Blog entry by Meguid El Nahas

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JAMA. 2015 May 29. doi: 10.1001/jama.2015.6731. [Epub ahead of print]

An Age-Calibrated Classification of Chronic Kidney Disease.


 The most practical way to separate age-related decline in eGFR from that associated with bona-fide kidney disease might be a persistent dipstick proteinuria of > 1+. While somewhat lacking in sensitivity it has reasonable specificity.  One needs to be careful about use of urine albumin to creatinine ratios (UACR) in the elderly as the expected decline in creatinine excretion with age (and frailty) leads to overestimation of albumin excretion, and thereby mis classification when one uses a KDIGO advocated schema.

The effect of ancestry and ethnicity on the age related changes in measured GFR or eGFR are not well studied.  Fitness and frailty, independent of ancestry or ethnicity, probably have a greater effect on eGFR (based on serum creatinine values). To my knowledge, the age-related decline in eGFR is seen in all ancestries, ethnicities but the rate of decline may vary, perhaps a consequence of the baseline nephron endowment at birth. The frequently cited Baltimore Longitudinal Study of Aging (BLSOG) was not a study of GFR per se, it was a study of true creatinine clearance and an unstated # of Type 2 diabetics were included-- it is not a useful study to examine the decline in eGFR in "healthy aging".  The findings of the BLSOG are frequently misquoted.  The cross-sectional data in very healthy subjects (living donors) strongly suggests that a decline in the functioning nephron population and whole kidney GFR is a fundamental biological phenomenon intimately entangled with organismal aging (organ senescence).  To designate an isolated decline in eGFR (using any equation you choose) to values less than 50% of that present in a healthy 20 year old without any other features of kidney damage as a disease per se is a mistake, in my judgement.
Richard Glassock
[ Modified: Thursday, 1 January 1970, 1:00 AM ]