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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#44;</span></p><p class="elsevierStylePara">Autosomal dominant polycystic kidney disease &#40;ADPKD&#41; is a hereditary disease caused by mutations in genes PKD1 and PKD2&#44; which codify polycystins 1 and 2<span class="elsevierStyleSup">1</span>&#46; The disease usually progresses more quickly in patients with PKD1 involvement&#44; although there is wide interindividual variability&#44; even within the same family&#46; Furthermore&#44; the progression of a given patient is not linear and may occasionally accelerate&#46; Explanations for this phenotypic variability include the existence of mutations of varying severity&#44; the individual&#8217;s genetic load&#44; the need for a second genetic hit and the impact of environmental factors or a third hit<span class="elsevierStyleSup">2</span>&#46; From the second hit hypothesis&#44; it is deduced that polycystic kidney disease is phenotypically dominant but molecularly recessive&#44; such that&#44; for a tubular cell to create a cyst&#44; a second somatic mutation in the second pkd1 or pkd2 gene would be necessary&#44; as well as the inherited genetic mutation&#46; With respect to the third hit&#44; there is evidence in animal models that inflammation may contribute to the progression of cystogenesis&#46; Tumour necrosis factor &#40;TNF&#41;&#44; the quintessential proinflammatory cytokine&#44; decreases the expression of polycystin 2 in mice<span class="elsevierStyleSup">3&#44;4</span>&#46; We reported the evolution of kidney function and volume in a patient with ADPKD treated for more than one year with TNF-neutralising antibodies due to another disease&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">CASE REPORT</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">A 35-year-old male diagnosed with HLA B27-positive ankylosing spondylitis in 2011&#46; An abdominal ultrasound displayed multiple hepatic and renal cysts&#46; The right kidney was 18cm and the left kidney was 19cm&#46; Given the lack of a family history of cystic diseases&#44; he was diagnosed with polycystic kidney disease due to <span class="elsevierStyleItalic">de novo </span><span class="elsevierStyleItalic">mutation</span>&#46;</p><p class="elsevierStylePara">In March 2011&#44; he began treatment with 40mg adalimumab &#40;Humira<span class="elsevierStyleSup">&#174;</span>&#41; every 15 days&#46; At that time he had&#58; haemoglobin &#40;Hb&#41; 12&#46;4g&#47;dl&#44; creatinine &#40;Cr&#41; 2&#46;3mg&#47;dl&#44; estimated glomerular filtration rate &#40;eGFR&#41; &#40;according to Modification of Diet in Renal Disease&#41; 34ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; proteinuria 10mg&#47;dl&#46; In September 2011 he had&#58; Cr 3&#46;24mg&#47;dl&#44; eGFR MDRD 23ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; proteinuria 1&#46;78g&#47;24h &#40;Figure 1&#41;&#46; Treatment was discontinued in January 2012 because the patient developed polyneuropathy and purpura&#46; In February 2012 a nuclear magnetic resonance &#40;NMR&#41; displayed a right kidney of 18cm &#40;volume of 2450ml&#41; and a left kidney of 18cm &#40;2250ml&#41;&#46; In April 2012 the patient began a course of 50mg Golimumab<span class="elsevierStyleBold"> </span>&#40;Simponi<span class="elsevierStyleSup">&#174;</span>&#41; every five weeks&#46; Six doses were administered and it was discontinued in September 2012 when the patient complained of a notable increase in his abdominal diameter and an umbilical hernia&#44; which was directly related to the administration of the drug&#46; A final dose was administered in December 2012&#46; In March 2013&#44; another NMR displayed a right kidney of 25&#46;4cm with a volume of 3899ml and a left kidney of 24&#46;1cm with a volume of 2739ml &#40;Figure 2&#41; and a slight increase in a much smaller amount of hepatic cysts&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">There is no specific treatment for ADPKD&#46; However&#44; various therapeutic approaches designed based on findings in experimental models and clinical observations are being studied&#46; The TEMPO 3&#58;4 trial observed that tolvaptan reduced the growth rate of cysts and the loss of glomerular filtration<span class="elsevierStyleSup">5</span>&#46; It had previously been observed that vaptans slowed down the progression of murine cystogenesis<span class="elsevierStyleSup">6</span>&#46; In clinical trials the mTOR &#40;<span class="elsevierStyleItalic">mammalian Target of Rapamycin</span>&#41; inhibitor sirolimus did not stop the growth of renal cysts and everolimus decreased the growth rate&#44; but not kidney function impairment<span class="elsevierStyleSup">7&#44;8</span>&#46; Again the rationale came from preclinical studies in animals<span class="elsevierStyleSup">9</span>&#46; The ALADIN trial demonstrated that long-lasting somatostatin slowed down cyst growth<span class="elsevierStyleSup">10</span>&#46; The choice of somatostatin was based on a case report&#46; A woman with ADPKD received treatment with somatostatin for a pituitary adenoma and her cystic nephropathy improved<span class="elsevierStyleSup">11</span>&#46; In this regard&#44; observations in a single patient may provide guidance on the potential usefulness of a therapeutic action&#46; In pkd2 &#43;&#47;- mice&#44; TNF increased cystogenesis and etanercept reduced it<span class="elsevierStyleSup">3</span>&#46; TNF reduced functioning polycystin 2 below a critical threshold as a result of the increased expression of protein FIP-2<span class="elsevierStyleSup">3</span>&#46; Therefore the evolution of the patient whose case we reported during treatment with anti-TNF for a concomitant disease is particularly interesting&#46; During this period&#44; ADPKD progressed rapidly&#46; The eGFR decreased with a slope of -1&#46;1ml&#47;min&#47;month homogenously over time &#40;and the volume of the kidneys increased by a mean of 71&#37; &#91;1938ml&#93;&#46; This progression speed is much higher than that of patients treated with a placebo in recent clinical trials &#40;Table 1&#41;<span class="elsevierStyleSup">5&#44;7&#44;8&#44;10&#44;12</span>&#46; Contrary to experimental observation<span class="elsevierStyleSup">3</span> and the hope placed in the potential efficacy of anti-TNF therapies<span class="elsevierStyleSup">4</span>&#44; there was no evidence of a therapeutic effect&#44; at least at this stage of the disease&#46; Since this was only one clinical case&#44; it is not a definitive observation&#46; In fact&#44; it may be argued that the existence of a systemic inflammatory disease could have contributed to accelerating the disease&#46; Nevertheless&#44; anti-TNF treatment was effective in controlling the activity of ankylosing spondylitis&#46;</p><p class="elsevierStylePara">In conclusion&#44; we reported the case of a patient with ADPKD treated with anti-TNF therapy due to a concomitant rheumatic disease&#44; whose kidney disease progressed quickly&#46; This case report argues against the efficacy of anti-TNF therapies for treating the human form of ADPKD&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12600&#95;16025&#95;61471&#95;en&#95;t1126003&#46;jpg" class="elsevierStyleCrossRefs"><img src="12600_16025_61471_en_t1126003.jpg" alt="Increased kidney volume in patients assigned to the placebo group in large observational studies and clinical trials and in the patient reported "></img></a></p><p class="elsevierStylePara">Table 1&#46; Increased kidney volume in patients assigned to the placebo group in large observational studies and clinical trials and in the patient reported </p><p class="elsevierStylePara"><a href="grande&#47;12600&#95;16025&#95;61472&#95;en&#95;f112600&#46;jpg" class="elsevierStyleCrossRefs"><img src="12600_16025_61472_en_f112600.jpg" alt="Evolution of renal function over 29 months&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Evolution of renal function over 29 months&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12600&#95;16025&#95;61473&#95;en&#95;f212600&#46;jpg" class="elsevierStyleCrossRefs"><img src="12600_16025_61473_en_f212600.jpg" alt="Image comparing kidney size in the nuclear magnetic resonances of 2012 &#40;left&#41; and 2013 &#40;right&#41;&#46;"></img></a></p><p class="elsevierStylePara">Figure 2&#46; Image comparing kidney size in the nuclear magnetic resonances of 2012 &#40;left&#41; and 2013 &#40;right&#41;&#46;</p>"
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