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Acute kidney injury laboratory findings

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Overview

Overview

In prerenal azotemia, tubular function is preserved and sodium reabsorption increases with the associated renal vasoconstriction. Hence the FENa is usually <1% in prerenal azotemia. A high FENa in the context of prerenal azotemia is possible during diuretic treatment and glycosuria. FEurea is of value in states of reduced effective circulating volume, and in cases where diuretics have been administered. In these situations, a low FEurea (<35%) has a higher sensitivity and specificity than FENa in differentiating between prerenal azotemia and renal AKI.

Laboratory Findings

Laboratory Findings

  • Laboratory findings consistent with the diagnosis of acute kidney injury include:[1][2][3][4]
Disease specific blood laboratory findings
Blood Laboratory Finding Related Etiologies
Severe hyperphosphatemia, hypocalcemia, elevated CPK and uric acid Tumor lysis syndrome, rhabdomyolysis
Increased anion gap and osmolal gap Ethylene glycol poisoning
Low anion gap Multiple myeloma
Low complement levels and high titers of ANAs, ANCAs and cryoglobulins Vasculitides
Severe anemia in the absence of bleeding Hemolysis, Multiple myeloma
Anemia, thrombocytopenia, schistocytes on peripheral blood smear, elevated LDH, and low haptoglobin Thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome, diffuse intravascular coagulation
Peripheral eosinophilia Acute interstitial nephritis, atheroembolic disease, polyarteritis nodosa, Churg-Strauss syndrome
Elevated BNP Heart failure
Bacteremia Sepsis


In prerenal azotemia, tubular function is preserved and sodium reabsorption increases with the associated renal vasoconstriction. Hence the FENa is usually <1% in prerenal azotemia. A high FENa in the context of prerenal azotemia is possible during diuretic treatment and glycosuria.

Another important index is the fractional excretion of urea (FEurea) calculated using the same equation for the fractional excretion of sodium. FEurea is of value in states of reduced effective circulating volume, and in cases where diuretics have been administered. In these situations, a low FEurea (<35%) has a higher sensitivity and specificity than FENa in differentiating between prerenal azotemia and renal AKI.[5]

Distinguishing Prerenal azotemia and ATN
Parameter Prerenal AKI Acute Tubular Necrosis
Urinary sediment Normal/Hyaline casts Epithelial cell casts
Urine specific gravity >1.020 <1.020
Urine sodium (mmol/L) <20 >40
FENa <1% >2%
FEurea <35% >50%
Urine osmolality (mOsmol/kg H2O) >500 <350
Urine-Plasma creatinine ratio >40 <10
Plasma BUN-creatinine ratio >20 <15
References

References

  1. Combadière C, Raoul W, Guillonneau X, Sennlaub F (2013). “Comment on “Ccl2, Cx3cr1 and Ccl2/Cx3cr1 chemokine deficiencies are not sufficient to cause age-related retinal degeneration” by Luhmann et al. (Exp. Eye Res. 2013; 107: 80.doi: 10.1016)”. Exp Eye Res. 111: 134–5. doi:10.1016/j.exer.2013.02.002. PMID 23402809.
  2. Schrier RW, Wang W, Poole B, Mitra A (2004). “Acute renal failure: definitions, diagnosis, pathogenesis, and therapy”. J Clin Invest. 114 (1): 5–14. doi:10.1172/JCI22353. PMC 437979. PMID 15232604.
  3. Ostermann M, Joannidis M (September 2016). “Acute kidney injury 2016: diagnosis and diagnostic workup”. Crit Care. 20 (1): 299. doi:10.1186/s13054-016-1478-z. PMC 5037640. PMID 27670788.
  4. Matheny ME, Peterson JF, Eden SK, Hung AM, Speroff T, Abdel-Kader K, Parr SK, Ikizler TA, Siew ED (2014). “Laboratory test surveillance following acute kidney injury”. PLoS ONE. 9 (8): e103746. doi:10.1371/journal.pone.0103746. PMC 4130516. PMID 25117447.
  5. Carvounis CP, Nisar S, Guro-Razuman S (2002). “Significance of the fractional excretion of urea in the differential diagnosis of acute renal failure”. Kidney Int. 62 (6): 2223–9. doi:10.1046/j.1523-1755.2002.00683.x. PMID 12427149.

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