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          "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Renal biopsy &#40;mother&#41;&#46; Massive glomerular deposit in cortex &#40;left&#41; and interstitial deposit in bone marrow &#40;right&#41; &#40;Congo red &#215;100&#41;&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Clinical case</span><p id="par0145" class="elsevierStylePara elsevierViewall">A 40-year-old male came to the emergency room complaining of oedemas&#46; Patient presented family history of mother with non-affiliated renal amyloidosis&#46; The mother&#39;s renal biopsy showed permanganate resistance&#44; which seemed to rule out AA amyloidosis&#44; and led to consider the possibility of AL amyloidosis&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">The patient did not receive any pharmacological treatment&#46; Upon physical examination&#44; the patient presented blood pressure of 135&#47;75<span class="elsevierStyleHsp" style=""></span>mmHg and bimalleolar oedemas&#44; without other data of interest&#46; Laboratory tests confirmed the presence of nephrotic syndrome &#40;serum albumin of 2&#46;5<span class="elsevierStyleHsp" style=""></span>g&#47;dl&#44; cholesterolaemia of 275<span class="elsevierStyleHsp" style=""></span>mg&#47;dl and urine protein of 6<span class="elsevierStyleHsp" style=""></span>g&#47;24<span class="elsevierStyleHsp" style=""></span>h&#41;&#44; without alterations in the sediment and with normal glomerular filtration rate&#46; Electrophoretic spectrum in blood and urine&#44; immunological study and renal ultrasound scan were normal&#46; A renal biopsy was performed that presented 19 glomeruli with fully distorted structure by a hyaline deposit in nodular disposition&#44; with positivity for Congo red and thioflavin&#46; Tubules and vessels did not show significant alterations and therefore the findings were compatible with amyloidosis&#46; The study of a paraffin sample showed a marked positivity for AP protein&#44; which is a part of the amyloid substance common in all amyloidosis types&#44; with negativity for light chains and AA protein&#44; B2 microglobulin and transthyretin&#46; A supplementary study was performed with antibodies to fibrinogen and lysozyme and the amyloid substance deposits resulted positive for the fibrinogen A-alpha chain &#40;AFib&#41;&#46; However&#44; the genetic study did not show any mutation in the AFib chain gene but there was a previously undescribed mutation in the Apolipoprotein A1 gene &#40;Apo AI&#41;&#46; Faced with this discrepancy&#44; the mother&#39;s biopsy was analysed&#46; The biopsy contained a glomerular deposit in the cortex and a massive deposit at the medullary level&#46; The deposit at the medullary level was not described in the AFib amyloidosis&#44; being very characteristic of the Apo AI&#46; The conclusion is that the first results of the immunohistochemistry were not completely reliable as it was not performed under adequate conditions&#46; The presence of Apo AI was later confirmed using the same technique&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">An extension study was performed&#44; with echocardiogram and electromyography&#44; without signs of heart condition or autonomic neuropathy&#46; The clinical evolution showed a progressive increase in transaminases&#44; suggesting hepatic involvement&#46; These results were in agreement with this type of familial amyloidosis which&#44; preferably&#44; involves the kidney and liver&#46; Although the intila GFR was normal&#44; renal function subsequently deteriorated progressively until renal replacement therapy was required after 2 years&#46; The patient received treatment with peritoneal dialysis for 4 years&#44; thereafter the patient underwent undergoing renal transplantation from a deceased donor&#46; The patient presented a complicated postoperative period with splenic rupture&#44; in the context of his disease&#44; with amyloid deposit in the spleen&#46; An urgent splenectomy was indicated&#46; Finally&#44; the patient was discharged in stable condition &#40;<a class="elsevierStyleCrossRefs" href="#fig0005">Figs&#46; 1&#8211;4</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia><elsevierMultimedia ident="fig0020"></elsevierMultimedia></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Discussion</span><p id="par0020" class="elsevierStylePara elsevierViewall">Hereditary non-neuropathic renal amyloidosis was first described by Ostertag in 1932&#46;<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">1</span></a> This name was given to emphasise the absence of peripheral nervous system involvement&#44; with the purpose of differentiating this pathology from other types of amyloidosis&#46; However&#44; this term is confusing and is not currently appropriate because several variants related to the apolipoprotein A1 associated with neuropathy have been described since then&#46;<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">2</span></a> In regards to this disease&#44; more than 25 mutations that alter the structure of different proteins&#44; causing the deposit in amyloid form&#44; have been identified&#46; These proteins are lysozyme&#44;<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">3</span></a> Apo AI&#44;<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">4&#44;5</span></a> Apolipoprotein A II &#40;Apo II&#41;<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">6&#44;7</span></a> and AFib chain&#46;<a class="elsevierStyleCrossRefs" href="#bib0195"><span class="elsevierStyleSup">8&#8211;12</span></a> Clinically&#44; all of them manifest themselves with renal failure at middle age and they have a dominant autosomic heritage&#44; although with highly variable penetrance and some specific clinic characteristics&#44; depending on the protein that originates the deposit&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Apo AI is the main protein that forms the high-density lipoprotein &#40;HDL&#41; structure&#46; It is secreted in the liver and the small intestine and catabolised mainly in the liver and kidneys&#46;<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">13&#8211;15</span></a> It is a co-factor for lecithin-cholesterol acetyltransferase &#40;LCAT&#41;&#44; and its function is linked to cholesterol elimination&#46;<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">13&#44;15&#44;16</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">To date&#44; at least 19 amyloidogenic mutations have been described in the APO AI gene&#46; A different clinical presentation of the disease has been observed depending on the region in which the mutation is located&#46; In this way&#44; mutations that affect the amino-terminal region manifest themselves with amyloid deposit at hepatic and renal level&#44; whereas mutations that affect the carboxi-terminal region manifest themselves with cutaneous&#44; laryngeal and cardiac amyloidosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0165"><span class="elsevierStyleSup">2&#44;15&#44;17</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">The Apo AI amyloidosis phenotype is very heterogeneous&#46; Some of the published cases describe extensive visceral amyloidosis and end-stage renal failure&#44; whereas others include larynx and skin involvement&#44; with minimal clinical consequences&#46; Clinical expression does not only depend on the mutation location&#44; since even patients with the same mutation may experience different clinical expression&#46; Phenotypic heterogeneity has also been observed between lineages with the same Apo AI mutation&#46; There are publications including series of patients with an elevated number of relatives affected and fast progression to end-stage renal disease &#40;10 out of 16 cases affected&#41;&#44;<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">15</span></a> which suggests the existence of a more aggressive phenotype or other genetic and environmental factors interacting or having an influence on clinical manifestations&#46; The possible amyloid deposit has been described in several organs&#44; among them the kidney&#44; gastrointestinal tract&#44; spleen&#44; liver&#44; heart&#44; peripheral nervous system&#44; larynx and skin&#46; The most common clinical presentation consists of high blood pressure&#44; mild proteinuria and slowly progressive renal failure deterioration between the ages of 18 and 55&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">The first mutation described&#44; and the most frequent in patients with Apo AI amyloidosis of Irish ancestry&#44; is Gly26Arg&#46; It is characterised by the progressive accumulation of amyloid fibrils composed by the amino-terminal polypeptide fragments of the Apo AI and it appears in young patients&#44; aged 20&#8211;46&#46; The amyloid deposit is located in the peripheral nerves&#44; kidneys&#44; liver and gastrointestinal tract&#44;<a class="elsevierStyleCrossRefs" href="#bib0165"><span class="elsevierStyleSup">2&#44;17</span></a> manifesting itself clinically with peripheral neuropathy&#44; peptic ulcer and nephropathy&#46;<a class="elsevierStyleCrossRefs" href="#bib0165"><span class="elsevierStyleSup">2&#44;18</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">At least up to 19 amyloidogenic mutations of Apo AI have been described since&#46; Here we describe a new mutation that we did not find in the literature&#44; the c&#46;220T&#62;C &#40;p&#46;Trp74Arg&#41;&#46; In our patient&#39;s case&#44; we were able to observe kidney involvement&#44; with renal function impairment within two years&#44; as well as liver and spleen involvement&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">The histological analysis of Apo AI amyloidosis shows predominant amyloid deposits at the medullary level with tubulointerstitial nephritis pattern&#44; characterised by tubular atrophy and interstitial fibrosis&#44; associated with secondary focal glomeruloesclerosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0230"><span class="elsevierStyleSup">15&#44;19</span></a> Although interstitial involvement is the most frequent&#44; there are also cases in which a deposit at glomerular level has been detected&#46;<a class="elsevierStyleCrossRefs" href="#bib0250"><span class="elsevierStyleSup">19&#8211;21</span></a> One case has even been published with predominant glomerular involvement&#44; associated with nephrotic syndrome&#44; as a result of Apo AI Leu64Pro amyloidosis&#46;<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">22</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">The preferred selectiveness of Apo AI amyloidosis for the renal medulla allows us to differentiate it from other types of hereditary and acquired systemic amyloidosis&#44;<a class="elsevierStyleCrossRefs" href="#bib0250"><span class="elsevierStyleSup">19&#44;23</span></a> since this preference for the medullary compartment is only shared with transthyretin amyloidosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0250"><span class="elsevierStyleSup">19&#44;24</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">In our case&#44; the patient&#39;s renal biopsy only contained cortex and the glomerular compartment was the only place where amyloid deposit was found&#46; These findings are in agreement with the clinical symptoms at diagnosis&#44; consistent nephrotic syndrome with posterior progressive worsening of renal function&#46; Initially&#44; this particular characteristic made us suspect fibrinogen A alpha chain amyloidosis&#44; since it is the most frequent cause of hereditary renal amyloidosis in Europe&#44; and its deposit is characteristically glomerular&#46; However&#44; the mother&#39;s biopsy had glomerular deposit in cortex&#44; but it also had medulla with massive deposit&#46; Finally&#44; the genetic study determined a new&#44; previously undescribed&#44; Apo AI mutation&#44; and the immunochemistry confirmed the diagnosis&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">A correct differential diagnosis in systemic amyloidosis is important since disease management and prognosis may be completely different depending on its origin&#46; This is the reason why it is particularly relevant to determine the protein that originates the deposit&#46; In accordance with a study performed in the United Kingdom National Amyloidosis Centre&#44; almost 10&#37; of the patients with a presumptive diagnosis of AL systemic amyloidosis actually suffer from a hereditary amyloidosis&#46;<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">25</span></a> This usually happens because it is quite common to consider AL amyloidosis as a diagnosis of exclusion&#44; due to the clinical overlapping between different types of amyloidosis&#44; the relatively frequent finding of a monoclonal protein in patients over 50&#44; and the difficulty to determine the type of fibril&#44; even when the AL amyloidosis diagnosis is correct&#44; since in up to 20&#37; of the cases the lambda or kappa light chain antibodies are not bound to it&#44; probably due to the alteration in their structure&#46; Moreover&#44; it is not always possible to verify the presence of family history of hereditary amyloidosis due to the variable penetrance of the disease and the diagnosis of new mutations&#46;</p><p id="par0070" class="elsevierStylePara elsevierViewall">Among the methods available to determine the protein composition of fibrils&#44; we find immunochemistry and direct protein sequencing&#46; In order to perform this last technique&#44; a considerable amount of tissue is required which is not always possible to obtain&#46; The recent development of proteomic techniques constitutes an advance in the diagnosis of amyloidosis since in order to identify the protein that forms the amyloid fibril only a small amount of fixed tissue is required&#46;<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">26</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Regarding disease treatment&#44; renal transplant due to Apo AI amyloidosis has had varied success&#46;<a class="elsevierStyleCrossRefs" href="#bib0250"><span class="elsevierStyleSup">19&#44;27&#44;28</span></a> There has been recurrence of amyloidosis in grafts&#44; but in most of the published cases graft survival was acceptable&#46; A study performed in the United Kingdom National Amyloidosis Centre revealed that out of 10 renal transplant recipients with APO AI amyloidosis&#44; five showed documented evidence of amyloid deposit in the transplanted kidney&#46; However&#44; only one patient&#44; after 25 years&#44; progressed to end-stage renal disease&#44; initiating dialysis again&#46;<a class="elsevierStyleCrossRefs" href="#bib0260"><span class="elsevierStyleSup">21&#44;29</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">Liver transplant is the final treatment for other types of hereditary amyloidosis&#44; since the amyloidogenic protein is synthesised in the liver&#46; However&#44; in the APO AI amyloidosis&#44; the amyloidogenic protein is also synthesised in the small intestine&#46; Although there have been cases like that of an Irish patient with the Apo AI Gly26Arg mutation&#44; who underwent hepatorenal transplant and two years later evidenced a regression of the amyloid deposits&#44;<a class="elsevierStyleCrossRefs" href="#bib0250"><span class="elsevierStyleSup">19&#44;30</span></a> double hepatorenal transplant is only considered in patients with significant impairment in both organs&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">In our patient&#39;s case&#44; we considered the best option was renal transplant since hepatic function was not very impaired&#46; However&#44; post-transplant evolution has become complicated by splenic rupture due to amyloid deposit&#46;</p><p id="par0090" class="elsevierStylePara elsevierViewall">We could assert that hereditary renal amyloidosis constitutes a diagnostic challenge due to the difficulty to identify the protein that originates the deposit&#44; and the importance of this aspect in prognosis and treatment&#46; In APO AI amyloidosis&#44; the indices cases diagnosis requires high clinical suspicion and a renal medulla biopsy is important to observe the amyloid deposit at this level&#46; The possibility of this diagnosis has to be considered in family cases of tubulointerstitial nephritis with hepatic involvement&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Questions</span><p id="par0095" class="elsevierStylePara elsevierViewall"><ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">1&#41;</span><p id="par0100" class="elsevierStylePara elsevierViewall">Dr&#46; Esther Rosello &#40;Valencia&#41;&#46; The diagnostic yield of amyloidosis often forces specialists to perform studies in fat&#44; rectal mucosa and&#44; in the end&#44; a renal biopsy&#46; What is the decision followed in the extraction of biopsies upon suspicion of amyloidosis&#63;</p><p id="par0105" class="elsevierStylePara elsevierViewall">Answer &#40;Kelly Samill&#225;n&#41;&#58; Upon suspicion of amyloidosis&#44; the diagnosis can frequently be confirmed through abdominal fat aspiration&#44; which is a mildly invasive technique&#46; The literature states that this technique provides high sensitivity for the diagnosis of AL amyloidosis &#40;between 80 and 90&#37;&#41; and a lower sensitivity &#40;between 65 and 75&#37;&#41; for AA amyloidosis diagnosis&#46; However&#44; in the case of familial amyloidosis&#44; the diagnostic yield is very low and the absence of positivity to Congo red in an abdominal fat biopsy does not exclude the diagnosis&#46;<a class="elsevierStyleCrossRef" href="#bib0310"><span class="elsevierStyleSup">31</span></a> In regards to the salivary gland and rectal mucosa biopsies&#44; they are also used as non-invasive diagnostic methods&#46; We believe that the diagnostic method in cases of amyloidosis must be individualised in accordance with the patient&#39;s characteristics and comorbidity&#46; In general&#44; if a patient presents apparent renal involvement&#44; particularly if the patient has nephrotic syndrome&#44; our group indicates the performance of a renal biopsy&#44; except in the exceptional cases in which the renal biopsy would not be decisive to take decisions or in which the patient&#39;s comorbidity does not allow it&#46; In the cases of Apo AI amyloidosis with renal involvement&#44; in our opinion&#44; it is advisable to perform the renal biopsy directly&#46;</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">2&#41;</span><p id="par0110" class="elsevierStylePara elsevierViewall">Dr&#46; Esther Rosell&#243; &#40;Valencia&#41;&#46; Do you think biopsy samples could be sent to referral centers for special amyloidosis techniques&#63;</p><p id="par0115" class="elsevierStylePara elsevierViewall">Answer &#40;Manuel Sol&#233;&#41;&#58; The diagnosis of amyloidosis presents difficulties at two levels&#58; the basic one&#44; the diagnosis with Congo red stain&#44; should be undertaken in the centre itself&#44; through adequate technique control&#44; although we are aware of the many problems this poses&#46; If typification is in question&#44; it is important to use an antibodies panel and the interpretation requires experience&#46; In this case&#44; it would be adequate to refer the sample to an amyloidosis unit&#46;</p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">3&#41;</span><p id="par0120" class="elsevierStylePara elsevierViewall">Dr&#46; Miguel &#193;ngel Mart&#237;nez &#40;Madrid&#41;&#58; I would like to mention that Congo red techniques are only successful if the cut sessions have a minimum of 6<span class="elsevierStyleHsp" style=""></span>&#956;m&#46; Does that coincide with your experience&#63;</p><p id="par0125" class="elsevierStylePara elsevierViewall">Answer &#40;Manuel Sol&#233;&#41;&#58; This is a very important technical aspect&#46; It is usually recommended to perform the stain on 8-&#956;m sections&#46; However&#44; this is not always possible&#44; particularly in renal biopsies in which routine unstained cut sections are performed for different techniques&#46; If the cut section is thin&#44; the stain will be pale&#44; but the green birefringence will remain&#44; although it may be more difficult to visualise&#46;</p></li><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">4&#41;</span><p id="par0130" class="elsevierStylePara elsevierViewall">Dr&#46; Julia Blanco &#40;Madrid&#41;&#46; I have noticed that you have obtained an excellent apple green in Congo red techniques&#44; do you have a secret formula&#63;</p><p id="par0135" class="elsevierStylePara elsevierViewall">Answer &#40;Manuel Sol&#233;&#41;&#58; It is essential that the observation with polarised light be made with a powerful light source&#46; Not just any microscope will do&#46; And remember that the main feature of Congo red is dichroism&#44; that is&#44; the change from red to golden and green when rotating the polarising filter&#46;</p></li></ul></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conflicts of interest</span><p id="par0140" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Hereditary renal amyloidosis is an autosomal dominant condition with considerable overlap with other amyloidosis types&#46; Differential diagnosis is complicated&#44; but is relevant for prognosis and treatment&#46; We describe a patient with nephrotic syndrome and progressive renal failure&#44; who had a mother with renal amyloidosis&#46;</p><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Renal biopsy revealed amyloid deposits in glomerular space&#44; with absence of light chains and protein AA&#46; We suspected amyloidosis with fibrinogen A alpha chain deposits&#44; which is the most frequent cause of hereditary amyloidosis in Europe&#44; with a glomerular preferential affectation&#46; However&#44; the genetic study showed a novel mutation in apolipoprotein AI&#46; On reviewing the biopsy of the patient&#39;s mother similar glomerular deposits were found&#44; but there were significant deposits in the renal medulla as well&#44; which is typical in APO AI amyloidosis&#46; The diagnosis was confirmed by immunohistochemistry&#46;</p><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Apo AI amyloidosis is characterised by slowly progressive renal disease and end-stage renal disease occurs approximately 3&#8211;15 years from initial diagnosis&#46; Renal transplantation offers an acceptable graft survival and in these patients with hepatorenal involvement simultaneous liver and kidney transplantation could be considered&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">La amiloidoisis renal hereditaria es un trastorno autos&#243;mico dominante cuya cl&#237;nica se solapa con la de otros tipos de amiloidoisis&#46; Hacer un adecuado diagn&#243;stico diferencial puede ser dif&#237;cil&#44; pero tiene una gran relevancia respecto al pron&#243;stico y tratamiento&#44; que difiere seg&#250;n sea el origen de la enfermedad&#46; Presentamos el caso cl&#237;nico de un paciente con s&#237;ndrome nefr&#243;tico e insuficiencia renal progresiva&#44; con antecedente familiar de madre con amiloidosis renal&#46;</p><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">En la biopsia renal se observ&#243; dep&#243;sito de amiloide a nivel glomerular&#44; con negatividad para cadenas ligeras y prote&#237;na AA&#46; La sospecha cl&#237;nica inicial fue la de amiloidosis por dep&#243;sito de cadena A alfa de fibrin&#243;geno&#44; que es la causa m&#225;s frecuente de amiloidosis hereditaria en Europa&#44; con afectaci&#243;n preferentemente glomerular&#46; Sin embargo&#44; el estudio gen&#233;tico determin&#243; una nueva mutaci&#243;n previamente no descrita de la Apolipoproteina AI &#40;APO AI&#41;&#46; En la biopsia de la madre se detect&#243; dep&#243;sito glomerular&#44; pero tambi&#233;n dep&#243;sito masivo en m&#233;dula&#44; lo que caracteriza a la amiloidosis por dep&#243;sito de APO AI&#46; El diagn&#243;stico se confirm&#243; mediante inmunohistoqu&#237;mica&#46;</p><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">La amiloidosis por dep&#243;sito de Apo AI progresa a enfermedad renal cr&#243;nica terminal en el plazo de de 3 a 15 a&#241;os&#46; Se diferencia cl&#237;nicamente de la amiloidosis AL por su menor afectaci&#243;n extrarrenal y su mejor pron&#243;stico&#46; El trasplante renal ofrece una supervivencia del injerto aceptable y el trasplante hepato-renal se podr&#237;a tener en cuenta en pacientes con disfunci&#243;n significativa de ambos &#243;rganos&#46;</p></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Samill&#225;n-Sosa KR&#44; Senci&#243;n-Mart&#237;nez G&#44; Lopes-Mart&#237;n V&#44; Mart&#237;nez-Gonz&#225;lez MA&#44; Sol&#233; M&#44; Arostegui JL&#44; et al&#46; Amiloidosis renal hereditaria por dep&#243;sito de apolipoprote&#237;na AI&#58; un reto diagn&#243;stico&#46; Nefrologia&#46; 2015&#59;35&#58;322&#8211;327&#46;</p>"
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Case report
Hereditary apolipoprotein AI-associated renal amyloidosis: A diagnostic challenge
Amiloidosis renal hereditaria por depósito de apolipoproteína AI: un reto diagnóstico
Kelly del Rocío Samillán-Sosaa, Gloria Sención-Martíneza, Vanessa Lopes-Martína, Miguel Angel Martínez-Gonzálezb, Manel Soléc, Jose Luis Arosteguid, Jose Mesae, Juan de Dios García-Díaze, Diego Rodríguez-Puyola, Patricia Martínez-Miguela,
Corresponding author
pmmiguel@salud.madrid.org

Corresponding author.
a Servicio de Nefrología, Hospital Universitario Príncipe de Asturias, Alcalá de Henares, Madrid, Spain
b Servicio de Anatomía Patológica, Hospital Universitario 12 de Octubre, Madrid, Spain
c Servicio de Anatomía Patológica, Hospital Clínic, Barcelona, Spain
d Servicio de Inmunología, Hospital Clínic, Barcelona, Spain
e Unidad de Genética Clínica, Medicina Interna, Hospital Universitario Príncipe de Asturias, Alcalá de Henares, Madrid, Spain
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cholesterolaemia of 275<span class="elsevierStyleHsp" style=""></span>mg&#47;dl and urine protein of 6<span class="elsevierStyleHsp" style=""></span>g&#47;24<span class="elsevierStyleHsp" style=""></span>h&#41;&#44; without alterations in the sediment and with normal glomerular filtration rate&#46; Electrophoretic spectrum in blood and urine&#44; immunological study and renal ultrasound scan were normal&#46; A renal biopsy was performed that presented 19 glomeruli with fully distorted structure by a hyaline deposit in nodular disposition&#44; with positivity for Congo red and thioflavin&#46; Tubules and vessels did not show significant alterations and therefore the findings were compatible with amyloidosis&#46; The study of a paraffin sample showed a marked positivity for AP protein&#44; which is a part of the amyloid substance common in all amyloidosis types&#44; with negativity for light chains and AA protein&#44; B2 microglobulin and transthyretin&#46; A supplementary study was performed with antibodies to fibrinogen and lysozyme and the amyloid substance deposits resulted positive for the fibrinogen A-alpha chain &#40;AFib&#41;&#46; However&#44; the genetic study did not show any mutation in the AFib chain gene but there was a previously undescribed mutation in the Apolipoprotein A1 gene &#40;Apo AI&#41;&#46; Faced with this discrepancy&#44; the mother&#39;s biopsy was analysed&#46; The biopsy contained a glomerular deposit in the cortex and a massive deposit at the medullary level&#46; The deposit at the medullary level was not described in the AFib amyloidosis&#44; being very characteristic of the Apo AI&#46; The conclusion is that the first results of the immunohistochemistry were not completely reliable as it was not performed under adequate conditions&#46; The presence of Apo AI was later confirmed using the same technique&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">An extension study was performed&#44; with echocardiogram and electromyography&#44; without signs of heart condition or autonomic neuropathy&#46; The clinical evolution showed a progressive increase in transaminases&#44; suggesting hepatic involvement&#46; These results were in agreement with this type of familial amyloidosis which&#44; preferably&#44; involves the kidney and liver&#46; Although the intila GFR was normal&#44; renal function subsequently deteriorated progressively until renal replacement therapy was required after 2 years&#46; The patient received treatment with peritoneal dialysis for 4 years&#44; thereafter the patient underwent undergoing renal transplantation from a deceased donor&#46; The patient presented a complicated postoperative period with splenic rupture&#44; in the context of his disease&#44; with amyloid deposit in the spleen&#46; An urgent splenectomy was indicated&#46; Finally&#44; the patient was discharged in stable condition &#40;<a class="elsevierStyleCrossRefs" href="#fig0005">Figs&#46; 1&#8211;4</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia><elsevierMultimedia ident="fig0020"></elsevierMultimedia></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Discussion</span><p id="par0020" class="elsevierStylePara elsevierViewall">Hereditary non-neuropathic renal amyloidosis was first described by Ostertag in 1932&#46;<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">1</span></a> This name was given to emphasise the absence of peripheral nervous system involvement&#44; with the purpose of differentiating this pathology from other types of amyloidosis&#46; However&#44; this term is confusing and is not currently appropriate because several variants related to the apolipoprotein A1 associated with neuropathy have been described since then&#46;<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">2</span></a> In regards to this disease&#44; more than 25 mutations that alter the structure of different proteins&#44; causing the deposit in amyloid form&#44; have been identified&#46; These proteins are lysozyme&#44;<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">3</span></a> Apo AI&#44;<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">4&#44;5</span></a> Apolipoprotein A II &#40;Apo II&#41;<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">6&#44;7</span></a> and AFib chain&#46;<a class="elsevierStyleCrossRefs" href="#bib0195"><span class="elsevierStyleSup">8&#8211;12</span></a> Clinically&#44; all of them manifest themselves with renal failure at middle age and they have a dominant autosomic heritage&#44; although with highly variable penetrance and some specific clinic characteristics&#44; depending on the protein that originates the deposit&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Apo AI is the main protein that forms the high-density lipoprotein &#40;HDL&#41; structure&#46; It is secreted in the liver and the small intestine and catabolised mainly in the liver and kidneys&#46;<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">13&#8211;15</span></a> It is a co-factor for lecithin-cholesterol acetyltransferase &#40;LCAT&#41;&#44; and its function is linked to cholesterol elimination&#46;<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">13&#44;15&#44;16</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">To date&#44; at least 19 amyloidogenic mutations have been described in the APO AI gene&#46; A different clinical presentation of the disease has been observed depending on the region in which the mutation is located&#46; In this way&#44; mutations that affect the amino-terminal region manifest themselves with amyloid deposit at hepatic and renal level&#44; whereas mutations that affect the carboxi-terminal region manifest themselves with cutaneous&#44; laryngeal and cardiac amyloidosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0165"><span class="elsevierStyleSup">2&#44;15&#44;17</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">The Apo AI amyloidosis phenotype is very heterogeneous&#46; Some of the published cases describe extensive visceral amyloidosis and end-stage renal failure&#44; whereas others include larynx and skin involvement&#44; with minimal clinical consequences&#46; Clinical expression does not only depend on the mutation location&#44; since even patients with the same mutation may experience different clinical expression&#46; Phenotypic heterogeneity has also been observed between lineages with the same Apo AI mutation&#46; There are publications including series of patients with an elevated number of relatives affected and fast progression to end-stage renal disease &#40;10 out of 16 cases affected&#41;&#44;<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">15</span></a> which suggests the existence of a more aggressive phenotype or other genetic and environmental factors interacting or having an influence on clinical manifestations&#46; The possible amyloid deposit has been described in several organs&#44; among them the kidney&#44; gastrointestinal tract&#44; spleen&#44; liver&#44; heart&#44; peripheral nervous system&#44; larynx and skin&#46; The most common clinical presentation consists of high blood pressure&#44; mild proteinuria and slowly progressive renal failure deterioration between the ages of 18 and 55&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">The first mutation described&#44; and the most frequent in patients with Apo AI amyloidosis of Irish ancestry&#44; is Gly26Arg&#46; It is characterised by the progressive accumulation of amyloid fibrils composed by the amino-terminal polypeptide fragments of the Apo AI and it appears in young patients&#44; aged 20&#8211;46&#46; The amyloid deposit is located in the peripheral nerves&#44; kidneys&#44; liver and gastrointestinal tract&#44;<a class="elsevierStyleCrossRefs" href="#bib0165"><span class="elsevierStyleSup">2&#44;17</span></a> manifesting itself clinically with peripheral neuropathy&#44; peptic ulcer and nephropathy&#46;<a class="elsevierStyleCrossRefs" href="#bib0165"><span class="elsevierStyleSup">2&#44;18</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">At least up to 19 amyloidogenic mutations of Apo AI have been described since&#46; Here we describe a new mutation that we did not find in the literature&#44; the c&#46;220T&#62;C &#40;p&#46;Trp74Arg&#41;&#46; In our patient&#39;s case&#44; we were able to observe kidney involvement&#44; with renal function impairment within two years&#44; as well as liver and spleen involvement&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">The histological analysis of Apo AI amyloidosis shows predominant amyloid deposits at the medullary level with tubulointerstitial nephritis pattern&#44; characterised by tubular atrophy and interstitial fibrosis&#44; associated with secondary focal glomeruloesclerosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0230"><span class="elsevierStyleSup">15&#44;19</span></a> Although interstitial involvement is the most frequent&#44; there are also cases in which a deposit at glomerular level has been detected&#46;<a class="elsevierStyleCrossRefs" href="#bib0250"><span class="elsevierStyleSup">19&#8211;21</span></a> One case has even been published with predominant glomerular involvement&#44; associated with nephrotic syndrome&#44; as a result of Apo AI Leu64Pro amyloidosis&#46;<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">22</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">The preferred selectiveness of Apo AI amyloidosis for the renal medulla allows us to differentiate it from other types of hereditary and acquired systemic amyloidosis&#44;<a class="elsevierStyleCrossRefs" href="#bib0250"><span class="elsevierStyleSup">19&#44;23</span></a> since this preference for the medullary compartment is only shared with transthyretin amyloidosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0250"><span class="elsevierStyleSup">19&#44;24</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">In our case&#44; the patient&#39;s renal biopsy only contained cortex and the glomerular compartment was the only place where amyloid deposit was found&#46; These findings are in agreement with the clinical symptoms at diagnosis&#44; consistent nephrotic syndrome with posterior progressive worsening of renal function&#46; Initially&#44; this particular characteristic made us suspect fibrinogen A alpha chain amyloidosis&#44; since it is the most frequent cause of hereditary renal amyloidosis in Europe&#44; and its deposit is characteristically glomerular&#46; However&#44; the mother&#39;s biopsy had glomerular deposit in cortex&#44; but it also had medulla with massive deposit&#46; Finally&#44; the genetic study determined a new&#44; previously undescribed&#44; Apo AI mutation&#44; and the immunochemistry confirmed the diagnosis&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">A correct differential diagnosis in systemic amyloidosis is important since disease management and prognosis may be completely different depending on its origin&#46; This is the reason why it is particularly relevant to determine the protein that originates the deposit&#46; In accordance with a study performed in the United Kingdom National Amyloidosis Centre&#44; almost 10&#37; of the patients with a presumptive diagnosis of AL systemic amyloidosis actually suffer from a hereditary amyloidosis&#46;<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">25</span></a> This usually happens because it is quite common to consider AL amyloidosis as a diagnosis of exclusion&#44; due to the clinical overlapping between different types of amyloidosis&#44; the relatively frequent finding of a monoclonal protein in patients over 50&#44; and the difficulty to determine the type of fibril&#44; even when the AL amyloidosis diagnosis is correct&#44; since in up to 20&#37; of the cases the lambda or kappa light chain antibodies are not bound to it&#44; probably due to the alteration in their structure&#46; Moreover&#44; it is not always possible to verify the presence of family history of hereditary amyloidosis due to the variable penetrance of the disease and the diagnosis of new mutations&#46;</p><p id="par0070" class="elsevierStylePara elsevierViewall">Among the methods available to determine the protein composition of fibrils&#44; we find immunochemistry and direct protein sequencing&#46; In order to perform this last technique&#44; a considerable amount of tissue is required which is not always possible to obtain&#46; The recent development of proteomic techniques constitutes an advance in the diagnosis of amyloidosis since in order to identify the protein that forms the amyloid fibril only a small amount of fixed tissue is required&#46;<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">26</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Regarding disease treatment&#44; renal transplant due to Apo AI amyloidosis has had varied success&#46;<a class="elsevierStyleCrossRefs" href="#bib0250"><span class="elsevierStyleSup">19&#44;27&#44;28</span></a> There has been recurrence of amyloidosis in grafts&#44; but in most of the published cases graft survival was acceptable&#46; A study performed in the United Kingdom National Amyloidosis Centre revealed that out of 10 renal transplant recipients with APO AI amyloidosis&#44; five showed documented evidence of amyloid deposit in the transplanted kidney&#46; However&#44; only one patient&#44; after 25 years&#44; progressed to end-stage renal disease&#44; initiating dialysis again&#46;<a class="elsevierStyleCrossRefs" href="#bib0260"><span class="elsevierStyleSup">21&#44;29</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">Liver transplant is the final treatment for other types of hereditary amyloidosis&#44; since the amyloidogenic protein is synthesised in the liver&#46; However&#44; in the APO AI amyloidosis&#44; the amyloidogenic protein is also synthesised in the small intestine&#46; Although there have been cases like that of an Irish patient with the Apo AI Gly26Arg mutation&#44; who underwent hepatorenal transplant and two years later evidenced a regression of the amyloid deposits&#44;<a class="elsevierStyleCrossRefs" href="#bib0250"><span class="elsevierStyleSup">19&#44;30</span></a> double hepatorenal transplant is only considered in patients with significant impairment in both organs&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">In our patient&#39;s case&#44; we considered the best option was renal transplant since hepatic function was not very impaired&#46; However&#44; post-transplant evolution has become complicated by splenic rupture due to amyloid deposit&#46;</p><p id="par0090" class="elsevierStylePara elsevierViewall">We could assert that hereditary renal amyloidosis constitutes a diagnostic challenge due to the difficulty to identify the protein that originates the deposit&#44; and the importance of this aspect in prognosis and treatment&#46; In APO AI amyloidosis&#44; the indices cases diagnosis requires high clinical suspicion and a renal medulla biopsy is important to observe the amyloid deposit at this level&#46; The possibility of this diagnosis has to be considered in family cases of tubulointerstitial nephritis with hepatic involvement&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Questions</span><p id="par0095" class="elsevierStylePara elsevierViewall"><ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">1&#41;</span><p id="par0100" class="elsevierStylePara elsevierViewall">Dr&#46; Esther Rosello &#40;Valencia&#41;&#46; The diagnostic yield of amyloidosis often forces specialists to perform studies in fat&#44; rectal mucosa and&#44; in the end&#44; a renal biopsy&#46; What is the decision followed in the extraction of biopsies upon suspicion of amyloidosis&#63;</p><p id="par0105" class="elsevierStylePara elsevierViewall">Answer &#40;Kelly Samill&#225;n&#41;&#58; Upon suspicion of amyloidosis&#44; the diagnosis can frequently be confirmed through abdominal fat aspiration&#44; which is a mildly invasive technique&#46; The literature states that this technique provides high sensitivity for the diagnosis of AL amyloidosis &#40;between 80 and 90&#37;&#41; and a lower sensitivity &#40;between 65 and 75&#37;&#41; for AA amyloidosis diagnosis&#46; However&#44; in the case of familial amyloidosis&#44; the diagnostic yield is very low and the absence of positivity to Congo red in an abdominal fat biopsy does not exclude the diagnosis&#46;<a class="elsevierStyleCrossRef" href="#bib0310"><span class="elsevierStyleSup">31</span></a> In regards to the salivary gland and rectal mucosa biopsies&#44; they are also used as non-invasive diagnostic methods&#46; We believe that the diagnostic method in cases of amyloidosis must be individualised in accordance with the patient&#39;s characteristics and comorbidity&#46; In general&#44; if a patient presents apparent renal involvement&#44; particularly if the patient has nephrotic syndrome&#44; our group indicates the performance of a renal biopsy&#44; except in the exceptional cases in which the renal biopsy would not be decisive to take decisions or in which the patient&#39;s comorbidity does not allow it&#46; In the cases of Apo AI amyloidosis with renal involvement&#44; in our opinion&#44; it is advisable to perform the renal biopsy directly&#46;</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">2&#41;</span><p id="par0110" class="elsevierStylePara elsevierViewall">Dr&#46; Esther Rosell&#243; &#40;Valencia&#41;&#46; Do you think biopsy samples could be sent to referral centers for special amyloidosis techniques&#63;</p><p id="par0115" class="elsevierStylePara elsevierViewall">Answer &#40;Manuel Sol&#233;&#41;&#58; The diagnosis of amyloidosis presents difficulties at two levels&#58; the basic one&#44; the diagnosis with Congo red stain&#44; should be undertaken in the centre itself&#44; through adequate technique control&#44; although we are aware of the many problems this poses&#46; If typification is in question&#44; it is important to use an antibodies panel and the interpretation requires experience&#46; In this case&#44; it would be adequate to refer the sample to an amyloidosis unit&#46;</p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">3&#41;</span><p id="par0120" class="elsevierStylePara elsevierViewall">Dr&#46; Miguel &#193;ngel Mart&#237;nez &#40;Madrid&#41;&#58; I would like to mention that Congo red techniques are only successful if the cut sessions have a minimum of 6<span class="elsevierStyleHsp" style=""></span>&#956;m&#46; Does that coincide with your experience&#63;</p><p id="par0125" class="elsevierStylePara elsevierViewall">Answer &#40;Manuel Sol&#233;&#41;&#58; This is a very important technical aspect&#46; It is usually recommended to perform the stain on 8-&#956;m sections&#46; However&#44; this is not always possible&#44; particularly in renal biopsies in which routine unstained cut sections are performed for different techniques&#46; If the cut section is thin&#44; the stain will be pale&#44; but the green birefringence will remain&#44; although it may be more difficult to visualise&#46;</p></li><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">4&#41;</span><p id="par0130" class="elsevierStylePara elsevierViewall">Dr&#46; Julia Blanco &#40;Madrid&#41;&#46; I have noticed that you have obtained an excellent apple green in Congo red techniques&#44; do you have a secret formula&#63;</p><p id="par0135" class="elsevierStylePara elsevierViewall">Answer &#40;Manuel Sol&#233;&#41;&#58; It is essential that the observation with polarised light be made with a powerful light source&#46; Not just any microscope will do&#46; And remember that the main feature of Congo red is dichroism&#44; that is&#44; the change from red to golden and green when rotating the polarising filter&#46;</p></li></ul></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conflicts of interest</span><p id="par0140" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Hereditary renal amyloidosis is an autosomal dominant condition with considerable overlap with other amyloidosis types&#46; Differential diagnosis is complicated&#44; but is relevant for prognosis and treatment&#46; We describe a patient with nephrotic syndrome and progressive renal failure&#44; who had a mother with renal amyloidosis&#46;</p><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Renal biopsy revealed amyloid deposits in glomerular space&#44; with absence of light chains and protein AA&#46; We suspected amyloidosis with fibrinogen A alpha chain deposits&#44; which is the most frequent cause of hereditary amyloidosis in Europe&#44; with a glomerular preferential affectation&#46; However&#44; the genetic study showed a novel mutation in apolipoprotein AI&#46; On reviewing the biopsy of the patient&#39;s mother similar glomerular deposits were found&#44; but there were significant deposits in the renal medulla as well&#44; which is typical in APO AI amyloidosis&#46; The diagnosis was confirmed by immunohistochemistry&#46;</p><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Apo AI amyloidosis is characterised by slowly progressive renal disease and end-stage renal disease occurs approximately 3&#8211;15 years from initial diagnosis&#46; Renal transplantation offers an acceptable graft survival and in these patients with hepatorenal involvement simultaneous liver and kidney transplantation could be considered&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">La amiloidoisis renal hereditaria es un trastorno autos&#243;mico dominante cuya cl&#237;nica se solapa con la de otros tipos de amiloidoisis&#46; Hacer un adecuado diagn&#243;stico diferencial puede ser dif&#237;cil&#44; pero tiene una gran relevancia respecto al pron&#243;stico y tratamiento&#44; que difiere seg&#250;n sea el origen de la enfermedad&#46; Presentamos el caso cl&#237;nico de un paciente con s&#237;ndrome nefr&#243;tico e insuficiencia renal progresiva&#44; con antecedente familiar de madre con amiloidosis renal&#46;</p><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">En la biopsia renal se observ&#243; dep&#243;sito de amiloide a nivel glomerular&#44; con negatividad para cadenas ligeras y prote&#237;na AA&#46; La sospecha cl&#237;nica inicial fue la de amiloidosis por dep&#243;sito de cadena A alfa de fibrin&#243;geno&#44; que es la causa m&#225;s frecuente de amiloidosis hereditaria en Europa&#44; con afectaci&#243;n preferentemente glomerular&#46; Sin embargo&#44; el estudio gen&#233;tico determin&#243; una nueva mutaci&#243;n previamente no descrita de la Apolipoproteina AI &#40;APO AI&#41;&#46; En la biopsia de la madre se detect&#243; dep&#243;sito glomerular&#44; pero tambi&#233;n dep&#243;sito masivo en m&#233;dula&#44; lo que caracteriza a la amiloidosis por dep&#243;sito de APO AI&#46; El diagn&#243;stico se confirm&#243; mediante inmunohistoqu&#237;mica&#46;</p><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">La amiloidosis por dep&#243;sito de Apo AI progresa a enfermedad renal cr&#243;nica terminal en el plazo de de 3 a 15 a&#241;os&#46; Se diferencia cl&#237;nicamente de la amiloidosis AL por su menor afectaci&#243;n extrarrenal y su mejor pron&#243;stico&#46; El trasplante renal ofrece una supervivencia del injerto aceptable y el trasplante hepato-renal se podr&#237;a tener en cuenta en pacientes con disfunci&#243;n significativa de ambos &#243;rganos&#46;</p></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Samill&#225;n-Sosa KR&#44; Senci&#243;n-Mart&#237;nez G&#44; Lopes-Mart&#237;n V&#44; Mart&#237;nez-Gonz&#225;lez MA&#44; Sol&#233; M&#44; Arostegui JL&#44; et al&#46; Amiloidosis renal hereditaria por dep&#243;sito de apolipoprote&#237;na AI&#58; un reto diagn&#243;stico&#46; Nefrologia&#46; 2015&#59;35&#58;322&#8211;327&#46;</p>"
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