Would FENa less than one apply for a situation like prerenal AKI with underlying CKD?
As you know FE Na is not absolute in the sense that there are limitations to its use and interpretation particularly in CKD patients.
Check out this article: http://cjasn.asnjournals.org/content/4/3/528.full.pdf+html
FE_Na less than one in AKI with or without underlying CKD should indicate prerenal etiology. But higher FE_Na, in this case, may not necessarily mean ATN.
In the case of CKD I would use “adequate fractional excretion of sodium”, it is value, which maintains normal serum concentration of sodium with respect to GFR and sodium intake.
Adequate FE_Na (%) = 0.0083 x (dUNa/CrCl)
/dUNa (mmol/24h) - corresponds to Na intake, CrCl (ml/s), 0.0083 is summary conversion coefficient (excretion in sec to day, mmol/day to ml/s)/
or
adequate FE_Na (%) = 0.14 x (NaCl_intake/CrCl) /NaCl_intake (g/24h)/
You compare FE_Na with adequate FE_Na to distinguish between tubular adaptation and dysfunction.
Patient with severe CKD can have adequate FE_Na > 1%, eg. 1.6 %, because the kidney maintain sodium homeostasis by decrease of sodium reabsorption (tubular adaptation).
It is preferable to use the KDIGO criteria for diagnosis of AKI which is defined by a) rise in serum creatinine of 0.3 mg / dl in 48 hrs above baseline b) rise in serum creatinine of 1.5 times above baseline in 1 week & c) Urine output < 0.5 ml / kg / hr for 6 - 12 hrs . The severity is further classified as Stage 1,2 & 3 .
It is preferable to avoid the term prerenal AKI , primarily because renal biomarkers are raised even in prerenal , suggesting that renal injury has occurred . The concept that prerenal AKI is only due to hemodynamic factors with no renal injury is questioned , because of raised renal biomarkers . Prerenal AKI might fit into Stage 1 & 2 .
The FeNa in CKD might be different in salt losing CKD due to chronic Interstitial nephritis , compared to chronic glomerulonephritis . Therefore , this parameter may be variable due to other factors .
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