Wednesday, August 4, 2010
Low Donor Kidney Weight ? Does it matter?
We have asked this question many times in conferences and especially when a pediatric kidney gets put in an adult recipient? Does it matter if the donor kidney weight is not compatible to the recipient's weight?
There is one study in 2005 that showed that low donor kidney weight to recipient weight ratio did not affect graft survival. That study only had 2.5 year follow up.
A recent study in JASN looked at >1000 patients for over 10 years and max of 7 year follow up. They found that with a low donor kidney to recipient kidney ratio of <2.3g/kg, initially the GFR increased, plateaued at 6 months but then decreased rapidly after 7 years at a mean rate of 3 ml/min.
With patients with >2.3g/kg, the the GFR after 7 years decreased at a much slower rate- 1.34ml/min.
The proteinuria was also higher in the low ratio group.FSGS was more common in the biopsies of the low ratio group.This is a retrospective analysis with its usual flaws but raises an important point of avoiding kidney and recipient weight incompatibility to avoid late clinical outcomes.
References:
http://www.ncbi.nlm.nih.gov/pubmed/20488949
http://www.ncbi.nlm.nih.gov/pubmed/15563571
There is one study in 2005 that showed that low donor kidney weight to recipient weight ratio did not affect graft survival. That study only had 2.5 year follow up.
A recent study in JASN looked at >1000 patients for over 10 years and max of 7 year follow up. They found that with a low donor kidney to recipient kidney ratio of <2.3g/kg, initially the GFR increased, plateaued at 6 months but then decreased rapidly after 7 years at a mean rate of 3 ml/min.
With patients with >2.3g/kg, the the GFR after 7 years decreased at a much slower rate- 1.34ml/min.
The proteinuria was also higher in the low ratio group.FSGS was more common in the biopsies of the low ratio group.This is a retrospective analysis with its usual flaws but raises an important point of avoiding kidney and recipient weight incompatibility to avoid late clinical outcomes.
References:
http://www.ncbi.nlm.nih.gov/pubmed/20488949
http://www.ncbi.nlm.nih.gov/pubmed/15563571
Renal Biopsy simulation
https://www.pediatric-nephrology.com/daily-updates/2010/08/04/259-kidneybx.html
Check out the above blog on Renal Biopsy simulation!
Check out the above blog on Renal Biopsy simulation!
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
Monday, August 2, 2010
TOPIC DISCUSSION: 25-OH Vitamin D and ESRD
The KDOQI has now started recommending that we check inactivated Vitamin D levels in all CKD patients with hyperparathyrodism and if the level is <30, to start replacing them with either D2 50,000 units once a week for 3 months or D3 1000 units once a day for 3 months. This is the nutritional deficiency recommendation based on the general population. There have been many studies in the general population with effects on even none bone/muscle organs: cancer prevention, decreased renin, decreased cardiac disease and so forth. 1. What are the implications of this in CKD and ESRD population?
2. Does it matter to replace inactivated vitamin D in ESRD patients?
3. Won't the inactivated D be more suppressed in our ESRD patients since we are giving them activated Vitamin D, sometimes in excess?
A recent study showed that lower levels of the inactivated Vitamin D was associated with increased mortality in HD patients but the administration of activated vitamin D to these patients decreased the mortality.
There is one study by Bert et al, that found that vitamin D3 was not as effective as activated vitamin D in decreasing pth levels in dialysis patients. Bone biopsies actually showed worsening of disease.
There is 1 alpha hydroxylation happening else where, mainly macrophages and other cells besides the kidney. Giving 25-OH might activated those cells to convert more and we can get extra renal activations.
But again, data is observational and there is no harm in giving nutritional supplemental vitamin D as long as the calcium and phosphorus are in good range.
The role of a combination of a calcimimetic and 25-0h vitamin D might be interesting to look at according to many experts. Well designed trials comparing both measures of just vitamin D alone vs vitamin D + calcimimetic vs activated vitamin D alone might be worth looking at.
Look at the below references
The first one is a nice review on all bone diseases in CKD( a nice table is in the article that summarizes a lot), good board prep table.
Kalantar-Zadeh K, Shah A, Duong U, Hechter RC, Dukkipati R, Kovesdy CP. Kidney Bone Disease and Mortality in CKD: Revisiting the role of Vitamin D, calcimimetics, alkaline phosphatase, and minerals. Kidney Int 2010:78 (suppl 117):S10-S21.
http://www.ncbi.nlm.nih.gov/pubmed/17687259
http://www.ncbi.nlm.nih.gov/pubmed/208439
IN THE NEWS:- MAYO CLINIC AND SOCIAL MEDIA
http://socialmedia.mayoclinic.org/
Check out the first center of Social Media by an University Medical Center. This is a true breakthrough.
I think that this will inspire many health care networks to have a more robust and prominent role of social media in health care.
Check out the first center of Social Media by an University Medical Center. This is a true breakthrough.
I think that this will inspire many health care networks to have a more robust and prominent role of social media in health care.
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