The author declares no conflict of interest.
State of the Art Review
Article first published online: 5 MAR 2013
© Veterinary Emergency and Critical Care Society 2013
Journal of Veterinary Emergency and Critical Care
Special Issue: Advances in Renal Physiology and Therapy
Volume 23, Issue 2, pages 163–173, March/April 2013
How to Cite
Littman, M. P. (2013), Lyme nephritis. Journal of Veterinary Emergency and Critical Care, 23: 163–173. doi: 10.1111/vec.12026
- Issue published online: 8 APR 2013
- Article first published online: 5 MAR 2013
- Manuscript Accepted: 21 JAN 2013
- Manuscript Received: 1 MAR 2012
- Borrelia burgdorferi;
- protein-losing nephropathy;
To review what is known and highlight knowledge gaps regarding Lyme nephritis (LN).
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.
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.