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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Lipodystrophy syndromes are a heterogeneous group of rare diseases characterised by selective loss of adipose tissue&#44; which often leads to insulin resistance with a tendency to develop diabetes&#44; dyslipidaemia&#44; hepatic steatosis&#44; acanthosis nigricans and hyperandrogenism&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> Acquired partial lipodystrophy &#40;APL&#59; OMIM&#58; <a id="intr0010" class="elsevierStyleInterRef" href="omim:608709">608709</a>&#41;&#44; also known as Barraquer&#8211;Simons syndrome&#44; is one of the most common&#44; and predominantly affects women &#40;4&#58;1&#41;&#46; It is characterised by a progressive loss of subcutaneous fat&#44; usually starting in childhood&#44;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> and progresses from the head down&#44; affecting the face&#44; upper limbs&#44; trunk and abdomen&#46; Unlike other types of lipodystrophy&#44; insulin resistance and metabolic complications&#44; apart from hepatomegaly &#40;60&#37;&#41;&#44; are rare&#46;<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1&#44;2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">In 10&#8211;20&#37; of cases&#44; APL is associated with autoimmune disorders&#44; especially lupus&#46; The most common complication &#40;20&#37;&#41; is the development of membranoproliferative glomerulonephritis type 2&#44; or dense deposit disease &#40;DDD&#41; approximately 8 years after onset of the disease&#46; The pathogenesis of such renal involvement includes activation of the alternative complement pathway &#40;ACP&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a> Patients show decreased serum C3 levels &#40;70&#37;&#41; and are positive for C3NeF &#40;80&#37;&#41;&#44;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> an autoantibody capable of altering the ACP and in the case of APL&#44; it is suspected to play a role in the destruction of fatty tissue&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">We had the case of a 15-year-old Caucasian girl with no relevant family or personal clinical history who was diagnosed of APL at the age of 5 due to progressive loss of subcutaneous fat from her face &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>a and b&#41;&#44; with subsequent involvement of neck and shoulders&#46; In her regular visits&#44; no clinical or laboratory abnormalities had been observed&#44; except for the slow progression of lipoatrophy and sustained decreased serum levels of C3 &#40;26&#8211;48<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; VN&#58; 86&#8211;184&#41;&#46; She had never had clinical or analytical data suggestive of nephropathy&#44; dyslipidaemia&#44; insulin resistance or hyperandrogenism&#46; Her serum leptin &#40;8&#46;03<span class="elsevierStyleHsp" style=""></span>ng&#47;ml&#59; NR&#58; 15&#46;3<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>8&#46;1 SD&#41; and adiponectin &#40;8&#46;3<span class="elsevierStyleHsp" style=""></span>mg&#47;ml&#59; NR&#58; 12&#46;0<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>3&#46;1 SD&#41; levels were slightly low and the DXA body composition study showed a reduction in total body fat &#40;17&#46;7&#37;&#59; NR&#58; 25&#46;9<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>6&#46;3&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">At the age of 13&#44; after three days of fever and in the context of acute gastroenteritis&#44; she was found to have macroscopic haematuria with non-nephrotic proteinuria &#40;13<span class="elsevierStyleHsp" style=""></span>mg&#47;kg&#47;day&#41; and transient elevation of creatinine &#40;maximum&#58; 0&#46;74<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#41;&#46; The pyrexia subsided 24<span class="elsevierStyleHsp" style=""></span>h later&#44; but the macroscopic haematuria persisted for two weeks&#44; with no other symptoms and with improvement in kidney function&#46; Serum levels of IgA were found to be high &#40;377<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; NR&#58; 40&#8211;350&#41;&#44; C3 remained low and C3NeF negative&#46; Studies of autoimmunity &#40;anti-thyroid&#44; anti-neutrophil and anti-nuclear antibodies&#41; were negative&#46; Percutaneous kidney biopsy was performed one month after the haematuria resolved&#46; The specimen contained 14 glomeruli and revealed the presence of focal and segmental mesangial hypercellularity &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>c&#41;&#58; M1&#44; E0&#44; S0 and T0 according to the Oxford classification<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> &#40;mesangial hypercellularity &#91;M&#93;&#44; endocapillary proliferation &#91;E&#93;&#44; segmental glomerulosclerosis &#91;S&#93; and interstitial fibrosis with tubular atrophy &#91;T&#93;&#41;&#46; Only one of the glomeruli had a crescent that occupied 26&#8211;50&#37; of the glomerulus&#46; Immunofluorescence showed granular mesangial IgA and C3 deposits &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>d&#41;&#46; Electron microscopy confirmed the presence of electron-dense deposits in the glomerulus&#44; ruling out DDD&#46; The patient was diagnosed with IgA nephropathy &#40;IgAN&#41;&#44; achieving clinical remission with spontaneous disappearance of the proteinuria and haematuria&#44; but maintaining decreased serum levels of C3 &#40;33<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#41; and increased serum IgA &#40;353<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#41;&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">APL is a rare disease of uncertain aetiology&#46; The association of APL with autoimmune diseases and DDD&#44; in addition to the decrease in C3 and C3NeF positivity point to an autoimmune basis<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a>&#59; although a possible genetic predisposition has also been suggested&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> IgAN&#44; meanwhile&#44; is the most common glomerular disease in the world&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> The aetiopathogenesis of IgAN&#44; which is not fully understood&#44; also involves complement activation through the ACP<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">7&#8211;9</span></a> and sometimes through the lectin pathway&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a> Diagnosis is histological and kidney biopsy shows mesangial immune deposits of IgA1 with C3 and occasionally IgG or IgM&#46; In the mesangial deposits&#44; it is common to find components of the ACP &#40;C3 and properdin&#41;&#44; but not of the classic pathway &#40;C1q and C4&#41; which&#44; taken together with normal serum C3 and other complement components&#44; suggests that the complement activation occurs in the kidney itself&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">To summarise&#44; we present the first reported case of APL associated to IgAN&#46; Although&#44; given the incidence of IgAN&#44; it could be a coincidence&#44; the fact that the APL is often associated with nephropathy&#44; the DDD&#44; whose pathogenesis&#44; like IgAN&#44; involves activation of the ACP&#44; raises the possibility of a common link between the two diseases&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0035" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest&#46;</p></span></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; de Lucas-Collantes C&#44; Pozo-Rom&#225;n J&#44; Aparicio-L&#243;pez C&#44; de Prada-Vicente I&#44; Argente J&#46; Lipodistrofia parcial adquirida &#40;s&#237;ndrome de Barraquer-Simons&#41; y nefropat&#237;a IgA&#46; Nefrolog&#237;a&#46; 2016&#59;36&#58;556&#8211;558&#46;</p>"
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Letter to the Editor
Acquired partial lipodystrophy (Barraquer–Simons syndrome) and IgA nephropathy
Lipodistrofia parcial adquirida (síndrome de Barraquer-Simons) y nefropatía IgA
Carmen de Lucas-Collantesa,e,
Corresponding author
mcdelucas@yahoo.es

Corresponding author.
, Jesús Pozo-Románb,c,d,e,f, Cristina Aparicio-Lópeza, Inmaculada de Prada-Vicentec, Jesús Argenteb,c,d,e,f
a Departamento de Nefrología Pediátrica, Hospital Infantil Universitario Niño Jesús, Madrid, Spain
b Departamento de Endocrinología Pediátrica, Hospital Infantil Universitario Niño Jesús, Madrid, Spain
c Departamento de Anatomía Patológica, Hospital Infantil Universitario Niño Jesús, Madrid, Spain
d Instituto de Investigación La Princesa, Madrid, Spain
e Departamento de Pediatría, Universidad Autónoma de Madrid, Madrid, Spain
f CIBEROBN, Instituto de Salud Carlos III, Madrid, Spain
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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">&#40;a and b&#41; Progression of the loss of facial fat&#59; &#40;c&#41; Glomeruli with increased mesangial cellularity&#44; and focal and segmental involvement &#40;H&#38;E &#215;100&#41; and &#40;d&#41; Mesangial granular immunofluorescence with anti-IgA&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Lipodystrophy syndromes are a heterogeneous group of rare diseases characterised by selective loss of adipose tissue&#44; which often leads to insulin resistance with a tendency to develop diabetes&#44; dyslipidaemia&#44; hepatic steatosis&#44; acanthosis nigricans and hyperandrogenism&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> Acquired partial lipodystrophy &#40;APL&#59; OMIM&#58; <a id="intr0010" class="elsevierStyleInterRef" href="omim:608709">608709</a>&#41;&#44; also known as Barraquer&#8211;Simons syndrome&#44; is one of the most common&#44; and predominantly affects women &#40;4&#58;1&#41;&#46; It is characterised by a progressive loss of subcutaneous fat&#44; usually starting in childhood&#44;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> and progresses from the head down&#44; affecting the face&#44; upper limbs&#44; trunk and abdomen&#46; Unlike other types of lipodystrophy&#44; insulin resistance and metabolic complications&#44; apart from hepatomegaly &#40;60&#37;&#41;&#44; are rare&#46;<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1&#44;2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">In 10&#8211;20&#37; of cases&#44; APL is associated with autoimmune disorders&#44; especially lupus&#46; The most common complication &#40;20&#37;&#41; is the development of membranoproliferative glomerulonephritis type 2&#44; or dense deposit disease &#40;DDD&#41; approximately 8 years after onset of the disease&#46; The pathogenesis of such renal involvement includes activation of the alternative complement pathway &#40;ACP&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a> Patients show decreased serum C3 levels &#40;70&#37;&#41; and are positive for C3NeF &#40;80&#37;&#41;&#44;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> an autoantibody capable of altering the ACP and in the case of APL&#44; it is suspected to play a role in the destruction of fatty tissue&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">We had the case of a 15-year-old Caucasian girl with no relevant family or personal clinical history who was diagnosed of APL at the age of 5 due to progressive loss of subcutaneous fat from her face &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>a and b&#41;&#44; with subsequent involvement of neck and shoulders&#46; In her regular visits&#44; no clinical or laboratory abnormalities had been observed&#44; except for the slow progression of lipoatrophy and sustained decreased serum levels of C3 &#40;26&#8211;48<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; VN&#58; 86&#8211;184&#41;&#46; She had never had clinical or analytical data suggestive of nephropathy&#44; dyslipidaemia&#44; insulin resistance or hyperandrogenism&#46; Her serum leptin &#40;8&#46;03<span class="elsevierStyleHsp" style=""></span>ng&#47;ml&#59; NR&#58; 15&#46;3<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>8&#46;1 SD&#41; and adiponectin &#40;8&#46;3<span class="elsevierStyleHsp" style=""></span>mg&#47;ml&#59; NR&#58; 12&#46;0<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>3&#46;1 SD&#41; levels were slightly low and the DXA body composition study showed a reduction in total body fat &#40;17&#46;7&#37;&#59; NR&#58; 25&#46;9<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>6&#46;3&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">At the age of 13&#44; after three days of fever and in the context of acute gastroenteritis&#44; she was found to have macroscopic haematuria with non-nephrotic proteinuria &#40;13<span class="elsevierStyleHsp" style=""></span>mg&#47;kg&#47;day&#41; and transient elevation of creatinine &#40;maximum&#58; 0&#46;74<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#41;&#46; The pyrexia subsided 24<span class="elsevierStyleHsp" style=""></span>h later&#44; but the macroscopic haematuria persisted for two weeks&#44; with no other symptoms and with improvement in kidney function&#46; Serum levels of IgA were found to be high &#40;377<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; NR&#58; 40&#8211;350&#41;&#44; C3 remained low and C3NeF negative&#46; Studies of autoimmunity &#40;anti-thyroid&#44; anti-neutrophil and anti-nuclear antibodies&#41; were negative&#46; Percutaneous kidney biopsy was performed one month after the haematuria resolved&#46; The specimen contained 14 glomeruli and revealed the presence of focal and segmental mesangial hypercellularity &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>c&#41;&#58; M1&#44; E0&#44; S0 and T0 according to the Oxford classification<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> &#40;mesangial hypercellularity &#91;M&#93;&#44; endocapillary proliferation &#91;E&#93;&#44; segmental glomerulosclerosis &#91;S&#93; and interstitial fibrosis with tubular atrophy &#91;T&#93;&#41;&#46; Only one of the glomeruli had a crescent that occupied 26&#8211;50&#37; of the glomerulus&#46; Immunofluorescence showed granular mesangial IgA and C3 deposits &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>d&#41;&#46; Electron microscopy confirmed the presence of electron-dense deposits in the glomerulus&#44; ruling out DDD&#46; The patient was diagnosed with IgA nephropathy &#40;IgAN&#41;&#44; achieving clinical remission with spontaneous disappearance of the proteinuria and haematuria&#44; but maintaining decreased serum levels of C3 &#40;33<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#41; and increased serum IgA &#40;353<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#41;&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">APL is a rare disease of uncertain aetiology&#46; The association of APL with autoimmune diseases and DDD&#44; in addition to the decrease in C3 and C3NeF positivity point to an autoimmune basis<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a>&#59; although a possible genetic predisposition has also been suggested&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> IgAN&#44; meanwhile&#44; is the most common glomerular disease in the world&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> The aetiopathogenesis of IgAN&#44; which is not fully understood&#44; also involves complement activation through the ACP<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">7&#8211;9</span></a> and sometimes through the lectin pathway&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a> Diagnosis is histological and kidney biopsy shows mesangial immune deposits of IgA1 with C3 and occasionally IgG or IgM&#46; In the mesangial deposits&#44; it is common to find components of the ACP &#40;C3 and properdin&#41;&#44; but not of the classic pathway &#40;C1q and C4&#41; which&#44; taken together with normal serum C3 and other complement components&#44; suggests that the complement activation occurs in the kidney itself&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">To summarise&#44; we present the first reported case of APL associated to IgAN&#46; Although&#44; given the incidence of IgAN&#44; it could be a coincidence&#44; the fact that the APL is often associated with nephropathy&#44; the DDD&#44; whose pathogenesis&#44; like IgAN&#44; involves activation of the ACP&#44; raises the possibility of a common link between the two diseases&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0035" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest&#46;</p></span></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; de Lucas-Collantes C&#44; Pozo-Rom&#225;n J&#44; Aparicio-L&#243;pez C&#44; de Prada-Vicente I&#44; Argente J&#46; Lipodistrofia parcial adquirida &#40;s&#237;ndrome de Barraquer-Simons&#41; y nefropat&#237;a IgA&#46; Nefrolog&#237;a&#46; 2016&#59;36&#58;556&#8211;558&#46;</p>"
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        "texto" => "<p id="par0040" class="elsevierStylePara elsevierViewall">The authors thank Dr Fernando Corvillo&#44; of the Immunology Department&#44; Hospital La Paz&#44; IdiPAZ&#44; Madrid&#44; for the study of C3Nef&#46;</p>"
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Article information
ISSN: 20132514
Original language: English
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Idiomas
Nefrología (English Edition)
es en

¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?