Letter to the Editor
Proteinury of nephrotic range in atypic uremic hemolytic syndrome by Clostridium difficile
Proteinuria de rango nefrótico en síndrome hemolítico urémico atípico por Clostridium difficile
Elena Borrego García
, Lidia Díaz Gómez, María Ramírez Gómez
Corresponding author
Servicio de Nefrología, Hospital Universitario San Cecilio, Granada, Spain
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It is a diagnosis of clinicopathological characteristics that presents with microangiopathic haemolytic anaemia, thrombocytopenia, and organ damage. The specific pathological lesion manifests itself with abnormalities in the endothelium and in the vascular wall, mainly affecting the renal vessels.<a class="elsevierStyleCrossRefs" href="#bib0030"><span class="elsevierStyleSup">1,2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Secondary aHUS can be caused by pregnancy/childbirth, systemic autoimmune diseases, drugs, solid organ transplantation/hematopoietic stem cells, infections, and other miscellaneous causes. <span class="elsevierStyleItalic">Chlostridium difficile</span> (CD) has been rarely identified as the infectious cause of the syndrome, with digestive symptoms (abdominal pain, diarrhoea) appearing days after oral-faecal contamination, followed by anaemia, thrombocytopenia, and renal failure (sometimes accompanied by haematuria and oliguria).<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">3,4</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">We report the rare case of a patient who began with significant proteinuria in nephrotic range, in the context of aHUS caused by CD.</p><p id="par0020" class="elsevierStylePara elsevierViewall">A 77-year-old patient with no medical history of interest. After a trip to Israel a few days ago, he went to the emergency department for a 48<span class="elsevierStyleHsp" style=""></span>h history of bloody diarrhoea (10–13<span class="elsevierStyleHsp" style=""></span>stools/day), asthenia and swelling of the lower limbs. On examination: BP 149/97; HR 73<span class="elsevierStyleHsp" style=""></span>bpm; SatO<span class="elsevierStyleInf">2</span> 99%; afebrile, generalized abdominal pain on superficial palpation and presence of moderate oedema up to the knees. No neurological focus or other signs. Diuresis was preserved at all times.</p><p id="par0025" class="elsevierStylePara elsevierViewall">The laboratory values that stood out were creatinine 2.7<span class="elsevierStyleHsp" style=""></span>mg/dl; urea 153<span class="elsevierStyleHsp" style=""></span>mg/dl; LDH 1510<span class="elsevierStyleHsp" style=""></span>U/l; haptoglobin 8<span class="elsevierStyleHsp" style=""></span>mg/dl; Hb 9.3<span class="elsevierStyleHsp" style=""></span>mg/dl; conjugated bilirubin 2.08<span class="elsevierStyleHsp" style=""></span>mg/dl; 44,000<span class="elsevierStyleHsp" style=""></span>mm<span class="elsevierStyleSup">3</span> platelets; peripheral blood schistocytes >7%; proteinuria of 10<span class="elsevierStyleHsp" style=""></span>g/24<span class="elsevierStyleHsp" style=""></span>h and blood cell casts. Stool culture showed growth of CD A<span class="elsevierStyleHsp" style=""></span>+<span class="elsevierStyleHsp" style=""></span>B toxin and an abdomen CT showed findings suggestive of infectious colitis with normal kidneys. The rest of the laboratory tests related to autoimmunity, complement, coagulation, Shiga toxin in stool, viral serology, direct Coombs and ADAMTS 13 protein determination, were normal, ruling out systemic disease. A renal biopsy was also performed, describing lesions typical of thrombotic microangiopathy with endothelial involvement.</p><p id="par0030" class="elsevierStylePara elsevierViewall">Given these results and the modification of terminology published in the KDIGO 2017 Guidelines,<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a> aHUS secondary to CD colitis was diagnosed. After failure to improve renal failure, despite symptomatic supportive treatment, the persistence of significant proteinuria, and persistent moderate thrombocytopenia, we started with corticosteroids boluses of 250<span class="elsevierStyleHsp" style=""></span>mg, daily plasmapheresis with fresh frozen plasma (total of 6 cycles) and empirical antibiotic therapy with oral vancomycin 500<span class="elsevierStyleHsp" style=""></span>mg/24<span class="elsevierStyleHsp" style=""></span>h and metronidazole 500<span class="elsevierStyleHsp" style=""></span>mg/8<span class="elsevierStyleHsp" style=""></span>h/for 10 days, with good progression and laboratory normalization of haemoglobin (12<span class="elsevierStyleHsp" style=""></span>mg/dl), platelets (220,000<span class="elsevierStyleHsp" style=""></span>mm<span class="elsevierStyleSup">3</span>), renal function (Cr 0.6<span class="elsevierStyleHsp" style=""></span>mg/dl), proteinuria of 266<span class="elsevierStyleHsp" style=""></span>mg/24<span class="elsevierStyleHsp" style=""></span>h, without new data on haemolysis and asymptomatic to date and without the need for haemodialysis.</p><p id="par0035" class="elsevierStylePara elsevierViewall">At present, the term aHUS is initially a diagnosis of exclusion, used to encompass those thrombotic microangiopathies that do not meet the criteria of thrombotic thrombocytopenic purpura or typical Shiga toxin-mediated HUS.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a> Among the most common causes of infectious origin of secondary aHUS are HIV, HCV, <span class="elsevierStyleItalic">Influenza</span>, CMV, <span class="elsevierStyleItalic">Rickettsia</span>, <span class="elsevierStyleItalic">Streptococcus pneumoniae</span> and malaria infection. CD is uncommon as the causative agent, and it mainly occurs in the paediatric population. The pathogenesis of the digestive symptoms caused by this gram-positive bacillus seems to be related to the binding of toxins A and B to specific receptors on colonic cells, inducing apoptosis, mucosal and microcirculatory damage, and increased pro-inflammatory cytokines. However, the role of DC in the kidney is still unclear and needs further study.</p><p id="par0040" class="elsevierStylePara elsevierViewall">The interest of our case was the atypical presentation with significant proteinuria, among other manifestations of aHUS, in addition to the unusual CD aetiopathogenesis. We also conclude by insisting on the need to make a good differential diagnosis that will help us to define thrombotic microangiopathies in order to propose an adequate treatment.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "⋆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Borrego García E, Díaz Gómez L, Ramírez Gómez M. Proteinuria de rango nefrótico en síndrome hemolítico urémico atípico por <span class="elsevierStyleItalic">Clostridium difficile</span>. 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