IN THE NEWS --> Cytoresistance and the kidney

What is cytoresistance? and why does it matter with the renal function.  There is some literature evidence that induction of either nephrotoxic or ischemic renal damage confers protection against the subsequent remaining renal parenchyma from the toxin.  This has been shown to be via heme-oxygenase 1 production increases and being a cytoprotective molecule. This concept of renal protection from a recent injury is referred to as cytoresistance.  This has been shown in experimental and surgical nephrectomy models in rats showing that there is protection against superimposed renal insults or acquired cytoresistance.
In the recent CJASN issue of Jan 2011, a clinical paper of this entity was reported in the post BMT patients with renal injury.  We know that Bone marrow nephropathy exists and there was multiple causes for it.  Close to >3000 cases were reviewed and the groups with >25% drop in GFR were assessed and then the absolute loss of GFR was noted.  Interestingly, they noted that the higher the baseline eGFR, the greater the risk and severity of subsequent loss of renal function with statistical P value. So if you had lower GFR to start with, there was "cytoresistance" to further renal damage.
This is an interesting concept. This is a retrospective review, only bone marrow transplant patients, they get a lot of immunomodulatory agents, including radiation, T cell depletion sometimes, and the eGFR was only one value after a year. When immunemodulatory agents are involved, don't know how we can really evaluate this concept. Perhaps a broader renal injury ( cardiac surgery, ATN sepsis) should be evaluate to see if this concept holds.
Ref:
http://www.ncbi.nlm.nih.gov/pubmed/20966118
http://www.ncbi.nlm.nih.gov/pubmed/19193722
http://www.ncbi.nlm.nih.gov/pubmed/9396240
http://www.ncbi.nlm.nih.gov/pubmed/3302505
Image source:
http://www.seputarforex.com/