Journal Information
Vol. 30. Issue. 3.May 2010
Pages 271-380
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Henoch-Schönlein nephritis triggered by Salmonella Enteritidis infection
Salmonella Enteritidis y nefropatia de Schönlein-Henoch
Andrea Venutaa, Fiorella Ballib
a Paediatric Department; Dipartimento materno-infantile, Modena University Hospital; Policlinico di Modena, Modena, Italy,
b Paediatric Department, Modena University Hospital, Modena, Italy,
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Dear Editor,

Henoch-Schönlein purpura  (HSP) is a common type of vasculitis in children. Renal involvement is frequent and not always benign. Prognostic factors have been recently reviewed by Garcia et al. on your journal, older age and relapses being related to a poorer renal prognosis1.

We present a case of  5-years old boy who was admitted to our hospital with a history of fever-chills, vomiting, abdominal cramping and diarrhoea.  He received IV and subsequent oral rehydration and his conditions improved in three days. A stool culture yielded Salmonella Enteritidis . After an interval of one week by the onset of gastrointestinal symptoms he developed symmetrical purpuric papules and plaques at the lower extremities and arthralgia of the tibio-tarsal joints. Two days later appeared frank hematuria lasting one day only and followed by microhematuria with mild proteinuria. Blood pressure was always normal. Among laboratory investigations creatinine was 77 μmol/L, platelet count, C3 and C4 levels were normal, antinuclear antibody and rheumatoid factor were absent, serum IgA levels were increased for his age (232 mg/dL). Characteristic skin manifestations, joint involvement and hematuria led us to the diagnosis of HSP nephritis (HSPN). Purpura and arthritis resolved in three weeks. Nephritis had a benign evolution. After six months the boy was normotensive without residual microhematuria nor proteinuria and his renal function was normal.

Pathogenesis of HSPN has very recently reviewed2. High levels of galactose-deficient IgA1 (Gd-IgA1) has been found in children with HSPN, but not in HSP affected patients without nephritis. Gd-IgA1 seems to have a pivotal role both in HSPN and IgA nephritis. Gd-IgA1 is recognised by anti-glycan antibodies and form large molecular immune complexes. Their deposit in renal mesangium is thought to initiate glomerular inflammation.

Many factors may activate IgA1 overproduction and subsequent disease: a list that includes various infective agents and medications has been published in a review by Rai et al., but it does not contain Salmonella Enteritidis3. Afterwards a case of HSP nephritis in a 50-year-old woman with Salmonella typhy septicaemia has been described4. At our knowledge our case of HSP nephritis induced by Salmonella enteritidis is the first described in literature. This pathogen, very common in children, should be included in the number of infectious agent that can trigger HSPN.

J. Lucas Garc��a, O. ��lvarez Blanco, M. J. Sanahuja Ib����ez, P. J. Ortega L��pez y I. Zamora Mart�� Evoluci��n de la nefropat��a de Sch��nlein-Henoch en pacientes pedi��tricos. Factores pron��sticos. Nefrolog��a 2008; 28 (6) 627-632
Lau KK, Suzuki H, Novak J, Wyatt RJ. Pathogenesis of Henoch-Sch��nlein purpura nephritis. Pediatr Nephrol. 2010 Jan; 25(1):179.
Rai A, Nast C, Adler S. Henoch-Sch��nlein Purpura Nephritis. J Am Soc Nephrol�� 1999;10:2637��2644 [Pubmed]
Youmbissi TJ, Malik TQ, Ajit Kumar S, Rafi A, Al Khursanny AI, Karkar A.�� Henoch-Sch��nlein nephritis and salmonella typhi septicaemia. Nephrol Dial Transplant. 2001 May;16(5):1081-2. [Pubmed]
Nefrología (English Edition)

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