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He was taking azithromycin&#46; The patient reported a reduction in diuresis in the previous days&#44; without lower urinary tract symptoms&#46; He was not taking NSAIDs or any other nephrotoxic drugs&#46; The medical history showed chronic obstructive pulmonary disease&#44; obstructive sleep apnoea syndrome&#44; chronic otitis media monitored by an otolaryngologist and botulism&#44; which required ICU admission in 2007&#46; No history of hypertension&#44; diabetes mellitus&#44; dyslipidaemia or any known heart disease&#46; The physical examination revealed a normal general state&#44; he was eupneic at rest&#44; conscious&#44; oriented&#44; collaborative&#44; with normal perfusion and hydration&#46; BP was 143&#47;95mm Hg&#44; HR was 75 beats&#47;min&#44; temperature 36&#46;5&#176;C&#44; and oxygen saturation 97&#37;&#46; There were no lesions on the skin or in the mucous membranes&#46;</p><p class="elsevierStylePara">Cardiopulmonary auscultation&#58; rhythmic without audible murmurs&#46; Vesicular murmur without superimposed noise was found&#46; Abdomen&#58; soft and palpable&#46; No signs of peritoneal irritation&#46; No masses or organomegaly on palpation&#46; The lower extremities showed pitting oedema to the root of the limbs&#44; without signs of deep vein thrombosis &#40;DVT&#41; or chronic venous insufficiency&#44; with positive pulses&#46; The neurological examination found isochoric and normally reactive pupils&#44; normal cranial nerves&#44; and segmentally conserved strength and sensitivity&#46; There were no signs of meningeal irritation&#46;</p><p class="elsevierStylePara">The analytical results on admission showed&#58; haemoglobin 11g&#47;dl&#44; haematocrit 34&#46;7&#37;&#44; MCV 92fl&#44; WBC 9000 &#40;85&#37; neutrophils&#44; 9&#46;1&#37; lymphocytes&#41;&#44; platelets 213 000&#44; glucose 102mg&#47;dl&#44; urea 265mg&#47;dl&#44; creatinine 12&#46;2mg&#47;dl&#44; sodium 137mEq&#47;l&#44; potassium 7mEq&#47;l&#44; chloride 107mEq&#47;l&#44; procalcitonin 0&#46;92mg&#47;dl&#44; protein 7g&#47;l&#44; calcium 9&#46;6mg&#47;dl&#44; corrected calcium 9&#46;8mg&#47;dl&#44; CRP 272&#46;8&#44; total bilirubin 0&#46;6mg&#47;dl&#44; AST 19U&#47;l&#44; ALT 39U&#47;l&#44; GGT 28U&#47;l&#44; ALP 61U&#47;L&#44; amylase 84&#46; Urinalysis&#58; protein 100mg&#47;dl&#44; 300 red cells&#44; negative nitrites&#44; no leukocyte&#46; Chest x-ray showed no signs of condensation or leakage&#44; and normal mediastinum&#46; The plain abdominal x-ray showed non-specific meteorism&#46;</p><p class="elsevierStylePara">Venous blood gases&#58; metabolic acidosis with pH 7&#46;28&#44; total CO<span class="elsevierStyleInf">2</span> 20mmol&#47;l&#44; HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">-</span>18&#46;8mmol&#47;l&#44; BE -7&#46;5&#46; ECG&#58; sinus rhythm at 75 beats&#47;min&#44; normal PR&#44; narrow QRS&#44; no acute repolarisation changes&#46; Abdominal ultrasound&#58; liver and spleen without ultrasound abnormalities&#46; Enlarged right kidney &#40;15cm&#41;&#44; with loss of cortico-medullary differentiation&#44; no observed dilation of the excretory tract&#46; Hypoplastic left kidney &#40;described in previous studies&#41;&#46; <span class="elsevierStyleSup">99m</span>Tc-MAG3 renal scan&#58; non-functioning left kidney&#46; Severe parenchymal nephropathy in the right kidney&#46; Immunology&#58; IgG 795mg&#47;dl&#44; IgA 123mg&#47;dl&#44; IgM 25&#46;1mg&#47;dl&#44; C3 133mg&#47;dl&#44; normal C4&#44; kappa chains 161mg&#47;dl&#44; normal lambda&#46;</p><p class="elsevierStylePara">Autoimmunity&#58; ANA&#44; anti-DNA Ab and c-ANCA negative&#44; p-ANCA 41U&#47;ml and anti-GBM Ab 287U&#47;ml&#46; Normal serum protein&#46; Serology for HBV and HCV negative&#46;</p><p class="elsevierStylePara">Given these clinical and analytical findings&#44; a renal biopsy was performed via open lumbotomy&#44; as the patient had a single functional kidney&#46;</p><p class="elsevierStylePara">The anatomical pathology described a total of 49 glomeruli&#44; three of them sclerosed and the structure of the others was extensively affected&#46; Fibrinoid necrosis and extracapillary cell and circumferential proliferation were found in 100&#37; of the glomeruli&#46; The small vessels also had necrotising vasculitis&#46; The direct IF study provided a linear and diffuse positive in the glomerular basement membrane&#44; with IgG positive and the rest of the antibodies negative&#46; In summary&#44; extracapillary glomerulonephritis was detected with intense involvement of 100&#37; of the glomeruli of the sample and IF typical of anti-GBM Ab-mediated extracapillary glomerulonephritis &#40;type I&#41;&#44; see Figures 1 and 2&#46;</p><p class="elsevierStylePara">From admission&#44; the patient required renal replacement therapy&#46; He was treated with intravenous cyclophosphamide at a dose of 1&#46;5mg&#47;kg&#47;day&#44; methylprednisolone 500mg&#47;24h for 3 days and plasmapheresis &#40;7 sessions&#41;&#46; The cyclophosphamide was discontinued due to thrombocytopaenia&#46; There was no pulmonary involvement at any time during evolution&#46;</p><p class="elsevierStylePara">Currently&#44; the patient is on haemodialysis with arteriovenous fistula as the vascular access&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Discussion </span></p><p class="elsevierStylePara">The percentage of serum coexistence of p-ANCA and anti-GBM Ab was quantified in different series at around 25&#37;&#46;<span class="elsevierStyleSup">1&#44;3-5</span> Currently&#44; the clinical profile&#44; the prognosis and the pathophysiological role of each antibody in the serum of patients with p-ANCA and anti-GBM Ab coexistence is still under investigation&#46; It is not clear whether the ANCA-associated GN predisposes the development of the anti-GBM Ab-mediated disease or if the ANCA becomes positive in the course of the anti-GBM Ab-mediated GN&#46;</p><p class="elsevierStylePara">However&#44; one of the most relevant factors is that IF studies are not routinely described in the literature&#46; Therefore&#44; we are not sure if &#8220;double positive&#8221; cases are type III or type I EGN&#46;</p><p class="elsevierStylePara">In type III ANCA&#43; EGN&#44; the existence of anti-GBM Ab has been described in up to 5&#37; of cases&#46; Due to the greater frequency of this disease&#44; most reported cases are included in this group&#46; Some studies suggest that ANCA GN appears first&#44; followed by anti-GBM Ab disease&#46;<span class="elsevierStyleSup">1&#44;3</span> In these cases&#44; it has been suggested that there is an exposure of the glomerular basement membrane antigens and the development of anti-GBM Ab&#46;</p><p class="elsevierStylePara">In type I EGN&#44; it has been reported that up to 30&#37; of cases may be associated with the existence of ANCA&#46; Due to the lower frequency of this disease&#44; fewer cases have been reported&#46;<span class="elsevierStyleSup">4&#44;5</span> The pathogenesis of this condition is not clear and it seems that altered immune regulation results in the development of both&#44; p-ANCA and anti-GBM Ab&#46;</p><p class="elsevierStylePara">In addition&#44; it has been suggested that patients with ANCA and anti-GBM Ab&#44; paradoxically&#44; have a better prognosis&#46;<span class="elsevierStyleSup">6</span> However&#44; this has not been confirmed&#44; and it has even been stated that renal survival in patients with dual positive is no better than those with only anti-GBM Ab&#46;<span class="elsevierStyleSup">1&#44;3&#44;8</span> In a study by Lindic et al&#46;&#44;<span class="elsevierStyleSup">10</span> patients with anti-GBM Ab&#44; ANCA and a creatinine of higher than 5&#46;6mg&#47;dl on admission did not recover renal function&#44; despite treatment with prednisolone&#44; cyclophosphamide and plasma exchange&#46;</p><p class="elsevierStylePara">We reported a case of type I EGN with positive linear IF and serum coexistence of anti-GBM Ab and p-ANCA&#46; The poor prognosis of renal function in these cases was seen in our patient&#44; who was dependent on haemodialysis despite aggressive treatment&#46;</p><p class="elsevierStylePara"><a href="grande&#47;10611&#95;108&#95;13109&#95;en&#95;10611&#95;f1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10611_108_13109_en_10611_f1.jpg" alt="Silver technique"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Silver technique</p><p class="elsevierStylePara"><a href="grande&#47;10611&#95;108&#95;13110&#95;en&#95;10611&#95;f2&#46;jpg" class="elsevierStyleCrossRefs"><img src="10611_108_13110_en_10611_f2.jpg" alt="Immunofluorescence"></img></a></p><p class="elsevierStylePara">Figure 2&#46; Immunofluorescence</p>"
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