thank u doctor Renovar
but if u kindly explain to me why u see the relation is always tight between secretion ability of kideny and GFR althougt this by tubules (which is intact in our case and not affected) and that by glomerulous which is diseased ?!
you said(Usually these two variables (renal filtration rate and your
kidney's ability to filter and secrete substances into the urine and
therefore "clear" your blood) are tightly coupled)
and can u see the explanation which say that (as glomerulonephritis show leakeage of protein so this make the increase in urea in its case not as much like pre renal azotemia , as bun is come from protein metabolism which is decreased already in blood) u can find this explanation working in give us picture why glomerulonephritis differ than pre renal in bun/cr ratio ,although both diseases based on decrease GFR?
thank u
The "explanation" in your second question is unsound because in GN, you will lose some protein but not that much. The "nephritic" range proteinuria is defined as less than 3 grams a day (and usually much less like 1 g or 500 mg) if you think about how much protein you eat (and hence, assuming steady state, your body turn over) in a day you'll realize thats a minute fraction to be affecting metabolism.
"GFR" and "creatinine clearance" not only tightly coupled, but in terms of creatinine, they are the same thing mathematically.
In a steady state, in = out, since you get rid of creatinine in your urine, your body's total creatinine production = creatinine in urine output. Creatinine is our serogate measure because it is similar to inulin (which is freely filtered, but not absorbed or secreted by kidney) so whatever amount is filtered is cleared. (This is why I initially said it is coupled, it is under this assumption) A big difference is that creatinie is secreted by the kidney to a certain extent.
So [Plasma creatinine][Renal blood flow rate] = [urine concentration][volume],
[renal blood flow rate] = GFR = UcrV/Pcr
The concept of renal blood flow rate (usually in cc/min) also denotes how fast creatinine is getting "cleared of" in the blood.
But to evaluate this you need 24 hour urine volume and urine concentration of creatinine, and assuming completely steady state. In pre-renal physiology you dont really have a steady state because your serum creatinine doesn't reflect a steady state concentration at that particular moment. GFR is low, but it is not permenent because the actual nephron is still alive and haven't reached ATN yet, and the impaired GFR (and impaired CrCl and therefore causing a building up of creatinine) haven't cause a significant impairment in the serum Cr measurement yet.
Based on physiology, theoretically if you can have a tubule that will not die in the setting of ischemia, a low GFR in pre-renal state will eventually lead to increase your serum creatinine because of the low GFR (and hence low creatinine clearance), and after rehydration your creatinine and BUN will go back to normal. In the real world, most of the time people's GFR decrease with prolonged prerenal state is due to tubular necrosis. That's why a transient hypotension episode likely sepsis or mass blood loss, sometimes their creatinine remains high after you correct their hypotension.
