Check out the latest on dual liver and kidney( live donor) combined transplants done recently.
http://www.ldnews.com/news/ci_17976156
Showing posts with label liver transplantation. Show all posts
Showing posts with label liver transplantation. Show all posts
Friday, May 6, 2011
Tuesday, August 3, 2010
Post transplant TMA, revisiting Atypical HUS
Post Transplantation is a real entity. Many causes have been identified. CNI toxicity, Sirolimus, ischemia, antibody mediated rejection or de novo carcinoma, antiphospholipid syndrome, post transplant SLE are a few possible diagnosis. One study showed that among 24 patients with post transplant TMA that was de novo, 7 carried a mutation in CFH or CFI or combined mutation, indicating a genetic abnormality that might be the first hit.
In the past decade, work has been very active in the field of Atypical HUS. Many complement abnormalities have been identified namely the CFH , CFI mutations, C3 mutations, CFB mutations, all which are mutations in the alternative pathway of complement leading to activation of MAC and TMA
A recent review in AJT July 2010 issue makes the following recs:
1. Screening for the above mutations to be done with all patients with aHUS prior to transplatation. I think that perhaps any non diarrheal related HUS should be screened as this might be the first hit.
2. Avoid Living related donation in such positive cases due to genetic transmission. Suggest a friend or spouse in such cases.
3. Studies have shown that aHUS MCP mutation can undergo kidney transplantation without increase risk of recurrence.
4. Anti CFH mutations might need pre emptive plasmapheresis, rituximab and steroids to lower the antibody levels.
5. The CFH and CFI mutations, the risk of recurrence is very high and transplant might be a risky procedure.
6. The options for CFH and CFI mutations might be combined liver-kidney transplantion along with TPE pre and post. Kidney alone with Pre and post TPE or kidney alone with eculizumab( anti complement agent).
All are only cases described, so no final decisions can be made. risk benefit has to be discussed with each case. Similar situations play part in C3 and CFB mutations as well. THBD mutations also are at risk but there is no data to do anything in these cases.
Does Nephrectomy of native kidneys help? Again, doesn't seem to be beneficial.
Check out these references:
http://www.ncbi.nlm.nih.gov/pubmed/20642678
http://www.ncbi.nlm.nih.gov/pubmed/20445192
http://www.ncbi.nlm.nih.gov/pubmed/20595690
Image source: http://www.profelis.org/amc/vorlesungen/immunologie/komplementsystem.html
Friday, April 23, 2010
Dual Liver and Kidney Transplantations
Tips from the NKF 2010 sessions
1. When to do both and when to do just Liver? It’s hard to figure this out as most of the kidney damage in liver associated kidney injury is ischemia and we don’t have good markers
2. A good strategy suggested was using biopsy as a guide and using the Interstitial fibrosis, tubular injury as a tool for seeing if they need a SLK or just a liver transplant.
3. When this strategy was used in some centers, and crt compared after going ahead with a respective transplants ( SLK or just liver), crt were 1.2 at 6 months in both groups.
4. Most common biopsy finding: ischemic ATN, followed by other primary GNs, (MPGN, IgA, FSGS, TMA) and vascular disease
5. If the patient has ESLD and is on dialysis < 6 weeks, perhaps just a liver is fine but otherwise might need a SLK. But with the biopsy method, we might achieve more accuracy
1. When to do both and when to do just Liver? It’s hard to figure this out as most of the kidney damage in liver associated kidney injury is ischemia and we don’t have good markers
2. A good strategy suggested was using biopsy as a guide and using the Interstitial fibrosis, tubular injury as a tool for seeing if they need a SLK or just a liver transplant.
3. When this strategy was used in some centers, and crt compared after going ahead with a respective transplants ( SLK or just liver), crt were 1.2 at 6 months in both groups.
4. Most common biopsy finding: ischemic ATN, followed by other primary GNs, (MPGN, IgA, FSGS, TMA) and vascular disease
5. If the patient has ESLD and is on dialysis < 6 weeks, perhaps just a liver is fine but otherwise might need a SLK. But with the biopsy method, we might achieve more accuracy
Sunday, February 21, 2010
New drugs for Hepatitis C
The latest AJT report introduces us to a new line of drugs for treatment of Hepatitis C. The two drugs that are closest to coming to the market are in Phase 3 trials are will be submitted to FDA soon. They are telaprevir and boceprevir. Protease inhibitors have been discussed in treating hepatitis C for years now and this brings it to the forefront.
Allowing to treat patients prior to liver transplantation might be the most benefit as the interactions post transplants with immunosuppresive medications is always a challenge. We see that in HIV patients who get kidney transplants.
The article summarizes that the future of treating primary Hep C infection or recurrence in the liver graft is going to be a cocktail of medications that will include standard medications like interferon and ribavarin but also protease inhibitors. Recurrence of Hep c in the transplanted liver is a commonly encountered problem and this might hopefully help in the near future.
Treatment of Hep C might tag behind how HIV is being treated.
Allowing to treat patients prior to liver transplantation might be the most benefit as the interactions post transplants with immunosuppresive medications is always a challenge. We see that in HIV patients who get kidney transplants.
The article summarizes that the future of treating primary Hep C infection or recurrence in the liver graft is going to be a cocktail of medications that will include standard medications like interferon and ribavarin but also protease inhibitors. Recurrence of Hep c in the transplanted liver is a commonly encountered problem and this might hopefully help in the near future.
Treatment of Hep C might tag behind how HIV is being treated.
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