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Why #kidney function does not equal #GFR (and certainly not Cr), making it an elusive target in clinical practice & the latter a poor surrogate outcome, despite its robust correlation with prognosis. Caring for kidneys versus improving Cr/GFR. A thread below:
The kidneys in essence have 3 functions:
1. Glomerular function = Clearance
2. Tubular function = Homeostasis
3. Neurohumoral function
GFR mainly reflects 1. So why do we take GFR (or its estimate Cr) as a surrogate for renal function?
1. Glomerular function = Clearance
2. Tubular function = Homeostasis
3. Neurohumoral function
GFR mainly reflects 1. So why do we take GFR (or its estimate Cr) as a surrogate for renal function?
Look at GFR determinants (=N x snGFR).
In stable circumstances, GFR mainly reflects the number of functional nephrons.
Starting from 1 million per kidney at birth, one loses 5,000-10,000 per year with aging: age-related GFR decline <1 mL/min/1.73m²/y
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299260/
In stable circumstances, GFR mainly reflects the number of functional nephrons.
Starting from 1 million per kidney at birth, one loses 5,000-10,000 per year with aging: age-related GFR decline <1 mL/min/1.73m²/y
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299260/
Degree of CKD ~ 1/N: prognostic! Or otherwise, more functional nephrons equals better kidney function.
If you are a nephrologist, it thus makes sense to follow GFR over time as a surrogate for N & degree of #CKD.
But, this assumes that single-nephron GFR remains stable!
If you are a nephrologist, it thus makes sense to follow GFR over time as a surrogate for N & degree of #CKD.
But, this assumes that single-nephron GFR remains stable!
This is why KDIGO classification for CKD incorporates (micro-)albuminuria as well, as a surrogate for snGFR.
In conditions where snGFR
(albuminuria/proteinuria): GFR overestimates the number of functionally intact nephrons. CKD is thus more severe!
In conditions where snGFR
(albuminuria/proteinuria): GFR overestimates the number of functionally intact nephrons. CKD is thus more severe!
During decongestion in #AHF or in #ICU however, snGFR is highly dynamic. Thus, GFR, even if we would be able to measure it easily and perfect (not the case with Cr), poorly reflects number of functionally intact nephrons (N). One might even say, poorly reflects renal function!
Biggest problem in #ICU is often homeostasis (volume, electrolytes) rather than clearance (uremia).
Remember, homeostasis is mostly a tubular rather than glomerular function. Even with GFR 15 mL/min, one filters >20 L & 184 g salt per day! More than enough to get rid of those!
Remember, homeostasis is mostly a tubular rather than glomerular function. Even with GFR 15 mL/min, one filters >20 L & 184 g salt per day! More than enough to get rid of those!
That's why I am not so worried at ICU if Cr rises, but urine output remains preserved!
Actually, I don't care about Cr too much at all & do not try to prevent a rise. Instead, I'll try to keep good perfusion & get rid of congestion. This saves nephrons & kidney on the long run!
Actually, I don't care about Cr too much at all & do not try to prevent a rise. Instead, I'll try to keep good perfusion & get rid of congestion. This saves nephrons & kidney on the long run!
Please throw away every single paper on #AKI at #ICU if defined according to Cr only. Those serve to keep you warm in wintertime! Literature is massively flawed! #AKI correlates with prognosis, just like CO. Preventing AKI or increasing CO has never shown to be of any benefit!
