Both NAG and KIM are usefull, but KIM has a potential to indicate you earlier proximal tubule adverse effects than NAG. Nag has the advantage of being probably more widely used, (KIM is a more recent biomarker), thus the optimal experimental conditions are likely better knbown for NAG than KIM. Both NAG and KIM are stable in acid urines, which may not be the case of the other biomarkers you mention.

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What about NGAL? what type of biomarker should be considered for detect tubulo interstitial injury?

Biomarkers of acute kidney injury -

Neutrophil gelatinase-associated lipocalin (NGAL) in urine  is best

Interleukin-18 (IL-18)

Kidney injury molecule 1 (KIM-1)

Cystatin C

Liver-type fatty acid–binding protein (L-FABP)

Urinary insulin like growth factor–binding protein 7 (IGFBP7)

Tissue inhibitor of metalloproteinases–2 (TIMP-2)

http://jasn.asnjournals.org/content/22/5/810.full.pdf

http://emedicine.medscape.com/article/1925619-overview#aw2aab6b4

NAG has the advantage of being easily measurable by colorimetry and easily automated.

Consider also the low MW protein assay as alpha1microglobuline. It increases in urine soon after aggression and is also easy to measure. You can also assaying beta2microglobuline, but it is less sensitive. Urine cystatin is not a sensitive marker. 

About NGAL, this marker is used primarily in the context of AKI, no personal opinion on the utility to detect a toxic effect in the short or long term

There's some great work being done by  Fahim Mohamed in his PhD on the topic (I'm helping him out).  I've linked to an article below concerning paraquat poisoning. Interestingly creatinine rises very quickly in this group.  

http://www.sciencedirect.com/science/article/pii/S0378427411000269?np=y

Except for all "special" markers discussed, I whould in the first line determine also the standard markers of renal function, at least eGFR and (micro)albuminuria/proteinuria. 

What is best to assay depends on what question one wants to ask.

The most clinically useful measure of kidney function is glomerular filtration rate (GFR), and although many of the methods of obtaining GFR values are wonky, not all of them are. For example, the Tk-GV method (1) is very approximately 10 fold more precise than estimating GFR from plasma creatinine. The motive for measuring GFR rather than a marker of acute toxicity would be to asses what renal function remains, and whether there is any recovery of function in time. For that, one may need to measure GFR precisely.

1. Wesolowski CA, Ling L, Xirouchakis E, Burniston MT, Puetter RC, Babyn PS, et al. (2011) Validation of Tikhonov adaptively regularized gamma variate fitting with 24-h plasma clearance in cirrhotic patients with ascites. Eur J Nucl Med Mol Imaging 38(12):2247-56.

Katarina ... I agree with proteniuria.  Indeed we and others have found albuminuria is at least as good as some of the novel biomarkers at predicting a later increase in plasma creatinine.  I would, though, not use eGFR as it is not designed for non-steady state conditions.  The recently introduced kinetic eGFR (Chan et al) is worth a look, but it won't give a measure of overall "kidney damage" that question was about.

Not suggesting eGFR, would not use it, too inaccurate. Suggesting GFR, actual, like from inulin constant infusion, or easier to perform and more accurate (I think) Tk-GV. Have never heard of "kinetic" eGFR, please give reference.

Thank you to Carl Wesolowski for this information about  this new approach to the determination of GFR (unknown to me)

Isotopic techniques are unfortunately not always accessible

Hi Carl, the kinetic (e)GFR reference is: 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. doi:10.1681/ASN.2012070653

It's yet to be validated in many populations.

We've shown a 4hour creatinine clearance has value in the ICU but not a specifically nephrotoxic population. Pickering, J. W., Frampton, C. M., Walker, R. J., Shaw, G. M., & Endre, Z. H. (2012). Four hour creatinine clearance is better than plasma creatinine for monitoring renal function in critically ill patients. Critical Care (London, England), 16(3), R107. doi:10.1186/cc11391

I agree that attempting to measure GFR is more ideal, especially if only one measure is needed - I understand most GFR measurements take ~4hours. If, though, it is a matter of monitoring GFR then technicium based measures may not be able to be repeated.  There is, however, some work by Rabito and colleagues of a continuous monitoring of GFR.  Also Bruce Molitoris's group is working on dual fluorescence for monitoring GFR (still only animal experimentation at this stage I think).  A couple of references:

Rabito, C. A., Halpern, E. F., Scott, J., & Tolkoff-Rubin, N. (2010). Accurate, fast, and convenient measurement of glomerular filtration rate in potential renal transplant donors. Transplantation, 90(5), 510–517. doi:10.1097/TP.0b013e3181e9139d

Yu, W., Sandoval, R. M., & Molitoris, B. A. (2007). Rapid determination of renal filtration function using an optical ratiometric imaging approach. American Journal of Physiology-Renal Physiology, 292(6), F1873–80. doi:10.1152/ajprenal.00218.2006

Hi John, Very interesting articles. Would not use those methods, however, not precise nor accurate enough to detect small changes in GFR in time, and not likely impervious  to fluid disturbances. At least, that is my estimate based on what I read and the methods used. Would be happy to discuss it, if you wish. But, as an introduction to why, I would suggest

Fleming JS, Zivanovic MA, Blake GM, Burniston M, Cosgriff PS (2004 Aug) Guidelines for the measurement of glomerular filtration rate using plasma sampling. Nucl Med Commun 25(8):759-69.

And as for why one model is better than another I suggest reading

Wesolowski CA, Puetter RC, Ling L, Babyn PS (2010) Tikhonov adaptively regularized gamma variate fitting to assess plasma clearance of inert renal markers. J Pharmacokinet Pharmacodyn 37:435-74.

But, that is 40 pages to slog through. Basically it boils down to exponential function being not very good models of early concentration (i.e., less than 120 min), see

Wanasundara SN, Wesolowski MJ, Puetter RC, Burniston MT, Xirouchakis E, Giamalis IG, et al. (2015) The early plasma concentration of 51Cr-EDTA in patients with cirrhosis and ascites: a comparison of three models. Nucl Med Commun:On line ahead of print.

One could adapt the methods you cited to be more mathematically sound, however, they need work, at least I think so.

Nephrotoxicity induced by herbicides is a tubular disorder. The best method to detect a tubular disorder in humans is urine micoelectro-phoresis. You can find a nonglomerular, tubular type of proteinuria.

http://www.ncbi.nlm.nih.gov/pubmed/434971

http://www.ncbi.nlm.nih.gov/pubmed/23954200