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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Dear Editor&#44;</span></p><p class="elsevierStylePara">Patients with acute renal failure due to pauci-immune necrotizing and crescentic glomerulonephritis with antinuclear antibody &#40;ANCA&#41; seropositivity can present with positive lupus serologies&#46;<span class="elsevierStyleSup">1</span> On the other hand&#44; patients with lupus nephritis present with ANCA seroconversion in 20&#37; of cases&#46; The fact that systemic lupus erythematosus &#40;SLE&#41; and positive myeloperoxidase &#40;MPO&#41; ANCA titers with kidney involvement can present with scant subendothelial deposits in the kidney biopsy&#44; may suggest a forme fruste of lupus nephritis or a concomitant renal vasculitis with neutrophil priming&#46;</p><p class="elsevierStylePara">A 77-year-old man with chronic kidney disease due to hypertension&#44; presented with hematuria&#44; nausea&#44; and vomiting and red discoloration of urine&#46; Laboratory data Table 1&#44; serology tests Table 2&#46; Renal ultrasonography unremarkable&#46; Patient developed hemoptysis&#46; Chest radiograph revealed bilateral diffuse airspace opacities&#46; Intravenous methylprednisolone was administered&#46; The patient received hemodialysis&#46; Renal biopsy showed mesangial hypercellularity &#40;Figure 1&#41;&#44; crescents &#40;Figure 2&#41;&#44; segmental necrosis &#40;Figure 1&#41;&#46; There was moderate tubular atrophy an occasional eosinophil&#46; Immunofluorescence microscopy demonstrated granular IgG &#40;1&#43;&#41;&#44; C3 &#40;2&#43;&#41;&#44; and C1q &#40;1&#43;&#41; deposition in the mesangial areas and glomerular basement membranes &#40;Figure 3&#41;&#46; EM showed numerous electron-dense deposits in the mesangial areas and few subepithelial and subendothelial electron-dense deposits &#40;Figure 4&#41;&#46; Focal effacement of podocyte foot processes was noted&#46; Histological diagnosis&#58; immune complex-mediated necrotizing and crescentic glomerulonephritis&#46;</p><p class="elsevierStylePara">Patient received pulse Rituximab and cyclophosphamide&#46; The hospital course was complicated by hypoxic respiratory failure&#46; Folow up computed tomography of the chest showed a right lower lobe pulmonary embolism&#46; Anticoagulation with heparin was initiated&#46; Serological tests were repeated &#40;Table 2&#41; and showed normalization of p-ANCA &#40;&#60;1&#58;20&#41; and anti-double-stranded DNA antibodies&#46; Anti-MPO antibodies were reduced at 9&#46;8U&#47;mL after induction therapy&#46; The patient expired&#46;</p><p class="elsevierStylePara">Pauci-immune necrotizing and crescentic glomerulonephritis &#40;GN&#41; due to the activation of neutrophils by ANCA&#44; differs from lupus nephritis in that glomerular necrosis and crescent formation occurs in the absence of cellular proliferation and in the presence of scant immune-complex deposition&#46; ANCA are implicated in the pathogenesis targeting cytokine-primed leukocytes that expressed MPO or proteinase 3 &#40;PR 3&#41; instead the white blood cell surface&#46;<span class="elsevierStyleSup">2</span></p><p class="elsevierStylePara">Lupus nephritis is an immune complex-mediated renal disease were the formation of glomerular immune deposits results in complement activation&#44; leukocyte infiltration&#44; cytokine release&#44; cellular proliferation&#44; crescent formation&#44; and necrosis under certain circumstances&#46; The final result is glomerular scarring&#46;<span class="elsevierStyleSup">1</span> There are cases of lupus nephritis in which focal or diffuse glomerular necrosis and crescents occur without substantial subendothelial deposits&#46;<span class="elsevierStyleSup">3</span> Patients with lupus nephritis IV-S &#40;2003 International Society of Nephrology&#47;Renal Pathology Society classification&#47;&#40;endocapillary or extracapillary GN involving &#62;50&#37; of glomeruli with segmental lesions&#41; had extensive fibrinoid necrosis and less immune-complex deposition findings resembling a pauci-immune GN at times&#46;<span class="elsevierStyleSup">4</span> Approximately 20&#37; of patients with SLE have ANCA positivity by immunofluorescence microscopy &#40;IF&#41;&#44; mainly with a perinuclear &#40;p-ANCA&#41; pattern&#46;<span class="elsevierStyleSup">5</span> Antinuclear antibody seropositivity by enzyme-linked immune-sorbent assay &#40;ELISA&#41; is less frequent&#44; and target antigens are most commonly lactoferrin &#40;LF&#41;&#44; cathepsin G&#44; and MPO&#46;<span class="elsevierStyleSup">5</span> Galeazzi <span class="elsevierStyleItalic">et al&#46;</span> evaluated 566 patients with SLE and found ANCA positivity by immunofluorescence microscopy in 16&#46;4&#37; of them including 15&#46;4&#37; p-ANCA and 1&#37; c-ANCA&#160; pattern&#46; By ELISA&#44; 9&#46;3&#37; had MPO-ANCA positivity and 1&#46;7&#37; had PR3-ANCA positivity&#46;<span class="elsevierStyleSup">6</span> There is difficulty in distinguishing p-ANCA from ANA by immunofluorescence microscopy&#46;<span class="elsevierStyleSup">7</span> There are also conflicting reports on biological significance of ANCA in patients with SLE&#46; Antinuclear antibody positivity has been associated with the presence of nephritis&#44; particularly diffuse proliferative lupus nephritis&#44; as well as anti-dsDNA antibodies&#46;<span class="elsevierStyleSup">8</span> While other reports have failed to show a correlation between ANCA and organ involvement&#46;<span class="elsevierStyleSup">9</span> Nasr <span class="elsevierStyleItalic">et al&#46;</span> evaluated a cohort of ten patients with SLE&#44; ANCA positivity and renal biopsy findings of lupus nephritis and ANCA-associated GN&#46; All biopsies exhibited necrosis and crescents with no or rare subendothelial deposits&#46;<span class="elsevierStyleSup">7</span> Nine patients had p-ANCA positivity by IF&#46; The high incidence of MPO-ANCA seropositivity in patients with SLE&#44; raises the possibility that the findings are not coincidental occurrence of two unrelated diseases&#46; One condition might trigger the other one or vice versa&#46; Systemic lupus erythematous may facilitate MPO autoantibody formation by promoting neutrophil degranulation and priming neutrophils to increase surface expression of MPO&#46;<span class="elsevierStyleSup">7</span> On the other hand&#44; the association of autoantibodies to MPO in drug-induced SLE has been reported independently&#46;<span class="elsevierStyleSup">10</span> There are conflicting reports on the correlation between the presence of ANCA in SLE and clinical features&#46; Some reports show no correlation between organ involvement and the presence of ANCA&#44; whilst others report a link&#46; In the largest population of patients studied&#44; Galeazzi <span class="elsevierStyleItalic">et al&#46;</span> reported significant positive correlations between IF ANCA and venous thrombosis as well as serositis&#46;<span class="elsevierStyleSup">6</span> In this case&#44; our patient presented with an episode of pulmonary embolism&#44; which is consistent this hypothesis&#46; Here&#44; we presented a patient with systemic vasculitis with rapid progressive glomerulonephritis and necrotizing and crescentic changes&#46; Lupus serologies probably represented an autoimmune response to the antinuclear antibody activity&#46; The fact that he had few sub endothelial deposits and lack of hypocomplementemia goes against activation of immune complexes due to SLE&#46; In the other hand&#44; the possibility of a simultaneous ANCA&#47;lupus nephritis involvement represents an interesting hypothesis&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflict of interest</span></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;12561&#95;19904&#95;57679&#95;en&#95;12561&#95;t1&#46;jpg" class="elsevierStyleCrossRefs"><img src="12561_19904_57679_en_12561_t1.jpg" alt="Laboratory data"></img></a></p><p class="elsevierStylePara">Table 1&#46; Laboratory data</p><p class="elsevierStylePara"><a href="grande&#47;12561&#95;19904&#95;57680&#95;en&#95;12561&#95;t2&#46;jpg" class="elsevierStyleCrossRefs"><img src="12561_19904_57680_en_12561_t2.jpg" alt="Serologic tests"></img></a></p><p class="elsevierStylePara">Table 2&#46; Serologic tests</p><p class="elsevierStylePara"><a href="grande&#47;12561&#95;16025&#95;61075&#95;en&#95;12561&#95;pgina&#95;3&#95;imagen&#95;0001&#46;jpg" class="elsevierStyleCrossRefs"><img src="12561_16025_61075_en_12561_pgina_3_imagen_0001.jpg" alt="H&#38;E&#58; mesangial hyeprcellularity and necrotizing crescentic glomerulonephritis"></img></a></p><p class="elsevierStylePara">Figure 1&#46; H&#38;E&#58; mesangial hyeprcellularity and necrotizing crescentic glomerulonephritis</p><p class="elsevierStylePara"><a href="grande&#47;12561&#95;16025&#95;61077&#95;en&#95;12561&#95;pgina&#95;3&#95;imagen&#95;0002&#46;jpg" class="elsevierStyleCrossRefs"><img src="12561_16025_61077_en_12561_pgina_3_imagen_0002.jpg" alt="Tricrome&#58; shows cellular crescent &#40;stained red&#41; extending from 11 to 2 o&#39;clock postion"></img></a></p><p class="elsevierStylePara">Figure 2&#46; Tricrome&#58; shows cellular crescent &#40;stained red&#41; extending from 11 to 2 o&#39;clock postion</p><p class="elsevierStylePara"><a href="grande&#47;12561&#95;16025&#95;61079&#95;en&#95;12561&#95;pgina&#95;3&#95;imagen&#95;0003&#46;jpg" class="elsevierStyleCrossRefs"><img src="12561_16025_61079_en_12561_pgina_3_imagen_0003.jpg" alt="IF for C3&#58; granular predominantly mesangial deposits"></img></a></p><p class="elsevierStylePara">Figure 3&#46; IF for C3&#58; granular predominantly mesangial deposits</p><p class="elsevierStylePara"><a href="grande&#47;12561&#95;16025&#95;61081&#95;en&#95;12561&#95;pgina&#95;3&#95;imagen&#95;0004&#46;jpg" class="elsevierStyleCrossRefs"><img src="12561_16025_61081_en_12561_pgina_3_imagen_0004.jpg" alt="EM&#58; electron dense immune complex deposits in glomerular mesangium &#40;high power&#41;"></img></a></p><p class="elsevierStylePara">Figure 4&#46; EM&#58; electron dense immune complex deposits in glomerular mesangium &#40;high power&#41;</p>"
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