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0 => array:2 [ "paginaInicial" => "194" "paginaFinal" => "196" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Maria Rullan, Joaquín Manrique, Loreto Fernandez Lorente, Diana Izquierdo, Fernanda Slon, Antonio José Rullan" "autores" => array:6 [ 0 => array:3 [ "nombre" => "Maria" "apellidos" => "Rullan" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 1 => array:4 [ "nombre" => "Joaquín" "apellidos" => "Manrique" "email" => array:1 [ 0 => "jmanriquees@gmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 2 => array:3 [ "nombre" => "Loreto Fernandez" "apellidos" => "Lorente" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 3 => array:3 [ "nombre" => "Diana" "apellidos" => "Izquierdo" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 4 => array:3 [ "nombre" => "Fernanda" "apellidos" => "Slon" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 5 => array:3 [ "nombre" => "Antonio José" "apellidos" => "Rullan" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Servicio de Digestivo, Complejo Hospitalario de Navarra, Pamplona, Navarra, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Servicio de Nefrología, Complejo Hospitalario de Navarra, Pamplona, Navarra, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Centro de Salud de Tafalla, Complejo Hospitalario de Navarra, Pamplona, Navarra, Spain" "etiqueta" => "c" "identificador" => "aff0015" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "<span class="elsevierStyleItalic">Corresponding author</span>." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Síndrome hemolítico urémico como forma de presentación de cáncer de próstata diseminado" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1210 "Ancho" => 3123 "Tamanyo" => 246560 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">(A)–(C) Changes in haemoglobin, creatinine, and platelets over time in each case, concurrently with haemodialysis sessions and plasmapheresis. The first patient (1A) showed baseline pCr of 6.29<span class="elsevierStyleHsp" style=""></span>mg/dl, Hb 7.6<span class="elsevierStyleHsp" style=""></span>g/dl, and platelet count 49<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span>/l. The patient underwent HD (magenta) and subsequently received PP (blue) every day. Two weeks after beginning treatment, diuresis and renal function were gradually recovered (13 HD sessions and 18 PP sessions). Baseline pCr figures were similar for the second patient (1B), who also presented anaemia and thrombocytopenia. He received 10 and 17 HD and PP sessions, respectively, recovering one month later. The third patient (1C) had a similar behaviour, received 10 and 15 sessions, respectively, and showed recovery within one month. Hb: haemoglobin; HD: haemodialysis; pCr: plasma creatinine; PP: plasmapheresis.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Ninety percent of the cases of haemolytic uraemic syndrome (HUS) are caused by the ingestion of food contaminated with Shiga toxin-producing <span class="elsevierStyleItalic">Escherichia coli</span> (STEC) (typical HUS), that activates the classical complement pathway.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> There are also thrombotic microangiopathies (TMA) secondary to drugs, autoimmune diseases, and malignancies, these are related to activation of the alternative complement pathway.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2–5</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">We present 3 patients from our hospital with advanced prostate cancer who developed severe TMA/HUS and had a good response to treatment (supportive, plasmapheresis, and haemodialysis).</p><p id="par0015" class="elsevierStylePara elsevierViewall">A 63-year old man, with no previous history of nephropathy, who presented at the emergency room with malaise and oliguria, no GI symptoms and without fever. Past medical history and physical exam were unremarkable. The patient had acute renal failure (pCr: 6.2<span class="elsevierStyleHsp" style=""></span>mg/dl), anaemia (Hb: 7.6<span class="elsevierStyleHsp" style=""></span>g/dl), and thrombocytopenia (platelets: 49<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span>/l); elevated LDH (1281<span class="elsevierStyleHsp" style=""></span>U/l), reticulocytosis, undetectable haptoglobin, and elevated number of schystocytes. Urine showed dysmorphic red blood cells, leukocyturia, and proteinuria (<1<span class="elsevierStyleHsp" style=""></span>g/24<span class="elsevierStyleHsp" style=""></span>h); obstructive uropathy was ruled out by ultrasound. Worsening renal function occurred at 24<span class="elsevierStyleHsp" style=""></span>h, auto-immunity markers were normal, the direct Coombs test was negative, and the activity of ADAMTS13 was normal (56.9%). Faeces were not tested because of the absence of clinical signs and symptoms. The patient was diagnosed with TMA/HUS and received daily haemodialysis (HD) and plasmapheresis (PP).</p><p id="par0020" class="elsevierStylePara elsevierViewall">Mean while, the patient was diagnosed of prostate adenocarcinoma (PSA 195.6<span class="elsevierStyleHsp" style=""></span>ng/ml and a biopsy: Gleason 9) with bone metastases (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>A). He completed 13 HD sessions, 18 PPs, and received bicalutamide, renal function and anaemia recovered, with no evidence of haemolysis (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>A). The patient was asymptomatic at the 8-month visit, and renal function, Hb, and platelets count were normal.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0025" class="elsevierStylePara elsevierViewall">An 82-year-old hypertensive COPD patient with a history of malaise, asthenia, micturition symptoms and oliguria. The patient complained of cough with production of white sputum, and a history of days of fever, with no GI symptoms or evidence volume expansion. Severe infection was ruled out and there was evidence of ARF (pCr: 7.5<span class="elsevierStyleHsp" style=""></span>mg/dl), accompanied by anaemia (Hb: 12.6<span class="elsevierStyleHsp" style=""></span>g/dl), and thrombocytopenia (platelets: 61<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span>/l), suggesting haemolysis (LDH 1600<span class="elsevierStyleHsp" style=""></span>U/l, with undetectable haptoglobin and reticulocytosis). Urine specific gravity was low, and there was microhaematuria, leukocyturia, and proteinuria (<1<span class="elsevierStyleHsp" style=""></span>g/24<span class="elsevierStyleHsp" style=""></span>h) with no evidence of obstructive uropathy in by ultrasound. Auto-immunity markers were normal, the patient showed increased schystocytes, negative direct Coombs test, and preserved ADAMTS13 activity (25.4%). Faeces were negative for STEC. After confirming TMA/HUS, the patient received HD and PP (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>B) and was diagnosed with advanced prostate cancer (PSA: 760<span class="elsevierStyleHsp" style=""></span>ng/ml with bone metastases, <a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>B), initiating treatment with bicalutamide. A month later his renal function had normalised, with discrete thrombocytopenia, and anaemia (Hb: 10.5<span class="elsevierStyleHsp" style=""></span>g/dl) (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>B).</p><p id="par0030" class="elsevierStylePara elsevierViewall">An 89-year old men with diabetes and benign prostate hyperplasia. He seek medical help because general deterioration, abdominal pain, macroscopic haematuria, and oliguria during the last a 6-days. No respiratory, cardiac, or gastrointestinal symptoms a physical exam without findings. The patient developed acute renal failure (pCr: 9.4<span class="elsevierStyleHsp" style=""></span>mg/dl), with haematuria and non-nephrotic proteinuria; haemolytic anaemia (Hb: 10.1<span class="elsevierStyleHsp" style=""></span>g/dl, reticulocytosis, LDH: 4411<span class="elsevierStyleHsp" style=""></span>U/l, haptoglobin: 54<span class="elsevierStyleHsp" style=""></span>mg/dl, increased schystocytes) and severe thrombocytopenia (platelets: 13<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span>/l). Obstructive aetiology of acute renal failure was ruled out by ultrasound. ADAMTS13 activity was preserved. The patient was diagnosed of TMA/HUS, and was treated with HD and PP for 3 weeks, with subsequent improvement of renal function, thrombocytopenia, and anaemia (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>C). The patient was diagnosed of prostate cancer and received specific treatment; the renal function did not recover totally and remained with some residual renal failure.</p><p id="par0035" class="elsevierStylePara elsevierViewall">In our three patients with TMA/HUS, disseminated intravascular coagulation (DIC) was ruled out and the diagnosis was made on the basis of the clinical history and precipitating causes, since signs and symptoms of aHUS are unexpectedly non-specific according to the consensus guidelines published in Nephrology (2013).<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Most cases of TMA/HUS are caused by STEC infections. Yet, there have been reports of TMA/HUS secondary to drugs, autoimmune diseases, or malignancies.<a class="elsevierStyleCrossRefs" href="#bib0075"><span class="elsevierStyleSup">5,7,8</span></a> In patients from oncologyin, the most common cause of TMA/HUS is in association with chemotherapy drugs (mainly mitomycin), whereas cases directly associated with malignancies are less common. The largest series available consists of 168 patients; being GI tumours are the most common kind (26%), followed by breast and prostate cancer,<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> thereby stressing the distinctiveness of our report.</p><p id="par0045" class="elsevierStylePara elsevierViewall">Complete response to classical treatment for TMA/HUS (PP, HD, and supportive) was observed in the cases presented here. Based on good response to treatment with PP, the deregulation of the alternative complement pathway, either resulting from individual susceptibilities because of mutations in regulatory proteins, or the presence of antibodies against them, may lead to this condition.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a> Resistance has also been reported with a positive transient response to anti-C5a (eculizumab).<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">The association of TMA/HUS to malignancies complicates the patient's outcome; the therapy employed against neoplasias are no always responsible for TMA/HUS. Early diagnosis and treatment of TMA/HUS may lead to resolution with no sequelae. The thriving research concerning the complement will help identify the causes and the right treatment for each patient.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Rullan M, Manrique J, Lorente LF, Izquierdo D, Slon F, Rullan AJ. Síndrome hemolítico urémico como forma de presentación de cáncer de próstata diseminado. Nefrologia. 2016;36:194–196.</p>" ] ] "multimedia" => array:2 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 913 "Ancho" => 1801 "Tamanyo" => 130029 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">(A) and (B) Bone scans showing disseminated bone lesions in cases 1 and 2.</p>" ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1210 "Ancho" => 3123 "Tamanyo" => 246560 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">(A)–(C) Changes in haemoglobin, creatinine, and platelets over time in each case, concurrently with haemodialysis sessions and plasmapheresis. The first patient (1A) showed baseline pCr of 6.29<span class="elsevierStyleHsp" style=""></span>mg/dl, Hb 7.6<span class="elsevierStyleHsp" style=""></span>g/dl, and platelet count 49<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span>/l. The patient underwent HD (magenta) and subsequently received PP (blue) every day. Two weeks after beginning treatment, diuresis and renal function were gradually recovered (13 HD sessions and 18 PP sessions). Baseline pCr figures were similar for the second patient (1B), who also presented anaemia and thrombocytopenia. He received 10 and 17 HD and PP sessions, respectively, recovering one month later. The third patient (1C) had a similar behaviour, received 10 and 15 sessions, respectively, and showed recovery within one month. 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