Blog entry by Meguid El Nahas

Anyone in the world

Semin Dial. 2012 Jan;25(1):9-14. doi: 10.1111/j.1525-139X.2011.01003.x. Epub 2011 Dec 6.


An Obituary for GFR as the Main Marker for Kidney Function?

This editorial review in NDT challenges the use of serum creatinine and derived eGFR to estimate kidney function in terms of glomerular filtration.
We forget all too often that serum creatinine is the result of creatinine homeostasis based on:
1. Intake, amino acids and creatine
2.Cr Metabolism  from creatine to creatinine; relying on muscle mass and related enzymes
3. Glomerular filtration
4. Secretion; renal tubular and intestinal
So any intervention that seemingly lowers serum creatinine or slow its rise may be the result of any of the above or a combination of some of them. Cionsequently, interventions pertaining to slow teh progression of CKD based on a slower rise in serum creatinine compared to control may be due to:
1. Decrease intake, metabolism and secretion as with Low protein Diet
2. Secretion as with ACE inhibitors and ARBs as they improve in CKD peritubular circulation and enhance the transport and secretion of Creatinine. This raise teh question as to whether the whole literature on ACE (RAAS) inhibition and CKD is a tubular secretion paraphenomenon of these agent... Not a single study bothered measuring or reporting GFR.
It is high time nephrologists go back to basics and remember how Creatinine is handling and stop equating changes in serum creatinine to changes in glomerular filtration alone... this is wrong and misleading!
[ Modified: Thursday, 1 January 1970, 1:00 AM ]