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ePublished: 08 Nov 2013
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J Renal Inj Prev. 2014;3(1): 17-20.
doi: 10.12861/jrip.2014.07
PMID: 25340158
PMCID: PMC4206044
  Abstract View: 4107
  PDF Download: 1689

Case Report

Post-infectious glomerulonephritis presenting as acute renal failure in a patient with Lyme disease

Davide Rolla 1*, Novella Conti 1, Francesca Ansaldo 1, Laura Panaro 1, Tiziano Lusenti 2

1 Division of Nephrology, IRCCS San Martino-IST, Genoa, Italy
2 Centro Medico Lazzaro Spallanzani, Reggio Emilia, It
*Corresponding Author: *Corresponding author: Davide Rolla, Clinica Nefrologica, Azienda Ospedaliera Universitaria S. Martino, Largo R. Benzi, 16132 Genova–Italy., Email: davide.rolla@hsanmartino.it

Abstract

Introduction: We report a case of a patient with acute renal failure in Lyme disease-associated focal proliferative mesangial nephropathy. Lyme disease is a vector-borne disease caused by Borrelia burgdorferi, transmitted by the bite of an infected ixodes tick. Post-infectious glomerulonephritis (GN)secondary to Borrelia burgdorferi infection in man could be fatal, as it is in canine Lyme borreliosis.Case: A 61-year old man with chronic ethanolic hepatitis was admitted to a provincial hospital, complaining of nausea, diarrhoea and loss of his sense of taste. A few days prior hospitalization, he had been bitten by a tick. He developed erythema gyratum repens in the right leg, thorax and face. Kidney function was altered despite normal urine flow: creatinine 5.04 mg/dl and BUN 126 mg/dl. Urinalysis showed light proteinuria and microscopic hematuria. IgG and IgM antibodies to Borrelia burgdorferi were detected by ELISA and Western blot confirmed the diagnosis. Renal biopsy showed mild mesangial proliferation and mesangial and paramesangial deposits on AFOG stain. A diagnosis of acute renal failure in Lyme disease-associated focal proliferative IgA nephropathy was made. Intravenous antibiotic medication was started (ceftriaxone 1 gram daily i.v.). The patient was later discharged, serum creatinine had decreased to 3.5 mg/dl with a BUN of 58 mg/dl, and a slight improvement was observed on follow-up.Conclusion: Borrelia burgdorferi is a possible cause of post-infectious GN in humans as it is in dogs. Difficulties in identifying Borrelia burgdorferi may also be one of the reasons for the paucity of reports on the association of this infection with glomerulonephritis in humans. Currently, various types of histological renal lesions have been reported.

Implication for health policy/practice/research/medical education:

The diagnosis of Lyme disease is based primarily on clinical history and on the presence of antibodies (IgM an IgG) to Borrelia burgdorferi. This vector-borne disease is a possible cause of post-infectious glomerulonephritis (GN) in humans as it is in dogs. It is likely that the immune-complex plays a role in the pathogenesis of this disorder, but acute Lyme disease may also contribute to the development of activation of previously immune-mediated glomerular disease.

Please cite this paper as: Rolla D, Conti N, Ansaldo F, Panaro L, Lusenti T. Post-infectious glomerulonephritis presenting as acute renal failure in a patient with Lyme disease. J Ren Inj Prev 2014; 3(1): 15-18. DOI: 10.12861/jrip.2014.06

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