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a nzyme synthetase, which mediates the binding of RNA to he specific amino acid, to form transfer RNA. Of the main SAbs described in the bibliography, the first and most comonly found (15%–30%) is anti-Jo1, which is directed against he synthetase that mediates binding between RNA and istidine.1 During the 1990s, authors began to describe clinical cases f patients with myositis, the presence of ASAbs in serum, nd some generally common clinical characteristics that came o be defined as ASS. AAS is characterized by the assoiation of inflammatory myopathy, which is clinically as uscle weakness; interstitial lung disease, which can lead o acute respiratory failure of different histological patterns bronchiolitis obliterans, interstitial infiltrates of predomiantly plasma cells and lymphocytes, and diffuse pulmonary brosis); non-erosive inflammatory arthritis; the so-called echanic’s hands, which have hyperkeratotic lesions accomanied by fissures, hyperpigmentation, and scaling on the alm and on the palmar and lateral surfaces of the fingers; nd other symptoms such as fever, Raynaud syndrome, and jögren syndrome.1,2 We present a case of a 59-year-old man, with no past edical history of note except for an 80 pack-year smokng history until 6 months before his admission. Over the revious 2 months he had developed symptoms of arthralia, myalgia, and oedema in the upper and lower limbs, with ssociated loss of muscle strength. He also had moderate exerional dyspnoea. On physical examination he had a blood

Nefropatía mesangial y síndrome antisintetasa: una forma curiosa de asociación