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Author Topic: Hyperfiltration After Donation and Living Kidney Donor Risk  (Read 1980 times)

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Offline Clark

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Hyperfiltration After Donation and Living Kidney Donor Risk
« on: November 11, 2017, 04:08:15 PM »

Hyperfiltration After Donation and Living Kidney Donor Risk
M. van Londen, J. van der Weijden, G. Navis
 American Journal of Transplantatio

DOI: 10.1111/ajt.14409

To the Editor:
The editorial by Dr. Steiner states that follow-up on living kidney donors in all current studies is too short for a good estimation of lifetime end-stage renal disease (ESRD) risk. We agree that follow-up should be longer, to allow the development of ESRD, but would like to add an important additional argument for this statement.
In the general population, the development of ESRD often is preceded by a period of chronic kidney disease with gradual renal function decline. But after living kidney donation, physiological hyperfiltration occurs in which the kidney uses its renal reserve capacity. This process can cause glomerular filtration rate to increase for up to 5 years after donation [1]. If a donor develops diabetic nephropathy, glomerular hyperfiltration also occurs early in the disease, although through a different mechanism [2]. Finally, during the past decades, the mean body mass index of the kidney donor population has increased [3], and obesity-associated hyperfiltration is strongly associated with ESRD risk in the long term [4]. These three causes of hyperfiltration cause an underestimation of ESRD risk in the short term, and the latter two contribute to the exponential risk in the long term that Dr. Steiner discusses. Studies with a follow-up of less than 10 years should take hyperfiltration into account when performing risk prediction.


Invited response to “Hyperfiltration After Donation and Living Kidney Donor Risk”
R. W. Steiner
 American Journal of Transplantatio

DOI: 10.1111/ajt.14445

To the Editor:
The concerns of Dr. van Londen and colleagues are well founded.[1] In the future, obesity and diabetes will occur more often as young adults age and will increase the exponential growth in ESRD rates 20-30 years later. These lifetime outcomes will remain distant and difficult to predict in young candidates. The risks of post-donation hyperfiltration are a separate issue that has concerned transplant centers for decades.[2]
But the potential contribution of hyperfiltration to increased long-term donor risk remains unclear. Drastically reducing renal mass by over 90% in rats produces hyperfiltration (an increased single nephron gfr, or sngfr) that is mediated by increased glomerular capillary pressure, causing mechanical damage and immediate, progressive loss of GFR. But a less severe 50% reduction in renal mass at donation has seemed benign.[2, 3] Sngfr initially increases by about 40% and keeps increasing for several years.[2-4] With obesity and/or diabetes in non transplant settings, sngfr typically increases even less than it does after donation,[4] raising questions about its pathogenic significance. The increased ESRD risks of obesity may principally be due to eventual diabetes or to direct vascular damage from the normoglycemic hyperinsulinemic state.[5] As the authors recognize, diabetic hyperfiltration is initially a physiologic maladaptation and not yet proven to be a contributor to progressive diabetic nephropathy.[4] Most importantly, once many kidney diseases begin, surviving glomeruli adapt by hyperfiltering, perhaps minimizing the relevance of preexisting hyperfiltration to disease progression.[4, 6]
The recently demonstrated increase in ESRD risk that is associated with donation may simply be due to loss of GFR at nephrectomy and have little to do with hyperfiltration. Lower postdonation GFRs provide less renal reserve, causing postdonation kidney diseases to reach ESRD sooner, if and when they begin. This also means that candidates with high-normal predonation GFRs will have higher postdonation GFRs and lower lifetime risks of ESRD. There is no evidence that such high-normal GFRs somehow represent a hyperfiltration risk that should be avoided.

Unrelated directed kidney donor in 2003, 62 gallon blood & platelet donor and counting!
Rep to the OPTN/UNOS Boards of Directors & Executive, Kidney Transplantation, & Ad Hoc Public Solicitation of Organ Donors Committees 2005-2011


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