Good question..

let me think about it??

I think that to use an estimation method to calculate  the residual GFR  in AKI  should be evaluated an erroneous choice.  These estimates  are based on serum creatinine value and eventually on other serum parameters and on age. But the serum creatinine value  in this clinical condition is practically always  influenced  by wasting  phenomena, due to the disease ( for instance a severe infection) or to a drug having nephrotoxicity  ,causes of  AKI , that is furthermore  always characterized  by  acidosis , a factor inducing per se muscle wasting. In consequence  of these metabolic events, the serum creatinine value is no more due simply to the loss of renal function, but  it is also and heavily  due to   the increasing muscle wasting , even if contrasted by adequate parenteral nutrition and correction of pH derangements  Consequently, if  AKI is characterized by the conservation of a urinary output , this often  having an adequate flow and even sometimes presenting a very high flow, the best choice is to measure a 24 hours creatinine clearance, a measure easy to realize and to repeat  over time, taking  into account that all these patients undergo an accurate follow- up of the urinary output, generally  based on an hourly measuring.  

the various formulas developed to estimate GFR were all derived from patients with stable renal function. These formulas will not be accurate in patients with either decreasing or increasing serum creatinine. If one needs to measure renal function in the presence of AKI then a nuclear medicine measured GFR can be done. Less accurate but easier to do would be a creatinine clearance based on a timed urine collection. This can overestimate true GFR by up to 40% due to tubular creatinine excretion. Taking the mean of urea and creatinine clearances is sometimes used as one overestimates true GFR and the other underestimates this.

Excellent answer thanks you so much!

the whole concept of measuring GFR whether, estimated, or direct is that there is  steady state with respect to the marker used. So using either Cr, BUN, or cystatin violates this principle since none of then are in steady state until they plateu. At that point the measurement or estimation of GFR is irrelevant since the decision for RRT will usually be made clinically based on symptoms, volume, and electrolyte/acid base status.   

I agree with the preceding answers. But, is important to remember that we need some marker to evaluate the renal function, mainly in critically ill patients. While we are waiting for the new biomarkers (NGAL, IL18, Kim-1, FABP) is, also important, use the new criterios to classify and diagnose AKI in different stages. I mean RIFLE or AKIN. It seems to me, if you diagnosis a patient in Risk of AKI you can immediately establish measures to protect the kidney and this way improve the prognosis of this patient.

As Dr. West notes,  you need to consider the importance of the steady-state, that is the assumption that serum levels of clearance markers reflect renal function when production = elimination, in which case GFR = U x V/P = production / blood level

Think about it this way: If I surgically remove one your kidneys, your post-op creatinine (or any other serum marker of GFR) will be ABSOLUTELY NORMAL. As production continues, it will climb asymptotically and again reflect GFR once a new steady-state is achieved (presumably close to twice the current value, though compensatory mechanisms in the healthy kidney will help). But until you achieve steady-state, it's not a marker of GFR, though rising values will tell you that bad things are happening (though not how bad, since you don't know if I actually removed both kidneys). If you want an instantaneous GFR not dependent on the steady-state assumption, then there are ways to measure it using isotope clearance, plasma elimination etc, which don't depend on the steady-state assumption. 

Dear Dr Shama, all your considerations are quite correct. and to state GFR n condition of AKI, that is to say during a continuous modification of renal function is similar to have the correct picture of the sunshine at dawn . From this, it is certainly correct that an isotope clearance can give us a GFR value to be considered probably  less or more the average GFR of that  day, but what the gain ? I think that what is pivotal is the continuous monitoring of the urine output.

Clearance is also important for drug dosing, particularly with nephrotoxic and ototoxic drugs like aminoglycosides and vancomycin.In this setting, pre-dose drug levels are probably more helpful than urine output. 

Thanks everybody!

Dear Dr Sharma, I think that we are speaking about two different problems concerning the follow up of AKI. Checking GFR is evidently very useful for drugs administration, but certainly a procedure impossible to frequently repeat if using methods of high precision. The urine output  survey  is directed to two different informations,  :  the first and most important reason to monitor the urine output is the balance with the mandatory input of fluids for nutrition and for replacing  any eventual loss of fluids for different causes, beyond  the perspiration ; if we already had to dialyze the patient using for instance an hemofiltration procedure, notwithstanding the persistent urine output, we  have to balance also the urine output whose amount we have to know;  secondly, to  check a  decreasing of the urine output particularly  if a rapid reduction: this should give us the mandatory alert to leave the conservative treatment for the substitutive therapy, if not yet started for other problems as hyperkalemia or heavy acidosis.        

Actually, I agree with you completely. I don't think the GFR estimate is helpful at all in this setting. I was replying to an earlier version of  the question, which asked about applying  the Schwartz formula for AKI, which I think it meaningless, for reasons I tried to explain. As you say, there are other issues (fluid balance, metabolic derangement, and drug clearance) that need to be addressed, but Schwartz-like equations won't help you with any of them. 

I fully agree

So do I. Knowing the exact level of "GFR" does not help manage th epatient.

I am really very much pleased that experienced researchers agree in considering GFR measuring in AKI to be a poor relevant need. A very different relevance I think could be this knowledge, when  the general   outline seems to be stabilizing, with an urine output  no more having a relevant polyuria, very often following the oliguria - anuria, or sometimes present and maintained from the hospitalization, the moment so to stop, if practiced, the substitutive therapy . From that moment  regular  controls of GFR have to start. This was , generally, my personal behavior.an my opinion about.        

Thanks you all for your comments!

CKD is a gradual & irreversible decline in GFR & therefore eGFR can be used , as the serum creatinine is stable over a period of time to measure GFR . AKI is a rapid & reversible decline in GFR & measuring eGFR may not represent the true GFR  at the time of estimation  Hence AKI is measured by serum creatinine & urine output , while CKD is measured by eGFR & proteinuria . The KDIGO guidelines on AKI & CKD are valuable to estimate the severity of these diseases.

AKI is not, per se, a decline in GFR if you think of GFR as a measure of funcional number of nephrons. It is a kontinuum of injury ( iscemic, toxic or other injury) that can result in temporary loss of funtional nephrons and sometimes also a chronic loss of nephrons. Often the cause of AKI is obvious ( hypotension/chock/sepsis/iscemic or due to toxins) and treatment and monitoring will typically focus on treatment of / removing thesese causes, and compensateing for potential fysiologi disadvantages to lack or decline of kidney funktion ( problems reg. uremia, acidosis, potassium and water metabolisme). In this setting eGFR adds no relevant information. Water excetion adds information and is of clinical value. What is needed is a biomarker that can discriminate between patients with compromized and good Tubular function prior to the development of AKI. When this biomarker is available de can develop treatment targeting this and probably lower the risk for AKI in this subsegment. GFR is of little value alone.

Dear Dr Jensen, I think that we are discussing in a confusion  of terms  of discussion -  It is well known that AKI in in many occasions is due an acute heavy damage of tubular system ,due for instance to interstitial nephritis or based on acute damage due to drugs,   but this will  cause  in any case an  high  reduction of GFR for a feed back mechanism due to the damaged tubular  cells in many collapsed by the infiltration of inflammatory cells an interstitial edema or obstructed  by cellular debris  . The rapidly increasing of serum creatinine, even  not a measure of GFR, is the same an approximated  index of GFR reduction, notwithstanding the glomeruli could be not yet  damaged. I would add that , as well known, in many cases AKI is due to a primary  GFR reduction, due in some cases of an acute prolonged hypotension as in shock condition, in this case without glomerular   damage in a first phase,  but in other cases due the direct damage of glomerular  structure, for instance as in acute post streptococcal glomerulonephritis , or acute vasculitis based on different pathogenic causes, including Lupus nephritis..          

Thanks you all for your comments and for make this question more interesting that I have thought. Grazie mille dottor Ruggieri per tutti i suoi commenti e per il suo tempo. Buon Natale.

Dear Dr Valarezo, thank you very much for your so kind appreciation of my intervention ed il mio apprezzamento per il cordiale saluto in italiano e per gli auguri che lericambio di cuore  

I'm late to the party, but noted nobody mentioned Kinetic GFR which Sseldon Chen designed specifically to get around the issue of non-steady state (Chen, S. (2013). Retooling the Creatinine Clearance Equation to Estimate Kinetic GFR when the Plasma Creatinine Is Changing Acutely. Journal of the American Society of Nephrology : JASN, 24(6), 877–888. http://doi.org/10.1681/ASN.2012070653).  

A short duration creatinine clearance is an alternative.  We tried a 4-h clearance in the ICU.

Article Four hour creatinine clearance is better than plasma creatin...

Thanks for your contribution Dr. Pickering.

Actually GFR is of only use in AKI for drugs dose adjustment, otherwise it has no clinical significance.