Acute Kidney Injury and Kidney Replacement Therapy in the Critically Ill Patient

assessment (TIMP-2•IGFBP7 greater than 2.0) into the classification of AKI as well as

the association with survival among patients with septic shock and similar AKI stage

classification. In patients with existing AKI, a positive biomarker was associated with

lower survival and higher mortality at 30 days. These data suggest that incorporation of

cell-cycle arrest biomarkers may augment AKI staging in patients who meet functional

criteria for AKI.

ii.

Early detection and diagnostic biomarkers (e.g., NGAL, KIM-1, L-FABP, NAG, urine cystatin

C, CCL14) have been studied as early indicators of kidney damage or predictors of persistent

AKI; each test has different performance characteristics

iii.

The cost-effectiveness of using these biomarkers to inform routine care has not been well

studied. Because of the high costs associated with the management of AKI, particularly when

dialysis is required, a systematic approach to biomarker use could prove economical. Additional

research is needed to explore this further.

Although the evidence is promising, novel biomarker use is not yet mainstream. Several factors,

including limited evidence, implementation challenges, and cost, have precluded widespread

adoption as an adjunct to SCr and UOP at this time. As use continues, additional information on the

logistics of successfully applying these tests is expected.

48 hours to increase from the onset of kidney damage. The kinetic eGFR equation is thought to provide

a quantitative solution to estimate kidney function in this difficult scenario. Using a simple algebraic

formula, including the initial creatinine content, the volume of distribution, the creatinine production

rate, and the change in SCr over time, inputs can be used to quantitatively interpret creatinine change.

Kinetic eGFR predicted AKI and the need for KRT more accurately than Modification of Diet in Renal

Disease (Clin Kidney J 2017;10:202-8). Published literature on the use of kinetic eGFR to inform

medication dosing remains in infancy.

Prerenal: AKI attributable to decreased kidney perfusion. Decreased kidney perfusion could be caused

by low effective arterial blood volume, as in hypovolemia or acute decompensated heart failure,

peripheral vasodilation, or renal vasoconstriction or renal occlusion. Some have suggested to do away

with the nomenclature “prerenal” because it could be misinterpreted to mean hypovolemia, which only

reflects a small subset of cases associated with decreased kidney perfusion.

example of this category of AKI in the hospital setting. AKI secondary to vasculitis, glomerulonephritis,

interstitial nephritis, infections, connective tissue disease, and crystalluria are in this category as well.

Postrenal: AKI associated with urinary tract obstruction. Common causes include prostatic hypertrophy,

nephrolithiasis, and tumor obstruction. If an obstruction is suspected, placing a urinary catheter may be

a sufficient temporizing measure. If higher in the urinary tract, nephrostomy tubes may be warranted to

alleviate hydronephrosis.