Borrelia-bakteeri voi aiheuttaa munuaiskerästulehduksen l. glomerulonefriitin.Alla kaksi tapausselostusta (57-vuotias nainen ja 40-vuotias mies) joissa molemmilla ilmeni borrelia-bakteerin aiheuttama munuaiskerästulehdus. Molemmat saivat hoidoksi antibiootteja ja steroideja ja tulivat kuntoon. Potilaiden pitkäaikaiseurannasta ei ole mainintaa.
Lyme disease-associated glomerulonephritis.
Mc Causland FR, Niedermaier S, Bijol V, Rennke HG, Choi ME, Forman JP
Nephrol Dial Transplant 2011 07 12
We report two cases of Lyme disease-associated glomerulonephritis. A 57-year-old female presented with rash, volume overload, hypertension and rapidly progressive glomerulonephritis. Biopsy confirmed an immune complex-mediated, membranoproliferative lesion. She was treated successfully with steroids and antibiotics. In a second case, a 40-year-old male, with a previously known microscopic hematuria, presented with rash, arthralgias, new proteinuria and gross hematuria following a tick bite. Biopsy revealed focal proliferative IgA nephropathy. Treatment with steroids and antibiotics resulted in rapid resolution of findings. Acute Lyme disease may contribute to the development of de novo, or activation of previously quiescent, immune-mediated glomerular disease.
BORRELIOOSI/MUNUAISSAIRAUDET
Valvojat: Jatta1001, Borrelioosiyhdistys, Bb
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PiHa
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Jatta1001
Re: BORRELIOOSI/MUNUAISSAIRAUDET
2013. Borreliabakteerin aiheuttama munuaistulehdus (glomerulonefriitti):
Lyme nephritis.
Authors: Littman MP
Citation: J Vet Emerg Crit Care (San Antonio) 2013(Mar)
Location: Department of Clinical Studies-Philadelphia, University
of Pennsylvania School of Veterinary Medicine, Philadelphia, PA, 19104-6010.
DOI: 10.1111/vec.12026
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.
© Veterinary Emergency and Critical Care Society 2013.
10.1111/vec.12026
Lyme nephritis.
Authors: Littman MP
Citation: J Vet Emerg Crit Care (San Antonio) 2013(Mar)
Location: Department of Clinical Studies-Philadelphia, University
of Pennsylvania School of Veterinary Medicine, Philadelphia, PA, 19104-6010.
DOI: 10.1111/vec.12026
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.
© Veterinary Emergency and Critical Care Society 2013.
10.1111/vec.12026