Lyme nephritis in humans: Physio-pathological bases and spectrum of kidney lesions
Known in less than half a century, borreliosis, or Lyme disease, is a zoonosis caused by the tick bite. It is the most common vector disease in Europe and the United States. Borrelia burgdorferi sensu lato, the bacterium in question, is fitted with a “cunning device” that allows it to trick the immune system and implant the infection chronically. It causes multi-system tissue damage mediated by the inflammatory response of the host.
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Renal involvement is rarely reported and is better known in dogs as Lyme nephritis. The first case of kidney impairment in the human being was described in 1999, and since then eight other cases have been reported. The involvement is preferentially glomerular; the histological forms vary between immune complex nephropathy and podocytopathy.
The pathophysiological mechanisms appear to be triple: immune complex deposits, podocytic hyper-expression of the B7-1 membrane protein, and renal infiltration of inflammatory cells.
On the basis of the accumulated knowledge of the disease in just over 40 years, this review aims at establishing the physio-pathological hypotheses of renal involvement in order to better define the histological lesions.
Source: By Gueye S1, Seck SM2, Kane Y3, Tosi PO4, Dahri S4, Kounde C4, Algouzmari I4, Gouin A4, Ged É4, Allal A4, Rostaing L5. [Lyme nephritis in humans: Physio-pathological bases and spectrum of kidney lesions]. Nephrol Ther. 2019 Jan 31. pii: S1769-7255(18)30655-2. doi: 10.1016/j.nephro.2018.09.004. [Epub ahead of print