk factors&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;5</span></a> Membranous nephropathy is not necessarily the most frequent cause of NS associated with AT&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;4</span></a> Our patient with popliteal vein&#44; femoral artery and aortic thrombosis and ischaemic stroke had risk factors for AT such as dyslipidaemia&#44; high blood pressure and smoking&#44; and other thrombogenic diatheses involved in AT such as protein C and S deficiency or antiphospholipid syndrome were ruled out&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a></p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">Moreover&#44; ACII is due to a mutation in the antithrombin gene&#44; which is of autosomal dominant inheritance and has variable penetrance&#46; This mutation provokes a local functional and non-circulating deficiency of antithrombin and its prevalence is probably underestimated with routine diagnostic methods since it does not affect activity on the levels of the coagulation parameters&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> ACII is a moderate venous and arterial thrombotic risk factor<a class="elsevierStyleCrossRefs" href="#bib0045"><span class="elsevierStyleSup">9&#44;10</span></a>&#59; in this latter territory&#44; it appears to alter thrombin regulation capacity at the endothelial level&#46; This dysfunction would be boosted in situations of hypercoagulability&#44;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> such as NS and it could feasibly have played some kind of a role in this patient&#8217;s thromboses&#46; From the therapeutic standpoint&#44; in the presence of ACII&#44; unfractionated heparin has apparently less anticoagulant efficacy than low molecular weight heparin&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">The pathogenesis of arterial disease involves multiple genetic and environmental phenomena&#44; which is why&#44; in the presence of AT in NS&#44; diagnostic possibilities permitting&#44; the presence of pro-thrombotic genetic factors should be ruled out on account of their potential prognostic and therapeutic relevance&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0040" class="elsevierStylePara elsevierViewall">The authors declare that they received no funding&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflict of interest</span><p id="par0045" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflict of interest&#46;</p></span></span>"
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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Aortic thrombosis&#46;</p> <p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Axial computed tomography of the abdomen following administration of arterial-phase intravenous contrast&#44; showing a 32<span class="elsevierStyleHsp" style=""></span>&#215;<span class="elsevierStyleHsp" style=""></span>27-mm dilation of the infrarenal aorta&#44; with a small 6-mm-thick intramural thrombus on the posterior left aspect &#40;arrow&#41;&#46;</p>"
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          "leyenda" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">NS&#58; nephrotic syndrome&#59; DVT LE&#58; deep vein thrombosis of the lower extremities&#46;</p>"
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                  <table border="0" frame="\n
                  \t\t\t\t\tvoid\n
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                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
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                  \t\t\t\t"><span class="elsevierStyleBold"><span class="elsevierStyleItalic">Mechanisms</span>&#58;</span> increase of factors&#58; V&#44; VII&#44; von Willebrand&#44; alpha-2 plasmin inhibitor&#44; plasminogen activator inhibitor&#44; fibrinogen&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n
                  \t\t\t\t\ttable-entry\n
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                  \t\t\t\t"><span class="elsevierStyleHsp" style=""></span>Urinary losses&#58; antithrombin&#44; possibly protein C and S&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n
                  \t\t\t\t\ttable-entry\n
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                  \t\t\t\t\ttop\n
                  \t\t\t\t"><span class="elsevierStyleHsp" style=""></span>Increased platelet aggregation&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
                  \t\t\t\t\ttop\n
                  \t\t\t\t"><span class="elsevierStyleHsp" style=""></span>Reduction in plasminogen&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n
                  \t\t\t\t\ttable-entry\n
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                  \t\t\t\t"><span class="elsevierStyleBold"><span class="elsevierStyleItalic">Nephropathies involved</span>&#58;</span> membranous&#44; membrano-proliferative&#44; minimal changes&#44; sclerosing and focal&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
                  \t\t\t\t\ttop\n
                  \t\t\t\t"><span class="elsevierStyleBold"><span class="elsevierStyleItalic">Risk factors</span>&#58;</span> membranous<a class="elsevierStyleCrossRef" href="#tblfn0005"><span class="elsevierStyleSup">a</span></a>&#44; diuretics&#44; steroids&#44; repeated venepuncture&#44; neoplasms<a class="elsevierStyleCrossRef" href="#tblfn0005"><span class="elsevierStyleSup">a</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
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                  \t\t\t\t"><span class="elsevierStyleBold"><span class="elsevierStyleItalic">Venous location</span></span>&#58; renal vein &#40;35&#37;&#41;&#44; pulmonary thromboembolism &#40;8&#37;&#41;&#44; DVT LE &#40;10&#37;&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n
                  \t\t\t\t\ttable-entry\n
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                  \t\t\t\t"><span class="elsevierStyleBold"><span class="elsevierStyleItalic">Arterial location&#58;</span></span> renal&#44; aortic&#44; femoral&#44; cerebral&#44; mesenteric&#44; coronary&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
                  \t\t\t\t\ttop\n
                  \t\t\t\t"><span class="elsevierStyleBold"><span class="elsevierStyleItalic">Prophylactic anticoagulation&#58;</span></span> in case of albuminuria &#60;2<span class="elsevierStyleHsp" style=""></span>g&#47;dL&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
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              "nota" => "<p class="elsevierStyleNotepara" id="npar0005">They favour preferentially venous thromboses&#46;</p>"
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        "descripcion" => array:1 [
          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Hypercoagulability of NS&#46;</p>"
        ]
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    ]
    "bibliografia" => array:2 [
      "titulo" => "References"
      "seccion" => array:1 [
        0 => array:2 [
          "identificador" => "bibs0005"
          "bibliografiaReferencia" => array:10 [
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              "etiqueta" => "1"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Hypercoagulability&#44; renal vein thrombosis&#44; and other thrombotic complications of nephrotic syndrome"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:1 [
                            0 => "F&#46; Llach"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:2 [
                      "doi" => "10.1038/ki.1985.149"
                      "Revista" => array:6 [
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                        "fecha" => "1985"
                        "volumen" => "28"
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                            "web" => "Medline"
                          ]
                        ]
                      ]
                    ]
                  ]
                ]
              ]
            ]
            1 => array:3 [
              "identificador" => "bib0010"
              "etiqueta" => "2"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Arterial thrombosis associated with nephrotic syndrome&#8212;a case report and review &#40;adult cases in the English literature&#41;"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:6 [
                            0 => "H&#46;J&#46; Kim"
                            1 => "C&#46;H&#46; Park"
                            2 => "C&#46;M&#46; Kang"
                            3 => "H&#46;C&#46; Park"
                            4 => "C&#46;Y&#46; Kim"
                            5 => "Y&#46;S&#46; Cho"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:2 [
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                            "web" => "Medline"
                          ]
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                    ]
                  ]
                ]
              ]
            ]
            2 => array:3 [
              "identificador" => "bib0015"
              "etiqueta" => "3"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Arterial thrombosis in the nephrotic syndrome"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:4 [
                            0 => "I&#46;H&#46; Fahal"
                            1 => "P&#46; McClelland"
                            2 => "C&#46;R&#46; Hay"
                            3 => "G&#46;M&#46; Bell"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:2 [
                      "doi" => "10.1136/pgmj.70.830.905"
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            3 => array:3 [
              "identificador" => "bib0020"
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              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Thrombose art&#233;rielle r&#233;cidivante de l&#8217;adulte au cours du syndrome n&#233;phrotique&#46; A propos d&#8217;un cas et revue de la litt&#233;rature"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:5 [
                            0 => "J&#46;C&#46; Farkas"
                            1 => "C&#46; Jacquot"
                            2 => "G&#46; Tabet"
                            3 => "C&#46; Laurian"
                            4 => "J&#46;M&#46; Cormier"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:1 [
                      "Revista" => array:6 [
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                          ]
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            ]
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              "identificador" => "bib0025"
              "etiqueta" => "5"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Acute arterial thrombosis with antithrombin III deficiency in nephrotic syndrome&#58; report of a case"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:5 [
                            0 => "M&#46; Nishimura"
                            1 => "J&#46; Shimada"
                            2 => "K&#46; Ito"
                            3 => "H&#46; Kawachi"
                            4 => "K&#46; Nishiyama"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:2 [
                      "doi" => "10.1007/s005950070110"
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            5 => array:3 [
              "identificador" => "bib0030"
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                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Venous thrombosis in the nephrotic syndrome"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
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                          ]
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                    0 => array:2 [
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                        "fecha" => "2013"
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                            "web" => "Medline"
                          ]
                        ]
                      ]
                    ]
                  ]
                ]
              ]
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Letter to the Editor
Arterial thrombosis in a patient with nephrotic syndrome and antithrombin Cambrigde II
Trombosis arteriales en un paciente con síndrome nefrótico y antitrombina Cambrigde II
Ana Esther Sirventa,
Corresponding author
anaesipe@gmail.com

Corresponding author.
, Giomar Urzola-Rodrígueza, Alicia Lorenzob, Ramiro Callejas-Martíneza, Ana Saizc, Leonardo Calle-Garcíaa, Álvaro Molina-Ordása, Astrid Rodríguez-Gómeza, Carmen Martin-Varasa, María José Fernández-Reyes-Luisa
a Servicio de Nefrología, Complejo Asistencial de Segovia, Segovia, Spain
b Servicio de Hematología, Complejo Asistencial de Segovia, Segovia, Spain
c Servicio de Anatomía Patológica, Hospital Universitario Ramón y Cajal, Madrid, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Thromboembolic phenomena are a serious complication of nephrotic syndrome &#40;NS&#41; with a general incidence of 20&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> However&#44; arterial thromboses &#40;AT&#41; are rare in adults&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;2</span></a> In this document&#44; we describe multiple AT in an adult with NS&#46; The genetic study pointed to an antithrombin Cambridge II &#40;ACII&#41; mutation&#46; To our knowledge&#44; this is the first case of NS with AT associated with this genetic thrombophilia&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">The patient is a 73-year-old male who consulted for oedemas coursing for two to three weeks and re-exacerbation of dyspnoea in the previous few hours&#46; Four weeks before he presented a right parietal lobe stroke &#40;albuminaemia 2&#46;7<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#41;&#46; In terms of personal background&#44; he was a smoker of 50 pack-years and had dyslipidaemia and arterial hypertension of several months&#8217; evolution&#46; His daily treatment included enalapril 20<span class="elsevierStyleHsp" style=""></span>mg&#44; atorvastatin 80<span class="elsevierStyleHsp" style=""></span>mg&#44; acetylsalicylic acid 100<span class="elsevierStyleHsp" style=""></span>mg and furosemide 60<span class="elsevierStyleHsp" style=""></span>mg&#46; The following results were obtained in the physical exploration&#58; blood pressure 120&#47;73<span class="elsevierStyleHsp" style=""></span>mmHg&#44; oxygen saturation 97&#37;&#44; pitting oedema as far as the knee&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">The analytical results were normal haemogram&#44; fibrinogen 706<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; D-dimer 1&#46;7 microg&#47;mL &#40;nv &#91;normal value&#93;&#58; 0&#46;3&#8211;0&#46;5&#41;&#44; rest of coagulation normal&#59; creatinine 1&#46;1<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; urea 39<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; albumin 2<span class="elsevierStyleHsp" style=""></span>g&#47;dL&#44; cholesterol 191<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; triglycerides 80<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; ions normal&#46; IgG 389<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; the other immunoglobulins were normal with no monoclonal component&#59; complements&#44; autoimmunity including anti-PLA2R&#44; thyroid hormones&#44; prostate-specific antigen &#40;PSA&#41;&#44; hepatitis markers&#44; human immunodeficiency virus &#40;HIV&#41; and normal or negative lues serology&#46; Proteinuria 6&#46;59<span class="elsevierStyleHsp" style=""></span>g&#47;24<span class="elsevierStyleHsp" style=""></span>h without a monoclonal component&#59; sediment with one to three red blood cells per field&#46; The electrocardiogram &#40;ECG&#41; and the echocardiogram were normal&#46; The computed tomography angiography &#40;CTA&#41; of the pulmonary arteries&#47;computed tomography &#40;CT&#41; of the chest showed a defect in the lateral segmental artery of the right basal pyramid consistent with pulmonary thromboembolism&#44; whereby anticoagulation was initiated &#40;suspended transiently as necessary&#41;&#59; a nodular opacity of 10<span class="elsevierStyleHsp" style=""></span>mm was also identified in the left upper lobe&#46; The lower extremity &#40;LE&#41; Doppler ultrasound identified an aneurysm of the left femoral&#47;popliteal arteries 2<span class="elsevierStyleHsp" style=""></span>cm in diameter&#44; partially thrombosed but no signs of deep vein thrombosis&#46; The renal artery abdominal ultrasound&#47;Doppler ultrasound showed no pathological findings in the renal echostructure&#44; nor renal artery thrombosis&#46; The thoracic-abdominal CT scan showed a 6-mm-thick mural thrombus in the infrarenal segment of the aorta &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; Ten glomeruli were identified by renal biopsy&#59; by optical microscopy and immunofluorescence lesions were compatible with membranous glomerulonephritis&#46; The gastroscopy was normal&#59; adenomas with low-grade dysplasia were identified in the colonoscopy and were resected&#46; A polypectomy of several low-grade dysplasia adenomas was performed&#46; In the thrombophilia study&#44; the results for anticardiolipin antibodies &#40;Ab&#41;&#44; lupus anticoagulant&#44; Factor V Leiden&#44; protein C and S and the prothrombin gene were negative or normal&#44; while antithrombin was 66&#37; &#40;NV 80&#37;&#8211;100&#37;&#41;&#44; and the ACII &#40;A384S&#41; heterozygous mutation was identified by means of the allele-specific polymerase chain reaction assay followed by restriction analysis&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">The pulmonary nodule was removed&#44; and the histological study showed an <span class="elsevierStyleItalic">in situ</span> bronchogenic carcinoma&#46; At discharge&#44; anticoagulation with low molecular weight heparin was maintained&#59; factor Xa levels showed adequate anticoagulation&#46; After one year of follow-up&#44; proteinuria of 6&#46;5<span class="elsevierStyleHsp" style=""></span>g in 24<span class="elsevierStyleHsp" style=""></span>h persisted&#44; with hypoalbuminaemia and preserved renal function&#44; negative anti-PLA2R&#44; with no tumour recurrence data&#44; and rituximab 1<span class="elsevierStyleHsp" style=""></span>g<span class="elsevierStyleHsp" style=""></span>&#215;<span class="elsevierStyleHsp" style=""></span>2 was subsequently given&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Antithrombin is the body&#8217;s most important physiological anticoagulant factor with a molecular weight similar to that of albumin and both levels are correlated in NS&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#8211;5</span></a> Antithrombin deficiency is present in 70&#37; of cases of NS<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> and promotes the multifactorial hypercoagulability status of this syndrome &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41; which usually induces venous thrombosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;7</span></a> On the other hand&#44; in NS&#44; AT is described in children and is usually in the lower extremities and coronary location&#59; aortic involvement is very rare and potentially catastrophic&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">8&#44;9</span></a> Some authors point to severe hypoalbuminaemia &#40;1&#46;6<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#41; and the use of diuretics and corticosteroids as risk factors&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;5</span></a> Membranous nephropathy is not necessarily the most frequent cause of NS associated with AT&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;4</span></a> Our patient with popliteal vein&#44; femoral artery and aortic thrombosis and ischaemic stroke had risk factors for AT such as dyslipidaemia&#44; high blood pressure and smoking&#44; and other thrombogenic diatheses involved in AT such as protein C and S deficiency or antiphospholipid syndrome were ruled out&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a></p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">Moreover&#44; ACII is due to a mutation in the antithrombin gene&#44; which is of autosomal dominant inheritance and has variable penetrance&#46; This mutation provokes a local functional and non-circulating deficiency of antithrombin and its prevalence is probably underestimated with routine diagnostic methods since it does not affect activity on the levels of the coagulation parameters&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> ACII is a moderate venous and arterial thrombotic risk factor<a class="elsevierStyleCrossRefs" href="#bib0045"><span class="elsevierStyleSup">9&#44;10</span></a>&#59; in this latter territory&#44; it appears to alter thrombin regulation capacity at the endothelial level&#46; This dysfunction would be boosted in situations of hypercoagulability&#44;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> such as NS and it could feasibly have played some kind of a role in this patient&#8217;s thromboses&#46; From the therapeutic standpoint&#44; in the presence of ACII&#44; unfractionated heparin has apparently less anticoagulant efficacy than low molecular weight heparin&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">The pathogenesis of arterial disease involves multiple genetic and environmental phenomena&#44; which is why&#44; in the presence of AT in NS&#44; diagnostic possibilities permitting&#44; the presence of pro-thrombotic genetic factors should be ruled out on account of their potential prognostic and therapeutic relevance&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0040" class="elsevierStylePara elsevierViewall">The authors declare that they received no funding&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflict of interest</span><p id="par0045" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflict of interest&#46;</p></span></span>"
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                  \t\t\t\t"><span class="elsevierStyleBold"><span class="elsevierStyleItalic">Mechanisms</span>&#58;</span> increase of factors&#58; V&#44; VII&#44; von Willebrand&#44; alpha-2 plasmin inhibitor&#44; plasminogen activator inhibitor&#44; fibrinogen&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleHsp" style=""></span>Urinary losses&#58; antithrombin&#44; possibly protein C and S&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleHsp" style=""></span>Increased platelet aggregation&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleHsp" style=""></span>Reduction in plasminogen&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleBold"><span class="elsevierStyleItalic">Nephropathies involved</span>&#58;</span> membranous&#44; membrano-proliferative&#44; minimal changes&#44; sclerosing and focal&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleBold"><span class="elsevierStyleItalic">Risk factors</span>&#58;</span> membranous<a class="elsevierStyleCrossRef" href="#tblfn0005"><span class="elsevierStyleSup">a</span></a>&#44; diuretics&#44; steroids&#44; repeated venepuncture&#44; neoplasms<a class="elsevierStyleCrossRef" href="#tblfn0005"><span class="elsevierStyleSup">a</span></a>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleBold"><span class="elsevierStyleItalic">Venous location</span></span>&#58; renal vein &#40;35&#37;&#41;&#44; pulmonary thromboembolism &#40;8&#37;&#41;&#44; DVT LE &#40;10&#37;&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleBold"><span class="elsevierStyleItalic">Arterial location&#58;</span></span> renal&#44; aortic&#44; femoral&#44; cerebral&#44; mesenteric&#44; coronary&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleBold"><span class="elsevierStyleItalic">Prophylactic anticoagulation&#58;</span></span> in case of albuminuria &#60;2<span class="elsevierStyleHsp" style=""></span>g&#47;dL&nbsp;\t\t\t\t\t\t\n
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                      "doi" => "10.1038/ki.1985.149"
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                        "tituloSerie" => "Kidney Int"
                        "fecha" => "1985"
                        "volumen" => "28"
                        "paginaInicial" => "429"
                        "paginaFinal" => "439"
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        "texto" => "<p id="par0050" class="elsevierStylePara elsevierViewall">Our thanks to Dr Jaime Corral&#44; who performed the antithrombin genetic study&#44; and to Dr Ricardo Enr&#237;quez for his collaboration&#46;</p>"
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ISSN: 20132514
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