Letter to the Editor
Renal involvement in Sneddon's syndrome
Afectación renal en el síndrome de Sneddon
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class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Sneddon's syndrome (SS) is a rare and slowly progressive vascular disease that affects small and medium-sized arteries, characterised by the association of <span class="elsevierStyleItalic">livedo reticularis</span> and recurrent cerebrovascular accidents (CVA).<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Approximately 80% of SS patients are women with a median age of 40 years.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> The aetiopathogenesis is unknown, with two proposed primary mechanisms (autoimmune/inflammatory versus thrombophilia), and it is classified mainly as positive or negative antiphospholipid.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> The main symptoms are cutaneous, which usually precede neurological symptoms by more than 10 years. The vast majority of patients present with labile systolic hypertension and it can also affect the heart valves or the kidneys, inter alia.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,2</span></a> After reviewing the literature, histopathological renal involvement in this syndrome is extremely rare.<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2,3</span></a> Below we describe a case of SS with biopsy-proven chronic kidney disease associated with features of membranous nephropathy:</p><p id="par0015" class="elsevierStylePara elsevierViewall">A 53-year-old woman diagnosed with SS, arterial hypertension, arterial toe ischaemia and an active smoker, receiving treatment with acetylsalicylic acid (ASA), atorvastatin and valsartan. She is referred to nephrology due to the onset of albuminuria. Asymptomatic, with good blood pressure control. Normal physical examination except for <span class="elsevierStyleItalic">livedo reticularis</span> in the facial area, back of the hands, upper and lower limbs. An investigation was started, which revealed plasma levels of creatinine of 1.3<span class="elsevierStyleHsp" style=""></span>mg/dl, urea 48<span class="elsevierStyleHsp" style=""></span>mg/dl, sodium 141<span class="elsevierStyleHsp" style=""></span>mEq/l, potassium 3.8<span class="elsevierStyleHsp" style=""></span>mEq/l, total cholesterol 155<span class="elsevierStyleHsp" style=""></span>mg/dl, triglycerides 153<span class="elsevierStyleHsp" style=""></span>mg/dl, total protein 6.5<span class="elsevierStyleHsp" style=""></span>mg/dl, albumin 3.9<span class="elsevierStyleHsp" style=""></span>mg/dl, normal immunoglobulins (Igs), C3 77.8<span class="elsevierStyleHsp" style=""></span>mg/dl, C4 18<span class="elsevierStyleHsp" style=""></span>mg/dl, positive antinuclear antibodies 1/1280 (1/320 centrometric), anti-Jo-1 1/18 and anticardiolipin antibodies >160. The remaining autoimmunity, including anti-phospholipase A2 antibodies, protein electrophoresis and serologies were negative. Normal blood count and coagulation. Urinalysis revealed an albumin/creatinine ratio (ACR) of 1478.8<span class="elsevierStyleHsp" style=""></span>mg/g. Sonography revealed kidneys of decreased size and a diffuse increase in bilateral cortical echogenicity.</p><p id="par0020" class="elsevierStylePara elsevierViewall">Due to renal involvement, a renal biopsy was performed that revealed chronic arteriolar/arterial vascular lesions with extensive interstitial and glomerular kidney damage associated with incipient membranous glomerulopathy. Glomerular damage was associated with ischaemia and deposition of immune complexes in capillary membranes without complement deposition. Immunofluorescence showed negativity for C1q, C3, C4, fibrinogen and albumin.</p><p id="par0025" class="elsevierStylePara elsevierViewall">To complete the study of this systemic entity, a cranial CT scan was performed, which found vascular-degenerative leukoencephalopathy.</p><p id="par0030" class="elsevierStylePara elsevierViewall">Regarding the treatment of SS, antiplatelets and anticoagulants are indicated as secondary CVA prophylaxis, in addition to improving the prognosis.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> In patients with antiphospholipid syndrome, anticoagulants give rise to a better outcome than antiplatelets.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> The use of anti-inflammatory or immunosuppressive therapies is controversial. In some cases, treatment has been started with intravenous immunoglobulins in patients with <span class="elsevierStyleItalic">livedoid</span> vasculopathy, with adequate outcomes.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> In our case, anticoagulant and antiproteinuric treatment was administered, with stability of renal function and a decrease in the ACR to 175<span class="elsevierStyleHsp" style=""></span>mg/g.</p><p id="par0035" class="elsevierStylePara elsevierViewall">In conclusion, it is a rare clinical syndrome that is probably underdiagnosed and in which kidney involvement is rare, so its detection adds complexity to the case.</p><p id="par0040" class="elsevierStylePara elsevierViewall">The case described is interesting since, in addition to presenting with vascular lesions associated with SS in the kidneys, there was associated membranous nephropathy, which has not been previously reported in conjunction with SS in the literature, and may be related to the existence of an associated antiphospholipid syndrome.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2020-01-12" "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: García EH, Torres MJS. Afectación renal en el síndrome de Sneddon. Nefrologia. 2021;41:81–82.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Sneddon syndrome: a comprehensive overview" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "D. Samanta" 1 => "S. Cobb" 2 => "K. 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