1. Role of diuresis in AKI management
W. Van Biesen,
Renal Division, Ghent University Hospital.

2. Declaration of interest:
Wim Van Biesen has no declaration of interest for this topic

3. Injury Markers Functional Markers Disease Available Therapies
Myocardial Infarction
EKG, ASTCKMB Troponin
Ejection Fraction, CO/CI
ASA, Heparin, β-blockers, IIB-IIIA, thrombolytics, PTCA, statins, ACE/ARB
ALI/ARDS
Acute Bilateral Infiltrates on CXR
Oxygenation
(P/F Ratio)
Low Tidal Volume Ventilation
Sepsis
Tissue Gram Stain, WBC count
SIRS Criteria
Activated Protein C, EGDT, steroids
Nephrology
.….
Serum Creatinine, Urine Output,
“renal bed rest”

4. Novel Biomarkers
Bonventre Nature Biot 28(5), 2010

5. Biomarker: Definition (FDA)
A characteristic, usually a laboratory test, that is objectively measured and evaluated as an indicator of normal biologic processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention.
Characteristics of an optimal biomarker:
Sensitive to derangement(s)
Specific to the disease(s)
Predictive of clinical outcomes
Robust, i.e. reproducible, inexpensive, simple, and accessible
The key points from this session include:
A definition of malnutrition as a syndrome that describes inappropriate intake, sometimes in conjunction with disease, that affects body composition, reduces functional capacity, and negatively impacts clinical outcome
Despite the negative effects of malnutrition on patients, hospital malnutrition is still prevalent and negatively affects patient outcomes
Physician training increases awareness and enhances clinical nutrition practice
The Total Nutrition Therapy (TNT) program was developed in response to studies such as those just described. The goal of this program is to increase physician awareness of the continuing problem of malnutrition and the benefits provided by appropriate nutrition therapy, and to provide information and tools to assist physicians in the daily practice of clinical nutrition.

6. Early Diagnosis of AKI: Hit or Miss?
KIM, CysC (0.83)
IL-18 (0.75)
Fold Increase in Concentration
A1M, AAG (0.87)
NGAL (0.95)
Marker (AUC)
Time post-CPB
Mishra et al, Lancet 2005
Portilla et al, Kidney Int 2008
Han et al, Kidney Int 2008
Parikh et al, Kidney Int 2006

8. Impact of using or not using the urinary output criterion in the definition of AKI
Vanmassenhove et al, ERA-EDTA Paris, 2012

9. Diuresis as AKI criterium
Macedo et al, KI, 2012

10. Impact of diuresis on mortality in AKI
Ralib et al, Critical Care, 2013

11. Oliguria as predictor of AKI in SEPSIS
Leedahl et al, cJASN, 2014

12. Oliguria as predictor of AKI in SEPSIS
Leedahl et al, cJASN, 2014

13. Leedahl et al, cJASN, 2014

14. Conceptual model for development and clinical course of AKI
of acute kidney injury. The concept of AKI includes both volume-
responsive and volume-unresponsive conditions. These
conditions are not mutually exclusive, and a given patient may
progress from one to the other. Time runs along the x-axis, and
the figure depicts a closing “therapeutic window” as injury
evolves and kidney function worsens. Biomarkers of injury and
function will begin to manifest as the condition worsens, but
traditional markers of function (e.g. urea nitrogen and creatinine)
will lag behind hypothetical “sensitive” markers of kidney
injury. Mortality increases as kidney function declines.
Himmelfarb et al, Clin J Am Soc Nephrol march,2008

16. Delayed vs timely nephrology consultation in AKI
Torres Costa e Silva, PloS, 2013

17. Diuresis as AKI criterium
Potential problems:
how to measure?
expressed as ml/min/kg:
what in overweight patients?
what in cachectic patients?
what in edematous patients?

21. Diuresis can only be measured in patients at ICU,
as they need an indwelling bladder catheter

22. Definition of AKI: KDIGO vision

23. ERBP Position statement on diagnosis of AKI
Fliser et al, NDT, 2012

25. Transient vs intrinsic AKI and tubular injury
Based on the creatinine criterion
Based on the urinary output criterion
Vanmassenhove et al, Istanbul, 2013

26. Transient vs intrinsic AKI and tubular injury
Based on the creatinine criterion
Based on the urinary output criterion
Vanmassenhove et al, Istanbul, 2013

27. AKI in the SAPS3 database
Joannidis M., Intensive Care Mecicine, 2009

28. Early intervention
Colpaert et al, CCM, 2012

29. 92.8% of alerts induced by low urinary output criterion
Early intervention
92.8% of alerts induced by low urinary output criterion
Colpaert et al, CCM, 2012

30. Fluid responsiveness

31. Furosemide stress test
Well rehydrated patients (clinical assumption)
AKIN stage I or II
IV Furosemide 1mg/kg
Hypothesis: Furosemide activity signals normal tubular function

32. Furosemide stress test
Well rehydrated patients (clinical assumption)
AKIN stage I or II
IV Furosemide 1mg/kg
Hypothesis: Furosemide activity signals normal tubular function

33. Furosemide stress test
Well rehydrated patients (clinical assumption)
AKIN stage I or II
IV Furosemide 1mg/kg
Hypothesis: Furosemide activity signals normal tubular function

34. Kaplan–Meier survival curves grouped by diuretic efficiency (DE) and diuretic dose in the Penn (A) and ESCAPE cohorts (B).
Kaplan–Meier survival curves grouped by diuretic efficiency (DE) and diuretic dose in the Penn (A) and ESCAPE cohorts (B). Loop diuretic dose and DE were dichotomized into high and low by the median value in each cohort. Low loop dose was also defined as a loop diuretic dose above or below the median value, which was 280 (interquartile range, 120–600) mg in the Penn cohort and 240 (interquartile range, 120–400) mg in 24 h in the ESCAPE cohort.
Jeffrey M. Testani et al. Circ Heart Fail. 2014;7:
Copyright © American Heart Association, Inc. All rights reserved.

36. Impact on outcome of increased awareness of AKI
Selby et al, Current Opin Nephrol Hypertension 2013

37. Conclusion
Diuresis and urinary output is an important biomarker for the prevention, diagnosis and management of AKI
Its implementation is a matter of WILLING rather than of possibility