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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#44; </span></p><p class="elsevierStylePara">A dermatological manifestation of chronic kidney disease &#40;CKD&#41; is calcific uraemic arteriolopathy &#40;CUA&#41; or calciphylaxis&#46; It is an anatomopathological entity characterised by necrosis of the skin and adipose tissue due to incorrect calcium salt deposits&#46;<span class="elsevierStyleSup">1</span> Morbidity and mortality of calciphylaxis is high due to the complications associated with it&#58; sepsis and ischaemia&#46; Different clinical entities can manifest calciphylaxis&#58; rheumatoid arthritis&#44; inflammatory bowel disease&#44; neoplasias&#44; CKD&#44; systemic lupus erythematosus or HIV infection&#46;<span class="elsevierStyleSup">1</span> Its treatment has to be aggressive&#46; Sodium thiosulfate has shown improvements in skin lesions caused by calciphylaxis&#46;</p><p class="elsevierStylePara">Our patient was a 78-year-old man with history of high blood pressure&#44; diabetes mellitus type 2&#44; dyslipidaemia&#44; CKD of unknown origin treated with haemodialysis three times a week for 3hr&#44; mineral and bone disorder associated with CKD &#40;MBD-CKD&#41;&#44; auricular fibrillation and ischaemic heart disease&#46; His usual treatment was sevelamer&#44; enalapril&#44; aspirin&#44; acenocumarol and insulin&#46;</p><p class="elsevierStylePara">He was admitted to hospital for painful skin erythematous lesions with necrotic edges on both lower limbs&#44; measuring 5x6cm&#46; Physical examination&#58; good general condition&#44; body mass index&#58; 23&#59; blood pressure 150&#47;63mm Hg&#59; heart rate 64bpm&#59; no fever&#46; Cardiopulmonary and abdominal auscultation&#58; painless&#46; Lower limbs&#58; normal pulse&#44; with no sign of deep vein thrombosis and showing previously described lesions&#46; Analyses&#58; parathyroid hormone &#40;PTH&#41;&#58; 826&#46;3pg&#47;ml&#44; calcium&#58; 8&#46;9mg&#47;dl&#59; phosphorus&#59; 7&#46;40&#59; creatinine&#58; 9&#46;8mg&#47;dl&#59; albumin&#58; 3g&#47;dl&#59; urea&#58; 156mg&#47;dl&#59; C-reactive protein&#59; 4&#46;3&#46; A cervical ultrasound and parathyroid gammagraphy were performed showing parathyroid hyperplasia free of adenomas&#46; The radiological study &#40;bone series and supra-aortic trunks Doppler&#41; showed vascular calcifications on the ascending and descending aorta&#46; Given the suspected calciphylaxis&#44; we performed a biopsy of one of the lesions&#44; with results compatible with calciphylaxis&#58; lesion with abundant calcium deposits compared with the walls of small vascular structures&#46; Swollen septa due to fibrosis &#40;Figure 1&#41;&#46; No signs of necrosis are observed&#46; Lastly&#44; we performed a technetium-99 gammagraphy which did not show that the calciphylaxis spread to the bones&#46;</p><p class="elsevierStylePara">We considered MBD-CKD to be the cause of calciphylaxis and intensified the treatment for it&#58; daily dialysis of 4hr was started with low calcium &#40;2&#46;5mEq&#47;l&#41; in the haemodialysis solution and high flux dialyser&#46; The treatment was intensified with calcium-free phosphate-binders&#58; lanthanum carbonate&#58; 750mg&#47;8hr and sevelamer&#58; 1600mg&#47;8hr&#44; and PTH control with calcimimetics&#58; 60mg&#47;24hr&#46; Acenocoumarol was withdrawn and treatment was started with 80ml of sodium thiosulfate at 25&#37; &#40;20g&#41; following haemodialysis &#40;three times per week&#41;&#46; Lesions improved 2 months later &#40;Figure 2&#41;&#46; Analytical parameters upon discharge&#58; P&#58; 3&#46;6mg&#47;dl&#59; total Ca&#58; 8&#46;9mg&#47;dl&#59; PTH&#58; 406&#46;90pg&#47;ml&#46;</p><p class="elsevierStylePara">CUA consists of a hydroxyapatite deposit in the skin and soft tissues with risk of necrosis&#46; In CKD&#44; CUA physiopathology is due to an alteration in phosphocalcic metabolism&#44; uraemic state&#44; increase in PTH &#40;although there are CUA cases following parathyroidectomy&#41;<span class="elsevierStyleSup">2</span>&#44; calcium-based phosphate binders and a high calcium concentration in the dialysis solution&#46;<span class="elsevierStyleSup">3</span> Phosphate and calcium are bound producing vascular&#44; skin and organic calcifications&#46;<span class="elsevierStyleSup">4</span></p><p class="elsevierStylePara">Other predisposing factors are&#58; female sex&#44; obesity&#44;<span class="elsevierStyleSup">5</span> hypoalbuminaemia &#40;&#60;2g&#47;dl&#41;&#44; diabetes mellitus&#44; C and S protein deficiency&#44;<span class="elsevierStyleSup">6</span> oral anticoagulants &#40;they inhibit synthesis of 4&#46;8-gamma-carboxyglumate&#41;<span class="elsevierStyleSup">7</span>&#44; intravenous iron and vitamin D due to its intestinal action on calcium reabsorption&#46;<span class="elsevierStyleSup">8</span></p><p class="elsevierStylePara">Lesions caused by CUA are often on the abdomen and the calf area&#44; given their abundance of subcutaneous tissue&#46; The lesion is similar to <span class="elsevierStyleItalic">livedo reticularis </span>progressing to ulceration&#46; Calcium deposits in skin are deposited in the dermis and subcutaneous tissue&#46; Physio-pathogenitically&#44; high levels of urea and phosphorus cause smooth muscle cells to convert into osteoblast cells that also increase osteopontin levels&#44; which together with proinflammatory and free radical molecules&#44; make it easier for phosphorus to adhere to calcium&#46;<span class="elsevierStyleSup">1&#44;7&#44;9&#44;10</span> This magma is mostly concentrated around calcium deposits that are also found in the arterioles<span class="elsevierStyleSup">1</span> and media of the vessels&#46;</p><p class="elsevierStylePara">The diagnosis is essentially clinical&#46; Lesion biopsy is not recommended given the risk of infection and ulceration&#46;<span class="elsevierStyleSup">10</span> Gammagraphy with technetium-99 is used to diagnose whether it has spread to the bones&#46;<span class="elsevierStyleSup">10</span> Calciphylaxis has a morbidity and mortality of 80&#37; given the risk of infection and necrosis&#46;</p><p class="elsevierStylePara">The CUA therapeutic approach must be aggressive&#44; controlling its associated alterations &#40;BMD-CKD control&#41;&#44; avoiding agents that could strengthen it&#44; and curing the lesion and infectious complications&#46;<span class="elsevierStyleSup">2</span> BMD-CKD control will be performed using calcium-free phosphate binders&#44; low calcium haemodialysis and peritoneal dialysis solutions &#40;CUA can develop above 4mEq&#47;l<span class="elsevierStyleSup">11</span>&#41; and implementing daily haemodialysis&#46; PTH control will be performed using calcimimetics and vitamin D&#44; preferably vitamin D analogues given that they have a lower calcifying and hyperphosphatemic effect&#46;<span class="elsevierStyleSup">2</span> Parathyroidectomy will be reserved for cases resistant to drug treatment&#46;</p><p class="elsevierStylePara">Dermal CUA lesions that have no ulcerations improve with corticoids&#46;<span class="elsevierStyleSup">10</span> However&#44; for those with ulceration&#44; the hyperbaric oxygen chamber is effective against anaerobic organims&#46;<span class="elsevierStyleSup">11</span> The sodium thiosulfate &#40;antidote against cynade&#44; used in skin treatments for acne and pityriasis versicolor&#44; and protection against carboplatin and cisplatin toxicity&#41; has proven a successful therapeutic measure in CUA lessions&#46;<span class="elsevierStyleSup">5&#44;14</span> Sodium thiosulfate inhibits calcium salt precipitation and dissolves calcium deposits&#46;<span class="elsevierStyleSup">12&#44;13</span> It does not have any effects on levels of calcium&#44; phosphorus or PTH&#46; The recommended dose is 20g I&#46;V&#46;&#44; three times a week during a minimum of 6 months&#46;<span class="elsevierStyleSup">2&#44;14</span> Its administration could lead to metabolic acidosis&#44; osteoclast activation&#44; volume overload and hypotension&#46;</p><p class="elsevierStylePara">In summary&#44; CUA is a serious entity among our patients&#46; Its treatment has to be aggressive&#46; Sodium thiosulfate is a valid therapeutic agent for treating CUA lesions&#46; It is safe to use and the benefits obtained mean that it can be considered a first-line drug for CUA lesions&#46;</p><p class="elsevierStylePara"><a href="grande&#47;10859&#95;108&#95;17671&#95;en&#95;f110859&#46;jpg" class="elsevierStyleCrossRefs"><img src="10859_108_17671_en_f110859.jpg" alt="Lesion on right leg prior to treatment with thiosulfate&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Lesion on right leg prior to treatment with thiosulfate&#46;</p><p class="elsevierStylePara"><a href="grande&#47;10859&#95;108&#95;17672&#95;en&#95;f210859&#46;jpg" class="elsevierStyleCrossRefs"><img src="10859_108_17672_en_f210859.jpg" alt="Lesion on right leg after two months of treatment with sodium thiosulfate&#46;"></img></a></p><p class="elsevierStylePara">Figure 2&#46; Lesion on right leg after two months of treatment with sodium thiosulfate&#46;</p>"
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