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Today, Lyme disease is the most common vector-borne disease in the US, with over 22 500 confirmed cases in 2010. Borrelia burgdorferi, a spirochete, is transmitted by the bite of infected Ixodes ticks. These ticks have a 3-stage lifecycle (larvae, nymph, and adult) and take 1 blood meal at each stage. They become infected by feeding on an infected wild animal—typically white-footed mice, voles, chipmunks, or birds—during the larval feeding. The infection is maintained during the tick molting process to the nymphal stage and can be transmitted to other animals to maintain the cycle of infection in the wild. Both nymphal and adult Ixodes ticks can transmit infection to humans.
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We have read the interesting review on Lyme disease by Linden Hu . As long as clinical presentation of the disease is actually protean and the disease is endemic in certain areas of the world, a thorough knowledge of its clinical presentation will help health professionals acquire high clinical suspicion for the disease. Following earlier similar reports in animals [2,3], we and others have reported several cases of Lyme-associated, apparently immune complex-mediated glomerulonephritis, often of the membranoproliferative type, manifested either as a nephritic, or nephrotic syndrome or even as acute renal failure of various gravity [4-8]. It is now seems possible that this has been an unreckognized, and still remains a rather under-reckognized condition  by primary care physicians as well as nephrologists and, as such, it often evades diagnosis or is mis-diagnosed as “primary” glomerulonephritis. In this context, it would seem appropriate that “Lyme-nephritis” is included into the clinical presentation of Lyme disease in the literature as well as in physicians’ diagnostic arsenal.
1.Hu LT. Lyme disease. Ann Intern Med 2012; 157(3):ITC2-1.
2.Dambach DM, Smith CA, Lewis RM, Van Winkle TJ: Morphologic, immunohistochemical, and ultrastructural characterization of a distinctive renal lesion in dogs putatively associated with Borrelia burgdorferi infection: 49 Cases (1987-1992). Vet Pathol 1997; 34: 85-96.
3.Grauer GF, Burgess EC, Cooley AJ, Hagee JH: Renal lesions associated with Borrelia burgdorferi infection in a dog. JAm Vet Med Assoc 1988; 193:237-9.
4.Kelly B, Finnegan P, Cormican M, et al. Lyme disease and glomerulonephritis. Ir Med J 1999; 92: 372-3.
5.Kirmizis D, Efstratiadis G, Economidou D et al. MPGN secondary to Lyme disease. Am J Kidney Dis 2004; 43: 544–51.
6.Papineni P, Doherty T, Pickett T, et al. Membranous glomerulonephritis secondary to Borrelia burgdorferi infection presenting as nephrotic syndrome. NDT Plus 2010; 3: 105-6.
7.Mc Causland FR, Niedermaier S, Bijo V, Rennke HG, Choi ME, Forman JP.
8.Kwiatkowska E, Gołembiewska E, Ciechanowski K, Kędzierska K. Minimal-Change Disease Secondary to Borrelia burgdorferi Infection. Case Reports in Nephrology 2012; doi:10.1155/2012/294532
9.Kirmizis D, Chatzidimitriou D. Comment on 'Membranous glomerulonephritis secondary to Borrelia burgdorferi infection presenting as nephrotic syndrome'. Nephrol Dial Transplant. 2010; 25: 1723-7.
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