Donor Risk Scores?

A recent review in Nature Nephrology discuses this important concept.  A large study out of Finland is discussed in this review and how the donor risk score was developed. What they describe is a donor allograft damage index which involves clinical components as well pathology components.
What constitutes the clinical components are: age >50, smoking, unstable blood pressure, HTN, need for CPR, alcohol abuse, untreated HTN, ischemic heart disease, arteriosclerosis, oliguria and the biopsy component is vascular intimal sclerosis, tubular atrophy, interstitial fibrosis, interstitial inflammation, mesangial matrix increase and glomerulosclerosis.  The Biopsies of the donors were graded with a 0-3 point system with each of the six histological criteria and the higher the points- the worse the kidney was.  The authors showed that the presence of >5 risk factors(clinical) and associated with an increase in mean allograft damage score from 0.5 to 1.4 and an increase in percent glomerulosclerosis from 1.5% to 8.1%.  And eventually higher donor risk scores were associated with long term graft outcomes over 5 years as well.
One of the few large studies to look at histological allograft data and comparing that to the clinical data.  Interesting to see what comes next.

Ref:
http://www.ncbi.nlm.nih.gov/pubmed/21303414
http://www.ncbi.nlm.nih.gov/pubmed/21522192

Dual Live Transplants performed

Check out the latest on dual liver and kidney( live donor) combined transplants done recently.

http://www.ldnews.com/news/ci_17976156

Fascinating Wordle in AJT 2011

Check out this picture that was created on most cited surgical articles in ten surgical journals.
Turns out Transplantation topics rule and show the most results.
Nice
http://onlinelibrary.wiley.com/doi/10.1111/j.1600-6143.2011.03459.x/full

Dichotomous Effects of Rapamycin

A recent review in AJT 2011 April issue reviews this concept nicely.

Rapamycin has many faces and many different effects on different cells. Lets summarize
1. Suppression of CD4 T+ differentiation
2. Increased T reg development
3. Decreased response to skin graft
4. Decreased dendritic cell maturation
5. Increased CD8 + T cell  memory differentiation
6. Increased CD8 T cell activation
7. Increased response to pathogen
8. Increased IL-12 production

Commonly noted side effects:- hyperlipidemia, thrombocytopenia, decreased wound healing
Ref and information obtained from:
http://www.ncbi.nlm.nih.gov/pubmed/21446969

Arteries and Kidney Transplant

http://consumer.healthday.com/Article.asp?AID=651907
Check out the news release from JASN

Pancreas Transplantation in the Treatment of Diabetes

A nice treat from Nephrology on Demand

Transplant Tourism and Malignancy

Transplant Tourism does still continue and many patients continue to get kidneys from other countries where it could be commercial possible.  A recent study showed that when groups were compared( tourism kidneys to home country based kidneys):- the graft and patient survivals were equal but the 10 year cumulative cancer risk was significantly higher in the transplant tourism kidneys; especially in the older age group.  What might be contributing to this? - immunosuppresive therapy, difficulty in follow ups and were some of the thoughts mentioned in this article. Check it out

Ref:
http://www.ncbi.nlm.nih.gov/pubmed/21270768

IVIG - how does it work from the Immunology blog?

http://allergynotes.blogspot.com/2011/04/intravenous-immune-globulin-ivig-in.html

Neutropenia from Tacrolimus

Post transplant neutropenia has many causes.  Etiology is usually medications, infections, cancer.
In a retrospective evaluation, 28% neutropenia was noted after first year of transplantation.  Most of this was sought to be from MMF-tacrolimus combination.
The drugs we usually consider are: MMF, azathioprine, acyclovir, gancyclovir, bactrim, valcyte.
A recent review on CJASN 2011, presents three patients with pure tacrolimus induced neutropenia and the mechanism behind it. All improved after they were switched to cyclosporine.

Why does it happen?
1. Direct inhibition of myeloid cells
2. effect of the drug on mononuclear accessory cells
3. pharmacokinetic interaction between MMF and tacrolimus
4. autoantibodies against myeloid precursors or mature neutrophils

Ref:
http://www.ncbi.nlm.nih.gov/pubmed/21258040
http://www.ncbi.nlm.nih.gov/pubmed/19538494