Showing posts with label hepatitis B. Show all posts
Showing posts with label hepatitis B. Show all posts

Thursday, July 28, 2011

Live from the consensus conference on "Optimal Testing of Live Donors to Prevent Transmission of Infectious Diseases"

What is the optimal testing strategy for testing live donors?

In a lecture given by Dr. Michael Ison, we can see that this is an area of great debate. We all agree that potential donors should have serology done for hepatitis b, hepatitis c, and HIV on initial visit. But should we repeat testing? Should we do repeat testing for everyone or should we repeat testing for high risk donors only? And what would this repeat testing mean? When is the optimal time to repeat this testing?
A suggestion was that possibly we can do repeat hepatitis B core and surface antigen testing, and nucleic acid testing for hcv and HIV. 7-14 weeks prior to surgery may be a good time to do these repeat testing.

Again, these tests can result in false positives, more costs, more patient anxiety, more visits and time spent to get blood drawn which can be looked at negatively.
More experience and studies are needed to tell us what exactly should be done. For now we need to follow our instincts and do what is best for the donor and recipient.

Thursday, July 14, 2011

CLINICAL CASE 39: ANSWERS AND SUMMARY


Which one of the following is NOT associated with Hepatitis B virus?
Membranous Glomerulopathy
  5 (5%)
Membrano proliferative GN
  1 (1%)
Mesangio proliferative GN
  6 (7%)
IgA nephropathy
  37 (43%)
Poly Arteritis Nadosa
  8 (9%)
All above are associated with Hepatitis B
  28 (32%)



Tough battle between All above and IgA Nephropathy. Traditionally, we think of Hep B and kidney disease as classically as Membranous GN.  So the most common finding is that.  MPGN, Mesangioproliferative and PAN have been also noted with Hep B.  Ig A has some rare associations with Hep B as well.  So the most probable answer should be All above are associated with Hep B.  The presence of immune complexes in the kidney suggests an immune complex basis for the disease like in MPGN sometimes, but a direct antigenic effect is the most likely cause of the proteinuria. Studies have shown that clearance of HBV antigens, either spontaneous or following antiviral treatments results in improvement in proteinuria. Thus, prompt recognition and specific antiviral treatment are critical in managing patients with HBV and renal involvement. Check out ref 1 and 2 for oldest literature on this topic. The last few references are linking IgA nephropathy and Hep B in endemic areas.

Here are some references:
http://www.ncbi.nlm.nih.gov/pubmed/605896
http://www.ncbi.nlm.nih.gov/pubmed/2023605
http://www.ncbi.nlm.nih.gov/pubmed/14988643
http://www.ncbi.nlm.nih.gov/pubmed/21677438
http://www.ncbi.nlm.nih.gov/pubmed/3293854
http://www.ncbi.nlm.nih.gov/pubmed/12970894

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