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4 How to Reduce AKI Mortality

4 How to Reduce AKI Mortality

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Z. Ricci and C. Ronco

identified, and we possibly will never see a single name on such treatment. However,

several approaches can be currently suggested.

Primum non nocere: the avoidance of useless and not effective treatments may

certainly help clinicians to focus on more consistent approaches [16].

In the same light, the earliest diagnosis of AKI is currently considered a fundamental aspect of plague’s management: the identification of renal dysfunction from

its milder forms [17] or, better, before the manifest sings are apparent [18] is useful

in order to promote preventive measures (e.g., administer antibiotics targeting

serum levels, reduce contrast media, avoid starches administration, etc.) and to keep

clinicians aware about kidney’s health in the eventual attempt of precluding the

worsening of AKI severity. Great expectations are currently trusted on renal biomarkers for early detection of AKI (see Chap. 2) [19] and “acute kidney stress”


Third, act upon disease pathogenesis. Sepsis, fluid overload, surgery, cardiac

dysfunction, and trauma: they all have partially different clinical pictures and

deserve tailored attention. Possibly, a surgical patient will benefit from an accurate

and aggressive goal-directed fluid replacement (see Chap. 10), whereas a septic one

should be “fluid restricted,” mostly avoiding starch infusion (see Chaps. 19 and 20).

Research is ongoing in every single setting, and scientific updating is certainly an

important part of clinicians’ efforts: we should attempt to administer the most

appropriate therapy according to the most recent evidences.

Then, do not delay RRT (see Chap. 5) and treat fluid accumulation. Importantly,

RRT dose should be closely monitored during the entire ICU stay and changed basing on clinical needs (see Chap. 6) [21].

Finally, read this book carefully: the most updated therapeutic approaches are

described in the next chapters in order to increase clinician’s awareness and good

clinical practice against AKI, the plague of critically ill patients.


1. Lameire NH, Bagga A, Cruz D et al (2013) Acute kidney injury: an increasing global concern.

Lancet 382:170–179

2. Bellomo R, Kellum JA, Ronco C (2012) Acute kidney injury. Lancet 380:756–766

3. Cruz DN, Ricci Z, Ronco C (2009) Clinical review: RIFLE and AKIN – time for reappraisal.

Crit Care 13:211

4. Hoste EA, Bagshaw SM, Bellomo R et al (2015) Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Med 41:1411–1423

5. Metnitz PGH, Krenn CG, Steltzer H et al (2002) Effect of acute renal failure requiring renal

replacement therapy on outcome in critically ill patients. Crit Care Med 30:2051–2058

6. Druml W, Lenz K, Laggner AN (2015) Our paper 20 years later: from acute renal failure to

acute kidney injury—the metamorphosis of a syndrome. Intensive Care Med


7. Vaara ST, Kaukonen K, Bendel S et al (2014) The attributable mortality of acute kidney injury:

a sequentially matched analysis. Crit Care Med 42:1–8

8. Druml W (2014) Systemic consequences of acute kidney injury. Curr Opin Crit Care



Acute Kidney Injury: The Plague of the New Millennium


9. Feltes CM, Van Eyk J, Rabb H (2008) Distant-organ changes after acute kidney injury.

Nephron Physiol 109(4):p80–p84

10. Ostermann M, Straaten HMO, Forni LG (2015) Fluid overload and acute kidney injury: cause

or consequence? Crit Care 19:443

11. Young P, Bailey M, Beasley R et al (2015) Effect of a buffered crystalloid solution vs saline on

acute kidney injury among patients in the intensive care unit. JAMA 314(16):1701–1710

12. Myburgh JA, Mythen MG (2013) Resuscitation fluids. N Engl J Med 369:1243–1251

13. Ricci Z, Romagnoli S, Ronco C (2012) Perioperative intravascular volume replacement and

kidney insufficiency. Best Pract Res Clin Anaesthesiol 26:463–474

14. RENAL replacement therapy study Investigators (2012) An observational study fluid balance

and patient outcomes in the randomized evaluation of normal vs. augmented level of replacement therapy trial. Crit Care Med 40:1753–1760

15. Heung M, Steffick DE, Zivin K et al (2016) Acute kidney injury recovery pattern and subsequent risk of CKD: an analysis of veterans health administration data. Am J Kidney Dis


16. Landoni G, Bove T, Székely A et al (2013) Reducing mortality in acute kidney injury patients:

systematic review and international web-based survey. J Cardiothorac Vasc Anesth


17. Kellum JA, Lameire N, Aspelin P et al (2012) KDIGO clinical practice guideline for acute

kidney injury. Kidney Int Suppl 2:1–138

18. Chawla LS, Goldstein SL, Kellum JA, Ronco C (2015) Renal angina: concept and development of pretest probability assessment in acute kidney injury. Crit Care 19:93

19. Kellum JA (2015) Diagnostic criteria for acute kidney injury: present and future. Crit Care

Clin 31:621–632

20. Katz N, Ronco C (2015) Acute kidney stress—a useful term based on evolution in the understanding of acute kidney injury. Crit Care 20:23

21. Villa G, Ricci Z, Ronco C (2015) Renal replacement therapy. Crit Care Clin 31:839–848


Acute Kidney Injury: Definitions,

Incidence, Diagnosis, and Outcome

Francis X. Dillon and Enrico M. Camporesi



Surgeons, anesthesiologists, intensivists, radiologists, interventional cardiologists,

and nephrologists, among others, are keenly interested in preserving renal function

in patients undergoing surgical interventions or other procedures, as well as in

intensive care unit (ICU) patients. The well-known strong association between

acute kidney injury (AKI) and its sequel, chronic kidney disease (CKD) with mortality and with severe cardiac and other organ morbidity [1–5] makes practitioners

even more mindful of kidney function in these patients. No effective new therapy

for AKI has been introduced so far; thus better avenues for progress may be novel

diagnostic tests and a clearer understanding of the factors associated with the development of AKI in both surgical and critically ill patients and how to prevent it.

Around 2000, the lack of novel pharmacologic strategies for AKI therapy seemed

to awaken a critical mass of epidemiologists and nephrologists: worldwide a reassessment of the most fundamental questions about AKI was spurred, and nephrology literature from 2004 onward was eventually unfolded.

F.X. Dillon, MD (*)

TEAMHealth Inc./Florida Gulf-to-Bay Anesthesia Associates LLC, Tampa General Hospital,

1 Tampa General Circle, Suite A327, Tampa, FL 33606, USA

Department of Surgery, University of South Florida, Tampa, FL 33606, USA

e-mail: fxdillon@gmail.com

E.M. Camporesi, MD

TEAMHealth Inc./Florida Gulf-to-Bay Anesthesia Associates LLC, Tampa General Hospital,

1 Tampa General Circle, Suite A327, Tampa, FL 33606, USA

Department of Surgery, University of South Florida, Tampa, FL 33606, USA

Department of Anesthesiology, Molecular Pharmacology and Physiology, University of South

Florida, Tampa, FL 33606, USA

e-mail: ecampore@health.usf.edu

© Springer International Publishing Switzerland 2016

G. Landoni et al. (eds.), Reducing Mortality in Acute Kidney Injury,

DOI 10.1007/978-3-319-33429-5_2



F.X. Dillon and E.M. Camporesi

The first most urgent questions were related on AKI definition, how best AKI

could be classified, what is its etiology, and how best to prevent it. If indeed prevention is the only way of reducing the burden of AKI and of its sequelae (outside of

renal replacement therapy [RRT]), then clarifying definition was the obligatory first



The Evolution of AKI Definition

The lack of uniformity in naming and defining AKI has been a serious impediment

to progress in the field’s epidemiology [6]. From the standpoint of nomenclature,

the older term “acute renal failure” (ARF) was predominant until 2005 when the

term AKI emerged. The term ARF is now obsolete as an acronym in medicine and


The significance of this change in nomenclature was felt by many in the nephrology community to be of great, even revolutionary importance because generally the

older references in the nephrology and critical care literature had often defined ARF

less precisely than the newer term AKI would be defined. For example, in a 1999

review Nissenson defined ARF in the critical care setting as “the abrupt decline in

glomerular filtration rate (GFR) resulting from ischemic or toxic injury to the kidney” [7]. Some authors defined ARF as azotemia with or without oliguria. Other

authors had recorded increases in blood urea nitrogen (BUN) to diagnose ARF and

omitted serum creatinine (sCr) measurements. In others, the timing of sCr or BUN

samples was incompletely documented. Some authors noted rehydration as a precondition for diagnosing ARF, while others did not specify the presence or absence

of rehydration as a part of this definition. In the seminal critical care paper in which

the first exact definition of AKI was introduced, Bellomo et al. [8] noted that some

30 definitions of ARF had hitherto been used at different times in the literature.

From 2002 onward, three different consensus definitions, from three different

workgroups, have emerged and become accepted, and the reader needs to be aware

of the differences between them when comparing studies. No single consensus definition has yet emerged as the standard definition, but the use of KDIGO definition [9]

(see below) is currently recommended for epidemiologic and research purposes.


The ADQI Workgroup Was Formed to Address a Lack

of Consensus Over How Best to Treat AKI with RRT:

Eventually, the Group Produced RIFLE, an Acronym

Defining AKI by Its Severity in Stages

The Acute Dialysis Quality Initiative (ADQI) [8, 10] Workgroup was founded in

2000 by representatives from the US National Institutes of Health (NIH), American

Society of Nephrology (ASN), and the Society of Critical Care Medicine (SCCM),

among others. In 2004, its founding members identified a definition and classification system for AKI. It employed the mnemonic acronym RIFLE (for “risk,”



Acute Kidney Injury: Definitions, Incidence, Diagnosis, and Outcome

“injury,” “failure,” “loss” of renal function, and “end-stage” kidney disease). The

various levels of AKI were defined according to azotemia (serum creatinine) and

urinary output (UO) criteria (Table 2.1) [8]. Note that the most severe criteria in

either the azotemia or oliguria columns should be applied when assigning a RIFLE

stratum: i.e., one should use whichever criterion that assigns the most severe class

of AKI.


The AKIN Diagnostic and Staging Criteria for AKI

Emphasize Azotemia

The members of the Acute Kidney Injury Network (AKIN) first met in 2005 and

proposed a diagnostic criterion for AKI [11] (see Table 2.2) in order to improve

some of RIFLE drawbacks. The AKIN workgroup classified AKI into three degrees

of severity called stages 1, 2, and 3 (Table 2.3). Note that, as the AQDI definition

did, these resemble the “R,” “I,” and “F” strata, which also take into account creatinine increase over baseline as well as oliguria. The AKIN guideline also stipulates

adequate fluid resuscitation prior to diagnosis of AKI.

Table 2.1 The acute dialysis quality initiative (ADQI) workgroup criteria and classification for









GFR criterion

Urine output criterion

Increased sCr × 1.5 or GFR

UO <0.5 mL/kg h ×

decrease ≥25 %


Increased sCr × 2 or GFR decrease UO <0.5 mL/kg h ×

≥50 %

12 h

Increased sCr × 3 or GFR decrease UO <0.3 mL/kg h ×

≥75 % or sCr ≥4 mg/dL (acute rise 24 h or anuria × 12 h

of ≥0.5 mg/dL)

Persistent ARF: complete loss of renal function >4 weeks

End-stage kidney disease

Sensitivity or


High sensitivity

High specificity

Modified from Bellomo et al. [8]

GFR glomerular filtration rate, UO urine output, sCr serum creatinine, and ARF acute renal



Select the highest (worst) RIFLE level using either the GFR or urine output criteria

Table 2.2 AKIN diagnostic criteria for AKI

An abrupt (within 48 h) reduction in kidney function defined as (one of the three below):

An absolute increase in serum creatinine of 0.3 mg/dl (26.4 μmol/l) or

A percentage increase in serum creatinine of 50 % (1.5-fold from baseline) or

A reduction in urine output (documented oliguria of <0.5 mL/kg h for >6 h)

Criteria to be applied in the context of the clinical presentation and following adequate fluid


Modified from Molitoris et al. [11] and Mehta et al. [72]

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