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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#44;</span></p><p class="elsevierStylePara">Autoimmune processes affecting the kidneys are heterogeneous clinical entities and their differential diagnosis is complex&#46; The best example is systemic lupus erythematosus &#40;SLE&#41;&#44; whose pleomorphisms can range from skin or joint lesions to lupus nephritis &#40;LN&#41;&#46; Its diagnostic criteria were revised in 1997 by the American College of Rheumatology &#40;ACR&#41;&#44; and by following them&#44; the syndrome can be defined with a sensitivity and specificity of 96&#37;&#46;<span class="elsevierStyleSup">1</span> However&#44; atypical clinical profiles are hard to interpret&#44; and the symptoms in such cases are often anachronical and non-specific&#46;</p><p class="elsevierStylePara">In this context&#44; we present the case of a 40 year old patient with a history of smoking&#44; obesity and high blood pressure &#40;HBP&#41; with no pharmacological treatment&#46; The patient was admitted to the nephrology department because he had experienced fever&#44; diarrhoea&#47;vomiting&#44; weight loss&#44; and progressive decrease in diuresis for 3 weeks&#46; Laboratory results then showed severe renal dysfunction &#40;urea 383mg&#47;dl&#59; creatinine 20&#46;3mg&#47;dl&#41;&#44; hypoalbuminaemia &#40;2&#46;3g&#47;dl&#41; and anaemia &#40;haematocrit 20&#37;&#59; haemoglobin 6&#46;9g&#47;dl&#59; mean cell volume 88 fL&#41;&#46; Meanwhile&#44; complementary tests found microhaematuria&#44; blood clotting disorders &#40;prothrombin activity 89&#37;&#59; haptoglobin 298mg&#47;dl&#59; reticulocytes 1&#46;5&#37;&#59; low schistocytosis&#59; positive direct Coombs test&#41; in addition to abnormalities found by ultrasound &#40;normal-sized kidneys with cortical hyperechogenicity&#41;&#46; In light of these results&#44; and suspecting a glomerular process&#44; with incomplete data suggesting haemolytic anaemia&#44; we performed emergency haemodialysis and a blood transfusion&#46;</p><p class="elsevierStylePara">Other results gathered at the same time were as follows&#58; negative stool and blood cultures&#59; negative serology for bacteria and parasites&#59; viral serology for hepatitis B&#44; C and HIV showing positive IgM and IgG for cytomegalovirus &#40;CMV&#41;&#44; Coxsackievirus&#44; herpes simplex and herpes varicella zoster&#59; and decreased C3 fraction &#40;51mg&#47;dl&#41;&#46; A renal biopsy showed generalised glomerulosclerosis in 60&#37; of the sample&#44; with fibrous crescents &#40;some glomeruli showing poorly defined margins&#41;&#44; cystic tubular atrophy&#44; fibrosis and interstitial lymphocytic infiltrate&#46; There were also signs of proliferative arteriopathy having to do with HBP &#40;Figure 1&#41;&#46;</p><p class="elsevierStylePara">With a presumed diagnosis of rapidly progressive extracapillary glomerulonephritis &#40;GN&#41; against the diagnosis of SLE&#44; we administered adjuvant immunosuppressive drugs with dialysis &#40;prednisone 1mg&#47;kg&#47;day and azathioprine &#40;AZA&#41; 2mg&#47;kg&#47;day&#41; while waiting for immunology test results&#46; Tests found the following results&#58; ANA &#40;&#43;&#41; at a titre of 1&#58;640&#59; anti-dsDNA &#40;&#43;&#41; 126IU&#47;ml&#59; anti-Sm &#40;&#43;&#41; 1&#46;54U&#47;ml and c-ANCA &#40;proteinase 3-specific cytoplasmic antineutrophil cytoplasmic antibodies&#41; &#40;&#43;&#41; 52&#46;8U&#47;ml&#46; Anticardiolipin and lupus anticoagulant antibodies were negative&#46; This was sufficient to diagnose the syndrome as WHO class VI lupus nephritis in a systemic context &#40;syndrome met 5 of the ACR criteria&#58; nephritis&#44; serositis&#44; abnormal blood tests&#44; ANA at high titres&#44; anti-dsDNA and anti-Sm&#41;&#46; Despite the positive results and proposed treatment&#44; the patient&#8217;s renal function never recovered and urine output remained below 500cc&#47;24h&#46;</p><p class="elsevierStylePara">Eight months after symptom onset &#40;during which time the patient&#8217;s anaemia could not be controlled correctly despite maintaining immunosuppressant treatment&#41; the patient suffered from numerous complications&#46; These included acute coronary syndrome &#40;ACS&#41;&#44; an episode of diarrhoea and high fever that did not respond to either astringent or antibiotic treatment&#44; and lastly&#44; severe pancytopoenia &#40;2320&#160;000 red blood cells&#47;&#181;l&#44; 890 leukocytes&#47;&#181;l&#44; 51&#160;000 platelets&#47;&#181;l&#41;&#44; with a low reticulocyte production index &#40;0&#46;2&#37;&#41; and negative direct and indirect Coombs test&#46; As there was a strong suspicion of a lupus flare and&#47;or myelotoxicity&#44; the recommendation was to intensify immunomodulatory treatment with a methylprednisolone bolus and discontinue AZA&#46; In addition&#44; we also decided to administer granulocyte colony-stimulating factors &#40;filgrastim&#58; 480&#181;g&#47;sc&#47;day&#41;&#46; However&#44; there was no megakaryocyte response&#44; and a bone marrow biopsy revealed intense hypoplasia with developmental anomalies&#44; and glycophorin-negative proerythroblasts which might be linked to SLE&#44; although it was impossible to rule out simultaneous chronic infection with parvovirus B19 &#40;Figure 2&#41;&#46; A new viral serology test also confirmed the presence of IgG antibodies &#40;against the diagnosis of parvovirus&#41; along with a blood count of 68&#160;000 copies&#47;ml of CMV DNA&#46; It was then decided to start foscarnet 50mg&#47;kg&#47;day to prevent the myelotoxic effect of ganciclovir&#44; and intravenous immunoglobulin &#40;60g&#47;day&#41;&#46; This association did not provide any haematological benefits and was manifestly unable to prevent a new episode of bloody diarrhoea complicated by a pulmonary haemorrhage which could not be resolved even by using combined treatment with daily dialysis and plasmapheresis&#46; In the end&#44; the patient died in the intensive care unit due to sepsis secondary to infection with <span class="elsevierStyleItalic">Escherichia coli</span>&#46;</p><p class="elsevierStylePara">In conclusion&#44; the case described is an excellent example of atypical SLE with severe LN with no classical signs of the disease such as skin and joint disorders&#44; with wasting syndrome &#40;fever&#44; anaemia&#41; and severe renal failure being predominant&#46; The main underlying conditions were generalised glomerulosclerosis&#47;fibrous crescents&#47;interstitial disorders &#40;compatible with advanced extracapillary GN&#41; without the lesions typical of proliferative forms of LN&#46;<span class="elsevierStyleSup">2</span> In addition&#44; obtaining a positive test for c-ANCA antibodies &#40;antiproteinase 3&#41; instead of p-ANCA was also uncommon&#59; p-ANCA is more prevalent according to most authors &#40;present in 15&#37;-30&#37; of cases of SLE&#41;&#46;<span class="elsevierStyleSup">3-5 </span>Complications that arose after diagnosis included ACS as an expression of systemic inflammation and atherosclerosis&#44; and evolution of the initial haemolytic anaemia to irreversible medullary aplasia of unknown aetiology &#40;possibly secondary to chronic infection with parvovirus B19&#41;&#46;<span class="elsevierStyleSup">6&#44;7</span> The patient did not respond to discontinuing AZA or to intensive treatment with intravenous gammaglobulins&#44; plasmapheresis or colony-stimulating factors&#46; This fact&#44; combined with the array of symptoms caused by CMV &#40;enteritis and pulmonary haemorrhage&#41; defined the final outcome and made us re-consider that both infections were co-existing opportunistic entities&#44; and perhaps&#44; the agents triggering the lupus flare&#46;<span class="elsevierStyleSup">7-10</span></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 affirm that they have no conflicts of interest related to the content of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11154&#95;19157&#95;29333&#95;en&#95;f1&#95;11154&#46;jpg" class="elsevierStyleCrossRefs"><img src="11154_19157_29333_en_f1_11154.jpg" alt="Renal Biopsy&#46; Severe glomerulosclerosis and tubular lesion"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Renal Biopsy&#46; Severe glomerulosclerosis and tubular lesion</p><p class="elsevierStylePara"><a href="grande&#47;11154&#95;19157&#95;29334&#95;en&#95;f2&#95;11154&#46;jpg" class="elsevierStyleCrossRefs"><img src="11154_19157_29334_en_f2_11154.jpg" alt="Bone marrow biopsy&#46; Developmental hypoplasia"></img></a></p><p class="elsevierStylePara">Figure 2&#46; Bone marrow biopsy&#46; Developmental hypoplasia</p>"
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