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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">INTRODUCTION</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Many authors now consider psoriasis to be an immune-mediated disease that primarily affects the skin&#46; There is no consensus as to whether or not the disease has an impact on the kidneys directly&#44; but the literature contains several cases of associated kidney diseases&#46; Etanercept is a tumour necrosis factor alpha &#40;TNF-alpha&#41; inhibitor used to treat this condition and others&#46; However&#44; cases of kidney injury have been associated with this drug&#46; In this study&#44; we present the case of a patient with membranous nephropathy &#40;MGN&#41; who later developed psoriasis&#44; which was treated with etanercept&#46; We observed complete remission of proteinuria during this treatment&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CASE STUDY</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Male patient 43 years of age with hypercholesterolaemia treated with statins&#44; non-hypertensive and non-diabetic&#46; Smoker and occasional drinker&#46; His nephrological symptoms began in April 2003&#44; when he presented with clinical and laboratory signs of a nephrotic syndrome while being treated for an ear infection with amoxicillin and clavulanic acid&#46; Since spontaneous partial remission of the syndrome occurred&#44; with residual proteinuria levels of approximately 1g&#47;24 hours and renal function normal at all times&#44; he did not undergo a biopsy and was monitored by the Nephrology Department on an outpatient basis&#46;</p><p class="elsevierStylePara">From that time on&#44; proteinuria &#40;selective&#41; gradually increased to 14g&#47;24h&#44; with no changes in urinary sediment&#46; An immunological study detected no antibodies&#44; and complement levels were normal according to multiple studies throughout the follow-up period&#46; The patient tested negative for hepatitis B&#44; C and human immunodeficiency virus&#46; In October 2003&#44; when renal function was normal&#44; the patient underwent a kidney biopsy that showed stage II MGN&#46; The immunofluorescence assay revealed intense granular parietal IgG&#44; C3 and C1q deposits&#46;</p><p class="elsevierStylePara">Prednisone treatment was started at doses of 1mg&#47;kg&#47;day&#44; resulting in partial remission of proteinuria&#44; which reached levels of 1&#46;3-0&#46;5g&#47;24h&#46; Treatment lasted 8 months&#44; with a progressive decrease in steroid doses&#46; At that time&#44; we initiated antiproteinuric treatment with enalapril and candesartan&#59; proteinuria persisted at levels of about 0&#46;5g&#47;24h&#46;</p><p class="elsevierStylePara">In December 2006&#44; the patient presented with scaly&#44; erythematous lesions on his hands&#44; feet and elbows&#44; and was diagnosed with psoriasis in the Dermatology department&#46; Treatment with acitretin failed and we decided to use an anti-TNF-alpha agent &#40;etanercept&#41; in April 2009&#59; treatment continued for 9 months and skin lesions improved significantly before resolving completely&#46; At the same time&#44; proteinuria decreased and was in complete remission 6 months after starting the treatment described above&#46;</p><p class="elsevierStylePara">The patient&#8217;s glomerular syndrome remained in complete remission during 11 months&#44; during which time no skin lesions were present&#46; In December 2010&#44; signs of psoriasis began to reappear slowly and progressively&#46; Proteinuria was detected again at that time&#44; at a level of 0&#46;5g&#47;24h&#46;</p><p class="elsevierStylePara">Figure 1 summarises the evolution of the case&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">This case led us to review three topics and the relationships between the two entities&#58;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Psoriasis and renal conditions</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Psoriasis is mainly a skin condition but it has some systemic repercussions&#46;<span class="elsevierStyleSup">1</span> It is characterised by the cutaneous infiltration of activated T cells and the proliferation of keratinocytes&#44; dendritic cells and Langerhans cells&#44; resulting in high concentrations of TNF-alpha in psoriatic lesions&#46;<span class="elsevierStyleSup">2</span> Decreasing intralesion and blood levels of TNF-alpha using agents that inhibit this cytokine is associated with clinical improvement&#46;<span class="elsevierStyleSup">3</span></p><p class="elsevierStylePara">Most reviews conclude that compromised renal function in psoriasis is very rare&#44; and may be directly related to a condition such as glomerulonephritis &#40;mainly membranous glomerulonephritis and IgA nephropathy&#41;&#44; microalbuminuria or secondary amyloidosis &#40;the literature reports some 20 cases of associated amyloidosis<span class="elsevierStyleSup">1</span>&#41;&#44; or related to psoriasis treatment with cyclosporine&#44; methotrexate or fumaric acid esters&#46;<span class="elsevierStyleSup">1&#44;2&#44;4-9</span> One study of 109 psoriasis patients and 178 controls observed that the former had significantly higher albuminuria levels and poorer creatinine clearance rates &#40;110ml&#47;min vs 109ml&#47;min&#41; measured using the Cockcroft-Gault formula&#46; Nevertheless&#44; the design and the discussion of that study are quite questionable&#59; among other issues&#44; there were no significant differences between subjects&#39; serum creatinine levels&#46;<span class="elsevierStyleSup">10</span></p><p class="elsevierStylePara">According to Zachariae&#44; incidental renal biopsies performed in psoriasis patients were normal&#46;<span class="elsevierStyleSup">4</span></p><p class="elsevierStylePara">As these patients&#8217; levels of beta 2-microglobulin in urine were within the upper limits of the normal range in 2 different analyses&#44; we conclude that tubular function is not affected in psoriasis&#46;<span class="elsevierStyleSup">11&#44;12</span></p><p class="elsevierStylePara">In the Szepietowki study&#44; the only renal anomaly detected was microalbuminuria&#44; which was present in 22&#37; of cases and in 42&#37; of those with severe skin lesions&#46;<span class="elsevierStyleSup">13</span> These data are comparable to recent findings published by Dervisoglu&#44; who found a correlation between proteinuria and the psoriasis activity&#47;severity index in 24&#37; of patients with microalbinuria&#46;<span class="elsevierStyleSup">14</span> Cecchi demonstrated the presence of significant microalbuminuria &#40;values &#62;20&#181;g&#47;min&#41; in 32 psoriasis patients compared to a control group&#44; and these values were correlated with the extent of the skin lesions&#46;<span class="elsevierStyleSup">15</span></p><p class="elsevierStylePara">Several cases of IgA nephropathy associated with psoriasis have been described&#46;<span class="elsevierStyleSup">7&#44;16</span> IgA levels are elevated in 50&#37; of psoriasis patients&#46;<span class="elsevierStyleSup">17</span> However&#44; in view of new findings about this nephropathy&#44; other factors must be at work in order for glomerular damage to occur&#46;</p><p class="elsevierStylePara">Sakemi et al described a similar case to our own in which a patient with MGN and nephrotic syndrome subsequently developed psoriasis&#46; These authors suggested that the immunological mechanism responsible for the association between systemic lupus erythematosus &#40;SLE&#41; or rheumatoid arthritis and secondary MGN could also be at work in psoriasis&#46;<span class="elsevierStyleSup">18</span></p><p class="elsevierStylePara">There are currently several approaches to explaining MGN pathogenesis&#46; One hypothesis is that it is caused by immune complexes &#40;formed by IgG1 and IgG4 directed against antigens on the epithelial side of the glomerular basement membrane and in podocytes&#44; associated with the complement&#41; that would alter the permeability of the filtration barrier&#46; Cellular immunity with increased TNF-alpha expression in the glomerulus<span class="elsevierStyleSup">19-21</span> and high levels of circulating TNF-alpha contribute to this damage&#46;<span class="elsevierStyleSup">22&#44;23</span> For that reason&#44; inhibition of this cytokine is proposed as a treatment objective in this disease&#46;<span class="elsevierStyleSup">20</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">The role played by tumour necrosis factor alpha</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">TNF-alpha is a cytokine produced by many cells having immunological activity in response to inflammation&#46;<span class="elsevierStyleSup">24</span> It is the main pro-inflammatory cytokine&#44; although there is evidence that it also acts as an immunomodulator&#46;<span class="elsevierStyleSup">25&#44;26</span></p><p class="elsevierStylePara">Etanercept is a dimeric molecule formed by the tumour necrosis factor receptor associated with the Fc region of IgG1&#46; This human recombinant protein inhibits TNF-alpha by competing with it to bind to its receptors TNFR1 &#40;55 kDa&#41; and TNFR2 &#40;75 kDa&#41;&#46;<span class="elsevierStyleSup">3&#44;20</span></p><p class="elsevierStylePara">Etanercept has been shown to be effective in treating psoriasis&#44; rheumatoid arthritis and juvenile idiopathic arthritis&#46;<span class="elsevierStyleSup">3&#44;27&#44;28</span></p><p class="elsevierStylePara">However&#44; due to its complex interactions with other immune system agents&#44; it has been found to stimulate autoimmunity&#46; This was demonstrated in published cases involving the appearance of new autoimmune disorders&#44; such as ANCA-positive vasculitis<span class="elsevierStyleSup">26</span> and lupus-like syndromes&#44;<span class="elsevierStyleSup">29-33</span> during treatment with this drug&#46; It has been observed that TNF-alpha plays an important role in the production of autoantibodies&#44; since it has different &#40;and sometimes contradictory&#41; effects on B cells&#44; dendritic cells&#44; T cells and the process of apoptosis&#46; These complex effects could explain the production of antinuclear antibodies &#40;anti-DNA&#44; anti-dsDNA&#41; and anti-cardiolipin antibodies&#44; which has been observed during treatment with anti-TNF-alpha&#46;<span class="elsevierStyleSup">26</span></p><p class="elsevierStylePara">Despite the importance of TNF-alpha in MGN pathogenesis&#44; TNF-alpha inhibition with etanercept was shown to decrease TNFR1 without any significant clinical improvement in a pilot study by Lionaki et al&#46;<span class="elsevierStyleSup">20</span> The authors concluded that this lack of efficacy could be caused by insufficient inhibition of TNF-alpha&#44; caused mainly by an unknown pharmacokinetic mechanism in nephrotic syndrome&#46;<span class="elsevierStyleSup">20&#44;34</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">C1q and kidney injury</span><span class="elsevierStyleItalic">&#160;</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">An unusual trait in this case was the presence of intense C1q deposits in the glomeruli&#46;</p><p class="elsevierStylePara">C1q is a complement component that is very important in triggering activation of the classical pathway&#46; When the Fc region of immune complexes &#40;mainly IgG and IgM&#41; binds to C1q&#44; the molecule dividing C4 and C2 into their subfractions undergoes a conformational change&#46; Among other functions&#44; this change stimulates phagocytosis and increases the production of cytokines &#40;TNF-alpha and IFN-gamma&#41;&#46;<span class="elsevierStyleSup">35</span> Unlike most complement proteins&#44; it is synthesised by antigen-presenting cells instead of hepatocytes&#46;<span class="elsevierStyleSup">36</span></p><p class="elsevierStylePara">The mechanisms by which C1q deposits are detected in renal biopsies are as follows&#58; 1&#41; C1q may bind to the Fc region of Ig or circulating immune complexes&#59; 2&#41; apoptotic debris may capture C1q and facilitate its clearance&#59; 3&#41; C1q may bind to C-reactive protein&#44; amyloid protein or Ig trapped in the glomerulus&#59; 4&#41; C1q may bind directly and specifically to renal parenchymal cells&#58; 5&#41; passive trapping and 6&#41; cross reaction with antigens similar to C1q&#46; This explains why every time we encounter a nephropathy affecting the classical pathway of complement activation&#44; we observe C1q deposits in the biopsy&#46;<span class="elsevierStyleSup">35</span></p><p class="elsevierStylePara">It is only when the renal biopsy shows a predominance of C1q deposits that C1q nephropathy may be considered as a diagnosis&#46; Its histological basis is highly variable&#44; ranging from different types of proliferative lesions to membranous nephropathies&#46;<span class="elsevierStyleSup">37&#44;38</span></p><p class="elsevierStylePara">There are studies in the literature that report the presence of such deposits in IgM nephropathy&#44; SLE&#44;<span class="elsevierStyleSup">34&#44;35</span> transplant glomerulopathy&#44;<span class="elsevierStyleSup">35&#44;36&#44;39-43</span> and many other very different entities&#44; such as nephrosclerosis&#44; tubulointerstitial nephritis and even in two donor kidneys with no clinical or laboratory abnormalities &#40;deposits are present in up to 19&#46;4&#37; of biopsies&#44; according to the biopsy series by Vizjak et al<span class="elsevierStyleSup">37</span>&#41;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CONCLUSIONS </span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Based on its evolution&#44; our case raises the question of a possible link between kidney injury and psoriasis&#59; clinical evolution suggests that this could be a secondary form of MGN that goes into complete remission at the same time as the skin symptoms&#44; with proteinuria reappearing when new psoriasis lesions are found on the skin&#46; We cannot exclude the possible effect that suspending renin-angiotensin-aldosterone blockers may have had on the recurrence of proteinuria&#46; Spontaneous&#44; idiopathic MGN remission cannot be ruled out either&#46; Given the presence of C1q&#44; this could also be an SLE-associated disease&#44; but it did not meet either clinical or laboratory criteria for SLE at any time during 9 years of follow-up&#46; It is known that membranous nephropathy can manifest several years before SLE does&#46; C1q nephropathy is an unlikely diagnosis in our case&#44; since immunofluorescence does not show a predominance of these deposits&#46;</p><p class="elsevierStylePara">No direct benefits of etanercept treatment have been described for MGN so far&#46; In this case&#44; treatment might have acted by controlling the primary illness&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The authors affirm that they have no conflicts of interest related to the content of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11112&#95;16025&#95;28220&#95;en&#95;f111112&#46;jpg" class="elsevierStyleCrossRefs"><img src="11112_16025_28220_en_f111112.jpg" alt="Evolution of the case described and treatment administered"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Evolution of the case described and treatment administered</p>"
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        "resumen" => "<p class="elsevierStylePara">La psoriasis es una enfermedad cut&#225;nea con afectaci&#243;n sist&#233;mica&#44; cuyo da&#241;o tisular se considera inmunomediado y que en la actualidad se trata eficazmente con etanercept&#46; El da&#241;o renal de esta patolog&#237;a no est&#225; completamente aclarado en la literatura&#46; Presentamos un caso de glomerulonefritis membranosa con dep&#243;sitos de C1q que posteriormente desarroll&#243; psoriasis&#46; En este art&#237;culo hacemos una revisi&#243;n de la posible asociaci&#243;n entre estas patolog&#237;as y la respuesta a esta mol&#233;cula biol&#243;gica&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">Psoriasis is a cutaneous disease with systemic involvement&#46; Tissue damage is considered to be immune-mediated&#44; and etanercept currently provides effective treatment&#46; Kidney injury arising from this condition has not yet been fully explained in the literature&#46; We present a case of membranous nephropathy with C1q deposits followed by development of psoriasis&#46; In this article we will review the possible association between these conditions and the response to this biological molecule&#46;</p>"
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