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Lyme nephritis

Authors

  • Meryl P. Littman VMD, DACVIM

    Corresponding author
    • Department of Clinical Studies–Philadelphia, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA
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  • The author declares no conflict of interest.

Address correspondence and reprint requests to

Dr. Meryl P. Littman, Department of Clinical Studies–Philadelphia, University of Pennsylvania School of Veterinary Medicine, 3900 Delancey Street, Philadelphia, PA 19104-6010, USA.

Email: merylitt@vet.upenn.edu

Abstract

Objective

To review what is known and highlight knowledge gaps regarding Lyme nephritis (LN).

Data Sources

Publications identified via PubMed using the keywords “Borrelia burgdorferi,” “Borreliosis,” “glomerulonephritis,” “protein-losing nephropathy,” “autoimmunity,” and “retriever,” and as generated by investigators working in the fields of Borreliosis and immune-mediated glomerulonephritis.

Human Data Synthesis

Postborrelial immune-mediated glomerulonephritis was described recently in 6 people; 3 responded to antimicrobials/steroids, 1 to antimicrobials/angiotensin-converting enzyme inhibitor/warfarin, 1 required hemodialysis but became hemodialysis independent after 5 months and treatment with antimicrobials, steroids, plasmapheresis, immunoglobulin, and 1 did not respond to steroids and angiotensin-converting enzyme inhibitor and still requires hemodialysis.

Veterinary Data Synthesis

Lyme nephritis is seen in <1–2% of Lyme seropositive dogs, with an average onset at 5–6 years. Labrador and Golden Retrievers are predisposed to this condition. Prior or concurrent lameness is described in 9–28% cases. Historical presentations include acute progressive protein-losing nephropathy with membranoproliferative glomerulonephritis, tubular necrosis/regeneration, and interstitial nephritis, but possibly milder forms exist. Complications include thromboembolic events, hypertension, effusive disease, and oliguric/anuric renal failure. Diagnostic tests help stage disease and rule out other causes. Renal biopsy is advocated early, when intervention may help, and to prove if immune-complex disease exists. Treatment includes standard therapy for protein-losing nephropathy, long-term antimicrobials, and perhaps immunosuppressive therapy.

Conclusions

There is no experimental model of LN to study predisposing factors, pathogenesis, onset, progression, treatment, or prevention. There are no predictive tests to identify the few individuals at highest risk, therefore all seropositive dogs should be screened and monitored for proteinuria. Lyme nephritis mimics other forms of protein-losing nephropathy and sometimes Leptospirosis. Renal biopsy helps show if immune-complex disease exists, but may not prove LN specifically. More studies are warranted on dogs with Lyme-specific immune-complex deposition to evaluate risk factors, understand pathogenesis, variability of expression, and to validate treatment and prevention protocols.

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