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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">We describe the course of a boy with atypical haemolytic uraemic syndrome &#40;aHUS&#41; with no mutation in the complement system&#44; who presented with two unusual extrarenal complications&#59; osteonecrosis of both femoral heads and cholelithiasis&#44; resulting from a relapse of aHUS caused after suspending eculizumab treatment&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">The case is an 8-year-old boy with a neonatal onset of aHUS with severe and multisystemic disease&#46; By administering eculizumab&#44; it was achieved full haematological and renal recovery&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> He continued the treatment with eculizumab from the neonatal period to the age of three years and six months&#44; and the disease was maintained in complete remission&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Exhaustive testing of all the known genes that could cause aHUS was carried out and no mutations were found&#46; Therefore the treatment was discontinued&#46; The genes studied were&#58; ADAMSTS13&#44; ARMS2&#44; C1S&#44; C2&#44; C3&#44; C3ARI&#44; C4BPA&#44; C4BPAP1&#44; C4BPAP2&#44; C4BPB&#44; C5&#44; C5ARI&#44; C6&#44; C7&#44; C8A&#44; C8B&#44; C8G&#44; C9&#44; CD46&#44; CD46&#44; CD55&#44; CD59&#44; CFB&#44; CFD&#44; CFH&#44; CFHR1&#44; CFHR2&#44; CFHR3&#44; CFHR4&#44; CFHR5&#44; CFI&#44; CFP&#44; CLU&#44; CPB2&#44; CR1&#44; CR1L&#44; CR2&#44; CRP&#44; DGKE&#44; F12&#44; F2&#44; F3&#44; FCN1&#44; HTRA1&#44; KDR&#44; MASP1&#44; MASP2&#44; MBL2&#44; NR5A2&#44; PHG&#44; PIGA&#44; PLG&#44; PROC&#44; PROCR&#44; PROS1&#44; PTX3&#44; RP1&#44; RP1L1&#44; SELP&#44; SERPING1&#44; TFP1&#44; THBD&#44; THBS1&#44; VSIG4&#44; VTN&#44; and VWF&#46; No variants &#40;haplotypes&#41; of risk in the MCP gene or the CFH gene were found&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Three months later&#44; after mild cold symptoms&#44; he was admitted for acute kidney failure&#46; Treatment was resumed with eculizumab&#44; and all parameters wee normalized within a few days &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41;&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0025" class="elsevierStylePara elsevierViewall">One year after the last relapse&#44; it was detected by chance&#44; synchronic and asymmetric bilateral necrosis of both femoral heads &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; Based on the stage of progression at which the lesions were found&#44; the osteonecrosis occurred during the relapse caused after withdrawing the medication&#46; The absence of a history of degenerative coxofemoral joint disease and other secondary causes of osteonecrosis enabled other possible aetiologies to be ruled out&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">In the same study&#44; asymptomatic gallstones were detected&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">Five years later&#44; the child continues to receive treatment with eculizumab&#44; with good tolerance &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41;&#44; without presenting evidence of thrombotic microangiopathy &#40;TMA&#41; activity&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Discussion</span><p id="par0040" class="elsevierStylePara elsevierViewall">In aHUS&#44; the membrane attack complex causes damage to the endothelium&#44; and this triggers TMA&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Although the aHUS lesions predominantly affect the kidney vessels&#44; the diffuse and systemic nature of TMA leads to microvasculature involvement of other organs &#40;brain&#44; heart&#44; intestines&#44; pancreas&#44; lungs&#44; etc&#46;&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">In addition to the triad of haemolytic anaemia&#44; thrombocytopoenia&#44; and acute kidney failure&#44; our patient presented avascular necrosis of both femoral heads&#44; presumably caused by the systemic TMA that occurred during the relapse&#46; Damage to the microvascular endothelium in the terminal circulation of the femoral head would cause tissue hypoperfusion with vascular supply interruption&#44; bone infarction&#44; and ultimately necrosis in both femoral heads&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> Its association with aHUS has not been reported&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">Among gastrointestinal complications&#44; some cases of gallstones have been published in the literature several months after an acute episode of typical HUS<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a>&#59; however&#44; this complication is rare in aHUS&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">One of the most currently debated topics is the duration of treatment with eculizumab<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#44;6</span></a> since the decision to withdraw treatment is not risk-free&#44; especially in patients with a very severe and life-threatening clinical presentation of aHUS at the start&#46; This controversy is accentuated in the paediatric age&#44; since the common events that lead to complement activation &#40;infections&#44; vaccines&#44; etc&#46;&#41; are common in this age group&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">No mutations in the complement genes are identified in 30&#8211;40&#37; of patients with aHUS&#46; There is evidence that the severity of aHUS and the response to eculizumab is similar in patients with or without an identified genetic risk&#44;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> although maintaining the treatment is more difficult in patients in whom no mutations were found in the complement system&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Funding</span><p id="par0070" class="elsevierStylePara elsevierViewall">No funding was received for this study&#46;</p></span></span>"
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