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This was consistent with acute myeloblastic leukaemia that was probably promyelocytic and a myelogram was subsequently performed&#44; which confirmed promyelocytic cell infiltration&#46; A cytogenetic study was carried out&#44; which confirmed translocation &#40;t15&#59;17&#41;&#46; On the same day&#44; we were consulted because the patient had sudden abdominal pain at the lumbar level during the night&#44; with oligoanuria&#46; We reviewed the peripheral blood smear&#44; in which we detected significant schistocytosis at around 8&#37;&#46; In this context&#44; the diagnosis of thrombotic microangiopathy was likely&#46; On 27 April 2013 we performed a computerised tomography &#40;CT&#41; scan of the abdomen&#44; which revealed a perfusion defect bilaterally at the renal cortex level with permeable renal arteries and veins&#44; consistent with cortical necrosis&#46; We also performed a renal scintigraphy&#44; which was indicative of cortical necrosis&#46; In the test carried out 6 hours later&#44; the patient already displayed sediment with microscopic haematuria and proteinuria of 100mg&#47;dl&#59; the blood test displayed Pcr of 4&#46;6mg&#47;dl&#44; with a slight elevation in liver enzymes&#44; with ultra-sensitive C-reactive protein &#40;CRP&#41; of 165mg&#47;l&#44; total bilirubin of 5&#46;9mg&#47;dl&#44; with coagulation &#40;D-dimer of 36mg&#47;l&#44; prothrombin activity of 53&#37;&#44; with the rest being normal&#41;&#44; normal direct and indirect Coombs tests&#44; and therefore&#44; given the high clinical suspicion of haemolytic-uraemic syndrome &#40;HUS&#41;&#44; we started treatment with daily plasmapheresis with 5 litres of fresh frozen plasma &#40;1&#46;5 plasma volumes&#41;&#44; with hypotensive therapy&#44; given the progressive increase in blood pressure&#58; 120&#47;70 to 170&#47;90mmHg&#46; The next day&#44; the patient remained oliguric with Pcr of 7mg&#47;dl and high blood pressure &#40;160&#47;80mmHg&#41;&#44; and therefore we began haemodialysis &#40;first session&#58; 28 April 2013&#41;&#46; We carried out a total of 12 plasmapheresis sessions &#40;7 consecutive and 5 on alternate days&#41;&#44; until haemolysis disappeared &#40;a decrease in lactate dehydrogenase &#91;LDH&#93;&#44; indirect bilirubin and schistocytes &#91;Figure 1&#93;&#44; along with an increase in haptoglobin&#58; mg&#47;dl &#91;70 &#40;1 May 2013 &#41; to 75 &#40; 13 May 2013 &#41; to 217 &#40;17 June 2013 &#41;&#93;&#44; and platelets&#41;&#46; On 1 May 2013&#44; after the fifth plasmapheresis session&#44; the patient had severe respiratory failure with mild haemoptysis and decreased consciousness&#44; and as such he was transferred to the intensive care unit &#40;ICU&#41;&#44; where he continued with plasmapheresis and haemodialysis&#46; In the ICU&#44; mechanical ventilation was required and a lung scintigraphy was carried out due to suspected pulmonary infarction with no signs of pulmonary thromboembolism&#59; a CT scan of the head was also performed&#46; Finally&#44; the patient left the ICU four days later spontaneously breathing with a respiratory infection due to <span class="elsevierStyleItalic">Acinetobacter </span>and <span class="elsevierStyleItalic">Pseudomona aeruginosa</span> and a urinary infection due to <span class="elsevierStyleItalic">Acinetobacter baumanii</span>&#46; The clinical response to chemotherapy with ATRA and idarubicin was satisfactory and the patient showed a good response to treatment&#46; He was discharged by haematology on 18 June 2013 with revisions in outpatient clinics&#46;</p><p class="elsevierStylePara">From the renal point of view&#44; the patient remained anuric thereafter and required haemodialysis&#44; without any sign of recovery&#46; We carried out a control CT angiogram&#44; which displayed cortical hypoperfusion&#46; Once platelet levels normalised with chemotherapy&#44; we performed a percutaneous renal biopsy &#40;7 June 2013&#41;&#58; 19 glomeruli&#44; 16 of which displayed severe changes typical of coagulative necrosis with complete destruction of all cellular elements secondary to ischaemia&#46; In three of them&#44; we observed the same signs&#44; but with preservation of their nuclei&#44; as well as mesangiolysis&#44; thickening of the membranes with the presence of red blood cells &#40;schistocytes&#41;&#44; and occasional neutrophils &#40;PMN&#41; without double contours or crescents or fibrinoid necrosis the glomerular capillary or the afferent arteriole&#46; In the interstitial area&#44; there was diffuse cortical necrosis with the presence&#44; in the cortico-medullary and medullary junction&#44; of tubules with red blood cell casts&#44; haemosiderin pigment&#44; cellular ischaemic changes with brush border loss and marked nuclear atypia and chronic inflammatory infiltrate and mild fibrosis patches&#46; At vascular level&#44; there were arteries with a medium-sized diameter&#44; the presence of intimal mucoid degeneration with luminal occlusion and incipient myointimal fibrous changes&#44; which confirmed the diagnosis of coagulative cortical necrosis with vascular changes consistent with HUS &#40;Figures 2 and 3&#41; and as such&#44; given the low expectation of renal recovery&#44; we requested an assessment by Vascular Surgery for a vascular access&#44; with the patient being included in a renal replacement programme through regular haemodialysis&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Diagnosis</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Renal failure due to bilateral renal cortical necrosis caused by ischaemia due to thrombotic microangiopathy in the context of acute myeloid leukaemia with myeloid crisis&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Cortical necrosis accounts for less than 2&#37; of all causes of acute renal failure in adults and represents 15&#37;-20&#37; of acute renal failure in the third trimester of pregnancy&#46; Renal cortical necrosis may have several degrees of extension&#58; minimal&#44; focal and massive and may be unilateral or bilateral&#46; Our patient&#8217;s necrosis was bilateral and massive&#44; given his poor clinical progression&#46; Generally&#44; the subcapsular and juxtamedullary cortical tissue is preserved&#44; except in cortical necrosis due to rejection&#44; in which the whole cortex tissue can become necrotic&#46;<span class="elsevierStyleSup">1&#44;2</span></p><p class="elsevierStylePara">Its most common causes include obstetric complications &#40;50&#37;-70&#37;&#41;&#44; and non-obstetric causes represent the remaining 20&#37;-30&#37;&#46; Premature placental abruption is the most common obstetric cause&#46; HUS is the most common non-obstetric cause &#40;around 50&#37;-70&#37; of the cases&#41;&#44; followed by septic situations&#46; Other causes are severe dehydration&#44; acute and hyperacute kidney rejection&#44; biological venoms and ethylene glycol&#44; etc&#46;</p><p class="elsevierStylePara">The exact mechanism behind renal cortical necrosis is unknown&#46; It is caused by a significant decrease in renal arterial perfusion secondary to vascular spasm&#44; or microvascular injury or intravascular coagulation&#44; and it is the pathological progression of acute tubular necrosis that results in cortical necrosis&#46; Clinically&#44; it usually presents with anuria&#44; and requires haemodialysis on most occasions&#46; Among the diagnostic tests&#44; imaging tests play a key role in preventing the risk of bleeding involved in renal biopsies in these patients&#44; due to their common clotting disorders&#46; The technique normally used to carry out the diagnosis is angiography&#44; which in addition to being a diagnostic tool is also useful for the prognosis of renal function&#44; since better renal perfusion results in a better prognosis of recovery&#46; However&#44; CT angiography or renal scintigraphy are also valid techniques that are useful for diagnosis&#46;<span class="elsevierStyleSup">3</span> Its prognosis is poor&#44; with a mortality rate of around 50&#37;&#46; The calcium deposits observed in the renal cortex suggest renal cortical necrosis&#44; but the latter appear late in the course of the disease as a result of chronicity and are only found in 20&#37;-50&#37; of cases&#46;<span class="elsevierStyleSup">4-7</span></p><p class="elsevierStylePara">In the prodromal phase of atypical HUS upper respiratory infection &#40;23&#37;&#41;&#44; unclassified fever &#40;46&#37;&#41; as our patient displayed&#44; and vomiting &#40;81&#37;&#41; have been observed&#46; The histological lesion characteristic of atypical HUS is arterial thrombotic microangiopathy&#44; while in the typical HUS group the most common lesion was glomerular thrombotic microangiopathy&#44; which corresponds to that observed in our patient&#46; Renal cortical necrosis is the most serious complication in this profile and most patients require dialysis&#46;<span class="elsevierStyleSup">8&#44;9</span></p><p class="elsevierStylePara">In summary&#44; we must say that&#44; with regard to the microangiopathy that the patient displayed&#44; in the context of the blast crisis&#44; HUS was secondary to a tumour process&#44; and that the aforementioned explosion of atypical cells resulted in the acute situation&#44; which led to renal failure due to renal cortical necrosis&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12162&#95;16025&#95;53035&#95;en&#95;f112&#46;12162&#95;02&#46;jpg" class="elsevierStyleCrossRefs"><img src="12162_16025_53035_en_f112.12162_02.jpg" alt="Graph showing progression&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Graph showing progression&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12162&#95;16025&#95;53036&#95;en&#95;f212&#46;12162&#95;02&#46;jpg" class="elsevierStyleCrossRefs"><img src="12162_16025_53036_en_f212.12162_02.jpg" alt="Renal cast&#46;"></img></a></p><p class="elsevierStylePara">Figure 2&#46; Renal cast&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12162&#95;16025&#95;53037&#95;en&#95;f312&#46;12162&#95;02&#46;jpg" class="elsevierStyleCrossRefs"><img src="12162_16025_53037_en_f312.12162_02.jpg" alt="Image of a typical artery in secondary haemolitic uraemic syndrome&#46;"></img></a></p><p class="elsevierStylePara">Figure 3&#46; Image of a typical artery in secondary haemolitic uraemic syndrome&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">Presentamos el caso de un paciente de 37 a&#241;os que ingresa a cargo de Hematolog&#237;a&#44; trasladado desde las Urgencias de Otorrinolaringolog&#237;a&#44; donde hab&#237;a acudido por amigdalitis&#46; All&#237; se demuestra anemia y leucopenia e ingresa con agranulocitosis en estudio&#46; Un d&#237;a m&#225;s tarde el paciente presenta crisis bl&#225;stica&#44; y se le diagnostica de leucemia aguda con crisis mieloide&#46; En dicha situaci&#243;n de crisis bl&#225;stica el paciente inicia un cuadro de dolor lumbar brusco&#44; con oliguria y deterioro de la funci&#243;n renal&#44; seguido de anemizaci&#243;n&#44; en el contexto de un cuadro de hem&#243;lisis compatible con microangiopat&#237;a tromb&#243;tica&#44; por lo que somos consultados&#46; Se inicia tratamiento con plasmaf&#233;resis y al d&#237;a siguiente hemodi&#225;lisis &#40;se realiza un total de 12 sesiones de plasmaf&#233;resis&#44; hasta desaparecer los datos de hem&#243;lisis&#41;&#46; Cinco d&#237;as m&#225;s tarde presenta cuadro de insuficiencia respiratoria&#44; por el que pasa a la Unidad de Cuidados Intensivos&#44; donde contin&#250;a con plasmaf&#233;resis y hemodi&#225;lisis&#46; El paciente se mantiene en anuria desde entonces&#44; con necesidad de hemodi&#225;lisis&#44; sin ning&#250;n signo de recuperaci&#243;n renal&#46; Una vez normalizadas las plaquetas&#44; con tratamiento quimioter&#225;pico hematol&#243;gico&#44; se realiza biopsia renal percut&#225;nea&#44; que confirma el diagn&#243;stico de necrosis cortical&#46; Finalmente el paciente queda incluido en programa sustitutivo de la funci&#243;n renal mediante hemodi&#225;lisis peri&#243;dica&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">A 37-year-old patient was transferred to Haematology from the ENT Emergency Department where he had been admitted due to tonsillitis&#46; He displayed anaemia and leukopenia and had agranulocytosis in the study&#46; A day later the patient had blast crisis&#44; and was diagnosed with myeloid acute leukaemia&#46; Due to blast crisis the patient experienced sudden back pain&#44; with oliguria and renal function deterioration followed by anaemia&#44; in the context of haemolysis consistent with thrombotic microangiopathy&#44; and as such&#44; we were consulted&#46; We began treatment with plasmapheresis and on the following day we performed haemodialysis &#40;we carried out a total of 12 sessions of plasmapheresis until haemolysis disappeared&#41;&#46; Five days later there was respiratory failure&#44; and the patient was consequently transferred to the Intensive Care Unit&#44; where he continued treatment with plasmapheresis and haemodialysis&#46; The patient remained anuric thereafter&#44; requiring haemodialysis&#44; with no sign of renal recovery&#46; Once platelet levels normalised with haematology chemotherapy&#44; a percutaneous renal biopsy was performed&#44; which confirmed the diagnosis of cortical necrosis&#46; Finally&#44; the patient underwent renal replacement therapy by regular haemodialysis&#46;</p>"
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Renal cortical necrosis secondary to thrombotic microangiopathy in the context of acute promyelocytic leukaemia blast crisis
Necrosis cortical renal secundaria a microangiopatía trombótica en el contexto de crisis blástica de leucemia aguda promielocítica
MANUEL Polaina Rusilloa, Manuel Polaina-Rusillob, MARIA DEL PILAR Pérez del Barrioa, M. del Pilar Pérez-del Barriob, ANA MARIA CARRILLO COLMENEROc, Ana M. Carrillo-Colmenerod, CESAR Ramírez-Tortosae, César Ramírez-Tortosaf, JOSEFA Borrego Hinojosaa, Josefa Borrego-Hinojosab, ANTONIO Liébana Cañadaa, Antonio Liébana-Cañadab
a Servicio de Nefrología, Complejo Hospitalario de Jaén, JAEN, JAEN, Spain,
b Servicio de Nefrología, Complejo Hospitalario de Jaén,
c Servicio de Radiología, Complejo Hospitalario de Jaén, JAEN, JAEN, Spain,
d Servicio de Radiología, Complejo Hospitalario de Jaén,
e SERVICIO DE ANATOMIA PATOLOGICA, Complejo Hospitalario de Jaén, JAEN, JAEN, Spain,
f Servicio de Anatomía Patológica, Complejo Hospitalario de Jaén,
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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Case study</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Our patient is a 37-year-old male without any relevant medical history&#44; except for recurrent tonsillitis&#44; being an ex-smoker and occasional cannabis user&#46; He came to the Emergency Department due to severe odynophagia lasting 24 hours&#46; Upon physical examination&#44; there was nothing remarkable&#44; except that the patient was slightly overweight &#40;body mass index&#58; 29kg&#47;m<span class="elsevierStyleSup">2</span>&#41;&#44; with hyperaemic tonsils&#46; Given the patient&#8217;s poor general condition&#44; low-grade fever &#40;37&#46;3&#186;C&#41; and tonsils that inhibited swallowing&#44; it was decided to admit the patient to the ENT Department on 25 April 2013&#46;</p><p class="elsevierStylePara">The day after admission&#44; the patient was transferred to Haematology due to agranulocytosis in the study&#44; after the test showed mild anaemia &#40;haemoglobin &#91;Hb&#93; 11&#46;9g&#47;dl&#41;&#44; leukopenia &#40;340&#47;l&#41;&#44; platelets 270&#44;000&#47;l&#44; with plasma creatinine &#40;PCr&#41; of 0&#46;9mg&#47;dl&#44; normal coagulation&#44; with an extension in peripheral blood with neutropenia&#44; without dysmorphias or immature cells&#44; with borderline macrocytosis and normal platelets&#46; Throat cultures were taken along with cytomegalovirus&#44; Epstein-Barr&#44; rubella&#44; toxoplasmosis&#44; human immunodeficiency virus and herpes serologies&#44; which were negative&#46;</p><p class="elsevierStylePara">The day after the transfer&#44; a control test showed 8290 leukocytes&#44; Hb of 11g&#47;dl&#44; 20&#44;000&#47;l platelets&#44; urea of 59mg&#47;dl and Pcr of 2&#46;3mg&#47;dl&#46; A peripheral blood smear was taken again&#44; in which a pathological population of immature cells was detected with a myeloid appearance and intense granulation&#46; Some of them had a 2-lobed cleft nucleus and erythroblastosis with atypical promyelocytes&#46; This was consistent with acute myeloblastic leukaemia that was probably promyelocytic and a myelogram was subsequently performed&#44; which confirmed promyelocytic cell infiltration&#46; A cytogenetic study was carried out&#44; which confirmed translocation &#40;t15&#59;17&#41;&#46; On the same day&#44; we were consulted because the patient had sudden abdominal pain at the lumbar level during the night&#44; with oligoanuria&#46; We reviewed the peripheral blood smear&#44; in which we detected significant schistocytosis at around 8&#37;&#46; In this context&#44; the diagnosis of thrombotic microangiopathy was likely&#46; On 27 April 2013 we performed a computerised tomography &#40;CT&#41; scan of the abdomen&#44; which revealed a perfusion defect bilaterally at the renal cortex level with permeable renal arteries and veins&#44; consistent with cortical necrosis&#46; We also performed a renal scintigraphy&#44; which was indicative of cortical necrosis&#46; In the test carried out 6 hours later&#44; the patient already displayed sediment with microscopic haematuria and proteinuria of 100mg&#47;dl&#59; the blood test displayed Pcr of 4&#46;6mg&#47;dl&#44; with a slight elevation in liver enzymes&#44; with ultra-sensitive C-reactive protein &#40;CRP&#41; of 165mg&#47;l&#44; total bilirubin of 5&#46;9mg&#47;dl&#44; with coagulation &#40;D-dimer of 36mg&#47;l&#44; prothrombin activity of 53&#37;&#44; with the rest being normal&#41;&#44; normal direct and indirect Coombs tests&#44; and therefore&#44; given the high clinical suspicion of haemolytic-uraemic syndrome &#40;HUS&#41;&#44; we started treatment with daily plasmapheresis with 5 litres of fresh frozen plasma &#40;1&#46;5 plasma volumes&#41;&#44; with hypotensive therapy&#44; given the progressive increase in blood pressure&#58; 120&#47;70 to 170&#47;90mmHg&#46; The next day&#44; the patient remained oliguric with Pcr of 7mg&#47;dl and high blood pressure &#40;160&#47;80mmHg&#41;&#44; and therefore we began haemodialysis &#40;first session&#58; 28 April 2013&#41;&#46; We carried out a total of 12 plasmapheresis sessions &#40;7 consecutive and 5 on alternate days&#41;&#44; until haemolysis disappeared &#40;a decrease in lactate dehydrogenase &#91;LDH&#93;&#44; indirect bilirubin and schistocytes &#91;Figure 1&#93;&#44; along with an increase in haptoglobin&#58; mg&#47;dl &#91;70 &#40;1 May 2013 &#41; to 75 &#40; 13 May 2013 &#41; to 217 &#40;17 June 2013 &#41;&#93;&#44; and platelets&#41;&#46; On 1 May 2013&#44; after the fifth plasmapheresis session&#44; the patient had severe respiratory failure with mild haemoptysis and decreased consciousness&#44; and as such he was transferred to the intensive care unit &#40;ICU&#41;&#44; where he continued with plasmapheresis and haemodialysis&#46; In the ICU&#44; mechanical ventilation was required and a lung scintigraphy was carried out due to suspected pulmonary infarction with no signs of pulmonary thromboembolism&#59; a CT scan of the head was also performed&#46; Finally&#44; the patient left the ICU four days later spontaneously breathing with a respiratory infection due to <span class="elsevierStyleItalic">Acinetobacter </span>and <span class="elsevierStyleItalic">Pseudomona aeruginosa</span> and a urinary infection due to <span class="elsevierStyleItalic">Acinetobacter baumanii</span>&#46; The clinical response to chemotherapy with ATRA and idarubicin was satisfactory and the patient showed a good response to treatment&#46; He was discharged by haematology on 18 June 2013 with revisions in outpatient clinics&#46;</p><p class="elsevierStylePara">From the renal point of view&#44; the patient remained anuric thereafter and required haemodialysis&#44; without any sign of recovery&#46; We carried out a control CT angiogram&#44; which displayed cortical hypoperfusion&#46; Once platelet levels normalised with chemotherapy&#44; we performed a percutaneous renal biopsy &#40;7 June 2013&#41;&#58; 19 glomeruli&#44; 16 of which displayed severe changes typical of coagulative necrosis with complete destruction of all cellular elements secondary to ischaemia&#46; In three of them&#44; we observed the same signs&#44; but with preservation of their nuclei&#44; as well as mesangiolysis&#44; thickening of the membranes with the presence of red blood cells &#40;schistocytes&#41;&#44; and occasional neutrophils &#40;PMN&#41; without double contours or crescents or fibrinoid necrosis the glomerular capillary or the afferent arteriole&#46; In the interstitial area&#44; there was diffuse cortical necrosis with the presence&#44; in the cortico-medullary and medullary junction&#44; of tubules with red blood cell casts&#44; haemosiderin pigment&#44; cellular ischaemic changes with brush border loss and marked nuclear atypia and chronic inflammatory infiltrate and mild fibrosis patches&#46; At vascular level&#44; there were arteries with a medium-sized diameter&#44; the presence of intimal mucoid degeneration with luminal occlusion and incipient myointimal fibrous changes&#44; which confirmed the diagnosis of coagulative cortical necrosis with vascular changes consistent with HUS &#40;Figures 2 and 3&#41; and as such&#44; given the low expectation of renal recovery&#44; we requested an assessment by Vascular Surgery for a vascular access&#44; with the patient being included in a renal replacement programme through regular haemodialysis&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Diagnosis</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Renal failure due to bilateral renal cortical necrosis caused by ischaemia due to thrombotic microangiopathy in the context of acute myeloid leukaemia with myeloid crisis&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Cortical necrosis accounts for less than 2&#37; of all causes of acute renal failure in adults and represents 15&#37;-20&#37; of acute renal failure in the third trimester of pregnancy&#46; Renal cortical necrosis may have several degrees of extension&#58; minimal&#44; focal and massive and may be unilateral or bilateral&#46; Our patient&#8217;s necrosis was bilateral and massive&#44; given his poor clinical progression&#46; Generally&#44; the subcapsular and juxtamedullary cortical tissue is preserved&#44; except in cortical necrosis due to rejection&#44; in which the whole cortex tissue can become necrotic&#46;<span class="elsevierStyleSup">1&#44;2</span></p><p class="elsevierStylePara">Its most common causes include obstetric complications &#40;50&#37;-70&#37;&#41;&#44; and non-obstetric causes represent the remaining 20&#37;-30&#37;&#46; Premature placental abruption is the most common obstetric cause&#46; HUS is the most common non-obstetric cause &#40;around 50&#37;-70&#37; of the cases&#41;&#44; followed by septic situations&#46; Other causes are severe dehydration&#44; acute and hyperacute kidney rejection&#44; biological venoms and ethylene glycol&#44; etc&#46;</p><p class="elsevierStylePara">The exact mechanism behind renal cortical necrosis is unknown&#46; It is caused by a significant decrease in renal arterial perfusion secondary to vascular spasm&#44; or microvascular injury or intravascular coagulation&#44; and it is the pathological progression of acute tubular necrosis that results in cortical necrosis&#46; Clinically&#44; it usually presents with anuria&#44; and requires haemodialysis on most occasions&#46; Among the diagnostic tests&#44; imaging tests play a key role in preventing the risk of bleeding involved in renal biopsies in these patients&#44; due to their common clotting disorders&#46; The technique normally used to carry out the diagnosis is angiography&#44; which in addition to being a diagnostic tool is also useful for the prognosis of renal function&#44; since better renal perfusion results in a better prognosis of recovery&#46; However&#44; CT angiography or renal scintigraphy are also valid techniques that are useful for diagnosis&#46;<span class="elsevierStyleSup">3</span> Its prognosis is poor&#44; with a mortality rate of around 50&#37;&#46; The calcium deposits observed in the renal cortex suggest renal cortical necrosis&#44; but the latter appear late in the course of the disease as a result of chronicity and are only found in 20&#37;-50&#37; of cases&#46;<span class="elsevierStyleSup">4-7</span></p><p class="elsevierStylePara">In the prodromal phase of atypical HUS upper respiratory infection &#40;23&#37;&#41;&#44; unclassified fever &#40;46&#37;&#41; as our patient displayed&#44; and vomiting &#40;81&#37;&#41; have been observed&#46; The histological lesion characteristic of atypical HUS is arterial thrombotic microangiopathy&#44; while in the typical HUS group the most common lesion was glomerular thrombotic microangiopathy&#44; which corresponds to that observed in our patient&#46; Renal cortical necrosis is the most serious complication in this profile and most patients require dialysis&#46;<span class="elsevierStyleSup">8&#44;9</span></p><p class="elsevierStylePara">In summary&#44; we must say that&#44; with regard to the microangiopathy that the patient displayed&#44; in the context of the blast crisis&#44; HUS was secondary to a tumour process&#44; and that the aforementioned explosion of atypical cells resulted in the acute situation&#44; which led to renal failure due to renal cortical necrosis&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12162&#95;16025&#95;53035&#95;en&#95;f112&#46;12162&#95;02&#46;jpg" class="elsevierStyleCrossRefs"><img src="12162_16025_53035_en_f112.12162_02.jpg" alt="Graph showing progression&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Graph showing progression&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12162&#95;16025&#95;53036&#95;en&#95;f212&#46;12162&#95;02&#46;jpg" class="elsevierStyleCrossRefs"><img src="12162_16025_53036_en_f212.12162_02.jpg" alt="Renal cast&#46;"></img></a></p><p class="elsevierStylePara">Figure 2&#46; Renal cast&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12162&#95;16025&#95;53037&#95;en&#95;f312&#46;12162&#95;02&#46;jpg" class="elsevierStyleCrossRefs"><img src="12162_16025_53037_en_f312.12162_02.jpg" alt="Image of a typical artery in secondary haemolitic uraemic syndrome&#46;"></img></a></p><p class="elsevierStylePara">Figure 3&#46; Image of a typical artery in secondary haemolitic uraemic syndrome&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">Presentamos el caso de un paciente de 37 a&#241;os que ingresa a cargo de Hematolog&#237;a&#44; trasladado desde las Urgencias de Otorrinolaringolog&#237;a&#44; donde hab&#237;a acudido por amigdalitis&#46; All&#237; se demuestra anemia y leucopenia e ingresa con agranulocitosis en estudio&#46; Un d&#237;a m&#225;s tarde el paciente presenta crisis bl&#225;stica&#44; y se le diagnostica de leucemia aguda con crisis mieloide&#46; En dicha situaci&#243;n de crisis bl&#225;stica el paciente inicia un cuadro de dolor lumbar brusco&#44; con oliguria y deterioro de la funci&#243;n renal&#44; seguido de anemizaci&#243;n&#44; en el contexto de un cuadro de hem&#243;lisis compatible con microangiopat&#237;a tromb&#243;tica&#44; por lo que somos consultados&#46; Se inicia tratamiento con plasmaf&#233;resis y al d&#237;a siguiente hemodi&#225;lisis &#40;se realiza un total de 12 sesiones de plasmaf&#233;resis&#44; hasta desaparecer los datos de hem&#243;lisis&#41;&#46; Cinco d&#237;as m&#225;s tarde presenta cuadro de insuficiencia respiratoria&#44; por el que pasa a la Unidad de Cuidados Intensivos&#44; donde contin&#250;a con plasmaf&#233;resis y hemodi&#225;lisis&#46; El paciente se mantiene en anuria desde entonces&#44; con necesidad de hemodi&#225;lisis&#44; sin ning&#250;n signo de recuperaci&#243;n renal&#46; Una vez normalizadas las plaquetas&#44; con tratamiento quimioter&#225;pico hematol&#243;gico&#44; se realiza biopsia renal percut&#225;nea&#44; que confirma el diagn&#243;stico de necrosis cortical&#46; Finalmente el paciente queda incluido en programa sustitutivo de la funci&#243;n renal mediante hemodi&#225;lisis peri&#243;dica&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">A 37-year-old patient was transferred to Haematology from the ENT Emergency Department where he had been admitted due to tonsillitis&#46; He displayed anaemia and leukopenia and had agranulocytosis in the study&#46; A day later the patient had blast crisis&#44; and was diagnosed with myeloid acute leukaemia&#46; Due to blast crisis the patient experienced sudden back pain&#44; with oliguria and renal function deterioration followed by anaemia&#44; in the context of haemolysis consistent with thrombotic microangiopathy&#44; and as such&#44; we were consulted&#46; We began treatment with plasmapheresis and on the following day we performed haemodialysis &#40;we carried out a total of 12 sessions of plasmapheresis until haemolysis disappeared&#41;&#46; Five days later there was respiratory failure&#44; and the patient was consequently transferred to the Intensive Care Unit&#44; where he continued treatment with plasmapheresis and haemodialysis&#46; The patient remained anuric thereafter&#44; requiring haemodialysis&#44; with no sign of renal recovery&#46; Once platelet levels normalised with haematology chemotherapy&#44; a percutaneous renal biopsy was performed&#44; which confirmed the diagnosis of cortical necrosis&#46; Finally&#44; the patient underwent renal replacement therapy by regular haemodialysis&#46;</p>"
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                  "referenciaCompleta" => "Prakash J, Vohra R, Wani IA, Murthy AS, Srivastva PK, Tripathi K, et al. Decreasing incidence of renal cortical necrosis in patients with acute renal failure in developing countries: a single-centre experience of 22 years from Eastern India. Nephrol Dial Transplant 2007;22(4):1213-7.  <a href="http://www.ncbi.nlm.nih.gov/pubmed/17267539" target="_blank">[Pubmed]</a>"
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Article information
ISSN: 20132514
Original language: English
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Idiomas
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