1. Kamran fazel MD, FCCM

2. AKI- Acute Kidney Injury

3. HISTORY
DEFINITION
EPIDEMIOLOGY
ETIOLOGY
SUBTYPE
PROGNOSIS
BIOMARKER
RISK FACTOR
EVALUATION
MANAGEMENT&GUIDELINE

4. 1-HISTORY

5. Acute Kidney Injury
2nd Century AD: Galen surmises urine formed from kidneys
AD: Byzantine physicians describe oliguria as symptom of AKI, as well as detailed urine findings in AKI; also, the transition to polyuric phase as late finding in AKI is recognized
AD: likely precursors to ATN described:
Aetius: “..the reasons for the destruction of the kidney are the toxic influence of remedies and poisons, and external pressure”
Nonus: “…hematuria results from poisonous drugs and serpent venom…” (Eftychiadis AC, Am J Nephrol 1997)

6. Acute Kidney Injury
1827: English physician Richard Bright describes microscopic hematuria, oliguria, and edema in acute and chronic renal inflammatory states, gives eponymic definition for .acute/chronic GN

7. Acute Kidney Injury
WWI & WWII: Post-traumatic oliguria seen in combatants, crush syndrome evolves as an AKI dx ’s: AKI found retrospectively in ~20% of post-op open heart/aortic surgery

8. Acute Kidney Injury
WW I: observations of thirst and oliguria in combat victims led to relationship between blunt trauma and AKI (Better, OS 1997)
WWII: Spanish surgeon Joseph Trueta observes same in Spanish Civil War, WWII combatants
Induces renal cortical vasospasm experimentally (Trueta, et al., 1947)
WWII: Bywaters and Beall link myoglobin to AKI in crush syndrome during London Blitz (1940)

9. 2-Definition of AKI

10. UK Renal Association 5th Edition, 2011
Acute kidney injury (AKI) has now replaced the term acute renal failure and an universal definition and staging system has been proposed to allow earlier detection and management of AKI. The new terminology enables healthcare professionals to consider the disease as a spectrum of injury. This spectrum extends from less severe forms of injury to more advanced injury when acute kidney failure may require renal replacement therapy (RRT)

11. Clinically AKI is characterised by a rapid reduction in kidney function resulting in a failure to maintain fluid, electrolyte and acid-base homoeostasis.

12. Definition of AKI
There are more than 35 definitions of AKI (formerly acute renal failure) in literature!
Mehta R, Chertow G: Acute renal failure definitions and classification: Time for change? Journal of American Society of Nephrology 2003; 14:

13. Acute Kidney Injury 2001 : Acute Dialysis Quality Initiative (ADQI)
Risk: 1.5x inc in SCr, GFR dec 25%, UOP<0.5 ml/kg/h x 6h
Injury: 2x inc SCr, GFR dec 50%, UOP<0.5 ml/kg/h x 12h
Failure: 3x inc SCr, GFR dec 75%, UOP<0.5/kg/h x 24h
Also anuria x 12 hr
Loss: complete loss (inc need for RRT) > 4 wks
ESRD: complete loss (inc need for RRT) > 3 months
2007: Acute Kidney Injury Network (AKIN)
Modified RIFLE to include ΔSCr o.3 mg/dL from baseline, within 48hr, based on 80% mortality risk

14. Definition of AKI As per the Acute Kidney Injury Network:
 An abrupt (within 48hrs) reduction in kidney function defined as an increase in serum creatinine level of 0.3mg/dl
                                            OR
 An increase in serum creatinine ≥ 50%
Urine output is < 0.5ml/kg/hr for >6 consecutive hours 
There are no consensus criteria for defining AKI, but it is worth KNOWING the above criteria to identify which of your patients has an AKI.

15. Definition of AKI
RIFLE classification AKIN classification

16. RIFLE classification
Bellomo R, Ronco C, Kellum J, et al.: Acute renal failure-definition, outcome measures, animal models, fluid therapy and information technology needs: The Second International Consensus Conference of the Acute Dialysis Initiative (ADQI) Group. Critical Care 2004; 8:R204-R212.

17. AKIN classification
Modification of the RIFLE classification by Acute Kidney Injury Network (AKIN).
Recognizes that small changes in serum creatinine (>0.3 mg/dl) adversely impact clinical outcome.
Uses serum creatinine, urinary output and time.
Coca S, Peixoto A, Garg A, et al.: The prognostic importance of a small acute decrement in kidney function in hospitalized patients: a systematic review and meta-analysis. American Journal of Kidney Diseases 2007; 50:

18. AKIN classification AKIN stage Serum Creatinine Criteria
Urinary Output Criteria
Time 1
 Cr ≥ 0.3 mg/dL or  ≥ % from baseline
< 0.5 mL/kg/hr
> 6 hrs 2
 Cr to > % from baseline
> 12 hrs 3
Cr to > 300% from baseline or Cr ≥ 4mg/dL with an acute rise of at least 0.5 mg/dL
or anuria
X 24 hrs
X 12 hrs
*Patients needing RRT are classified stage 3 despite the stage they were before starting RRT
Mehta R, Kellum J, Shah S, et al.: Acute kidney Injury Network: Report of an Initiative to improve outcomes in
Acute Kidney Injury. Critical Care 2007; 11: R31.

19. 3-Epidemiology

20. Epidemiology AKI occurs in ≈ 7% of hospitalized patients.
36 – 67% of critically ill patients (depending on the definition).
5-6% of ICU patients with AKI require RRT.
Nash K, Hafeez A, Hou S: Hospital-acquired renal insufficiency. American Journal of Kidney Diseases 2002; 39:
Hoste E, Clermont G, Kersten A, et al.: RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients: A cohort analysis. Critical Care 2006; 10:R73.
Osterman M, Chang R: Acute Kidney Injury in the Intensive Care Unit according to RIFLE. Critical Care Medicine 2007; 35:

21. Data from the Intensive Care National Audit Research Centre (ICNARC) suggests that AKI accounts for nearly 10 percent of all .ICU bed days

22. 4-Etiology

23. Etiology Hemodynamic 30% Parenchymal 65% Acute tubular necrosis 55%
Acute glomerulonephritis 5%
Vasculopathy 3%
Acute interstitial nephritis 2%
Obstruction 5%

24. Common causes of AKI in ICU
Sepsis
Major surgery
Low cardiac output
Hypovolemia
Medications (20%)
Uchino S, Kellum J, Bellomo R, et al.: Acute renal failure in critically ill patients: A multinational, multicenter study. JAMA 2005; 294:

25. Nephrotoxins NSAIDs Aminoglycosides Amphotericin Penicillins Acyclovir
Cytotoxics
Radiocontrast dye
Dennen P, Douglas I, Anderson R,: Acute Kidney Injury in the Intensive Care Unit: An update and primer for the Intensivist. Critical Care Medicine 2010; 38:

26. 5-Subtype

27. Subtype Acute Kidney Injury
AKI
PRERENAL
INTRINSIC
POSTRENAL

28. Acute Kidney Injury PRERENAL Net result: glomerular hypoperfusion
Volume loss/Sequestration
Impaired Cardiac Output
Hypotension (and potentially hypo-oncotic states)
Net result: glomerular hypoperfusion

29. Acute Kidney Injury RENAL/INTRINSIC Vascular disorders:
small vessel
large vessel
Glomerulonephritis
Interstitial disorders:
Inflammation
intercalative processes
Tubular necrosis:
Ischemia
Toxin
Pigmenturia

30. Acute Kidney Injury POSTRENAL Intrarenal Extrarenal Crystals Proteins
Pelvis/Ureter
Bladder/Urethra

31. 6-PROGNOSIS

32. Mortality according to RIFLE
Mortality increases proportionately with increasing severity of AKI (using RIFLE).
AKI requiring RRT is an independent risk factor for in-hospital mortality.
Mortality in pts with AKI requiring RRT 50-70%.
Even small changes in serum creatinine are associated with increased mortality.
Hoste E, Clermont G, Kersten A, et al.: RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients: A cohort analysis. Critical Care 2006; 10:R73.
Chertow G, Levy E, Hammermeister K, et al.: Independent association between acute renal failure and mortality following cardiac surgery. American Journal of Medicine 1998; 104:
Uchino S, Kellum J, Bellomo R, et al.: Acute renal failure in critically ill patients: A multinational, multicenter study. JAMA 2005; 294:
Coca S, Peixoto A, Garg A, et al.: The prognostic importance of a small acute decrement in kidney function in hospitalized patients: a systematic review and meta-analysis. American Journal of Kidney Diseases 2007; 50:

33. Acute kidney injury has a poor prognosis with the mortality ranging from 10%-80% Patients who present with uncomplicated AKI, have a mortality rate of up to 10%. In contrast, patients presenting with AKI and multiorgan failure have been reported to have mortality rates of over 50%. If renal replacement therapy is required the mortality rate rises further to as high as 80%

34. Non-Oliguric vs. Oliguric vs. Anuric
Oliguric renal failure.
Functionally, urine output less than that required to maintain solute balance (can’t excrete all solute taken in).
Defined as urine output < 400ml/24hr.
Anuric renal failure.
Defined as urine output < 100ml/24hr.
Less common – suggests complete obstruction, major vascular catastrophy, or more commonly severe ATN.

35. Non-Oliguric vs. Oliguric vs. Anuric
Classifying by urine output may help establish a cause.
Oliguria – more common with obstruction, prerenal azotemia
Nonoliguric – intrarenal causes – nephrotoxic ATN, acute GN, AIN.
More importantly, assists in prognosis.
Significantly higher mortality with oliguric renal failure.
80% vs. 25% mortality in Oliguric vs. non-oliguric ARF
Nonoliguric renal failure may also suggest greater liklihood of recovery of function.

36. 7-BIOMARKER

37. BIOMARKER RESEARCH IN DEFINITIONS AND GOALS
a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention
a biomarker is “any substance, structure or process that can be measured in the body or its products and influence or predict the incidence or outcome of disease”

38. What is GFR? How is it Calculated?
The Glomerular Filtration Rate (GFR) is the volume of fluid filtered from glomerular capillaries into the Bowman’s capsule per unit time
There are a number of different formulas to estimate the GFR. The Cockcroft-Gault formula is given above. It is perhaps more important to know what are the variables in this formula than the actual formula.
By looking at this equation, one can appreciate how serum creatinine, age, weight, gender, and race can influence the GFR and thus how one interprets renal function.

39. Suspect AKI in a sick patient with a modest rise in their creatinine
Large acute drop in GFR with oligoanuria
GFR falls rapidly to near zero
- only shown by oliguria
Slow rise in Cr until
eventually a new steady state is reached
Only a small early rise in Cr: not easy to recognise as AKI

40. Limitations to Serum Creatinine as a Reflection of GFR
The serum creatinine concentration does not increase above the normal range until the GFR declines below 50 mL/min, and large declines in GFR may occur above this level without a concomitant increase in the serum .creatinine value

41. Limitations to Serum Creatinine as a Reflection of GFR
In a cachectic patient with very low muscle mass, creatinine generation may be so feeble that the serum creatinine level remains “normal” (<0.9 mg/dL) even in the presence of a GFR less than 25 mL/min.

42. Serum creatinine is a useful marker of stable renal function, but it is unreliable when GFR is .rapidly changing

43. Because it may take up to 48 hours for GFR to return to baseline, in the postoperative period the serum creatinine value may still increase for a few days while GFR is actually recovering.

44. Urine flow rate is an unreliable marker of acute renal failure and may vary from anuric (zero flow), to oliguric (urinary flow rate <15 mL/hr), to nonoliguric (15-80 mL/hr), to polyuric (>80 mL/hr).

45. Indices of Tubular Injury
β2-Microglobulin
Urinary N-Acetyl-β-d-glucosaminidase
Neutrophil gelatinase-associated lipocalin (NGAL)

47. 8-Risk Factors

48. Risk Factors for AKI Age > 75 yrs
Chronic kidney disease (CKD, eGFR < 60 mls/min/1.73m2)
Cardiac failure 
Diabetes mellitus
Hypovolemia
Nephrotoxic medication
Atherosclerotic peripheral vascular disease
Liver disease
Sepsis
Patients may present to hospital with an AKI or it may arise while in hospital. It is thus important to understand which of your patients are at risk. Knowing these risk factors can often be helpful when determining the cause and tailoring the treatment to the patient.

49. Risk Factors for Ischemic Tubular Injury
Volume depletion
Aminoglycosides
Radiocontrast
NSAIDs, Cox-2 inhibitors
Sepsis
Rhabdomyolysis
Preexisting renal disease
HTN
Diabetes mellitus
Age > 50
Cirrhosis

50. Radiocontrast-Induced Acute Renal Failure
Induces renal vasoconstriction and direct cytotoxicity via oxygen free radical formation
Risk factors:
Renal insufficiency - Diabetes
Advanced age - > 125 ml contrast
Hypotension
Usually non-oliguric ARF; irreversible ARF rare

51. Prevention of Radiocontrast Nephropathy
Intervention
Strength of Evidence
Clarity of Risk-Benefit
Grade of Recommendation
Volume expansion with normal saline
Good
Clear
A: Intervention is always indicated
and acceptable
Volume expansion with sodium bicarbonate
Fair
B: Intervention may be effective and is acceptable
Iso-osmolar contrast
Theophylline
Unclear
C: May be considered; minimal or
no relative impact
N-acetylcysteine
Hemofiltration
I: Insufficient evidence to recommend for or against
Fenoldopam
D: Not useful
Hemodialysis

52. Prevention of Contrast-Induced Nephropathy
Avoid use of intravenous contrast in high risk patients if at all possible.
Use pre-procedure volume expansion using isotonic saline (?bicarbonate).
NAC
Avoid concomitant use of nephrotoxic medications if possible.
Use low volume low- or iso-osmolar contrast
Dennen P, Douglas I, Anderson R,: Acute Kidney Injury in the Intensive Care Unit: An update and primer for the Intensivist. Critical Care Medicine 2010; 38:

53. Prevention of AKI in ICU
Recognition of underlying risk factors
Diabetes
CKD
Age
HTN
Cardiac/liver dysfunction
Maintenance of renal perfusion
Avoidance of hyperglycemia
Avoidance of nephrotoxins
Dennen P, Douglas I, Anderson R,: Acute Kidney Injury in the Intensive Care Unit: An update and primer for the Intensivist. Critical Care Medicine 2010; 38:

54. Prevention of AKI in hepatic dysfunction
Intravenous albumin significantly reduces the incidence of AKI and mortality in patients with cirrhosis and SBP.
Albumin decreases the incidence of AKI after large volume paracentesis.
Albumin and terlipressin decrease mortality in HRS.
Sort P, Navasa M, Arroyo V, et al.: Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. New England Journal of Medicine 1999; 341:
Gines P, Tito L, Arroyo V, et al.: Randomised comparative study of therapeutic paracentesis with and without intravenous albumin in cirrhosis. Gastroenterology 1988; 94:
Gluud L, Kjaer M, Christensen E: Terlipressin for hepatorenal syndrome. Cochrane Database Systematic Reviews 2006; CD

55. KDIGO Clinical Practice Guideline for Acute Kidney Injury
4.4.3: We suggest using oral NAC, together with i.v. isotonic crystalloids, in patients at increased risk of CI-AKI.
4.4.4: We suggest not using theophylline to prevent CI-AKI.
4.4.5: We recommend not using fenoldopam to prevent CI-AKI.
4.5.1: We suggest not using prophylactic intermittent hemodialysis (IHD) or hemofiltration (HF) for contrast-mediaremoval in patients at increased risk for CI-AKI.
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56. 9-EVALUATION

57. Baseline Set of Laboratories to Consider
Biochemistry
urea and electrolytes
Hematology
CBC
Urinalysis (+/- microscopy, eosinophils)
Urinary Biochemistry
electrolytes, urea, osmolality
Microbiology
urine/blood culture when/if infection suspected
Imaging
renal ultrasound
CXR, abdominal x-ray
ECG
The above list of labs can be useful in narrowing down the differential diagnosis, the severity of the injury and in the initiation of treatment. As the problem is with kidney function, you can appreciate how many of these tests are focused on analysis of the urine.
Knowing patterns of urine characteristics associated with certain causes can narrow down the differential diagnosis (slide to follow with typical patterns).
Eosinophiluria is not a very specific test for interstitial nephritis and has a very poor positive predictive value. However, the value of eosinophiluria in interstitial nephritis is in ruling out the disease, the negative predictive value for patients with AKI is > 90%.
 Microscopy can be useful when poisoning/crystalluria is suspected
A CXR can help one assess volume status. An ultrasound can very quickly indicate if obstruction is the cause of the injury
An ECG has value in that one might be able to determine if a particular electrolyte disturbance is influencing the conduction system of the heart.

58. Acute Kidney Injury LABORATORY DATA Creatinine; also BUN/Cr ratio
CBC: anemia, thrombocytopenia
HCO3ˉ: anion gap, lactic acid, ketones K
CPK/LDH/Uric acid/liver panel
Serologies:
Complement
ESR, RF, ANA, ANCA, AntiGBM
Electrophoresis
Toxicology studies

59. Evaluation of Renal Failure
Is the renal failure acute or chronic?
laboratory values do not discriminate between acute vs. chronic
oliguria supports a diagnosis of acute renal failure
Clues to chronic disease
Pre-existing illness – DM, HTN, age, vascular disease.
Uremic symptoms – fatigue, nausea, anorexia, pruritis, altered taste sensation, hiccups.
Small, echogenic kidneys by ultrasound.

60. Diagnostic Evaluation of Renal Failure
100-
80-
60-
40-
20- 0-
15%
25%
Cumulative
% Correct
Diagnosis
60%
Hx, PE, Labs
Therapeutic
Trials
Renal
Biopsy

61. Renal Biopsy-When?
Exclude pre- and post-renal failure, and clinical findings are not typical for ATN
Extra-renal manifestations that suggest a systemic disorder
Heavy proteinuria
RBC casts

62. AKI Physical Exam. Assessing volume status.
Is the patient intravascularly volume depleted?
Neck veins – JVP
Peripheral edema or lack of.
Orthostatic vitals.
Not always straightforward.
Pt. may be edematous (low albumin) or have significant right sided heart disease.

63. Creatinine in anephric state typically only rises 1mg/dl/day.
BUN/Creatinine ratio.
> 20:1 – suggest prerenal or obstruction.
Can be elevated by anything leading to increased urea production/absorption.
GI bleed
TPN
Steroids
Drugs – Tigecycline.
Creatinine in anephric state typically only rises 1mg/dl/day.
If greater – should be concerned for rhabdomyolysis

64. AKI: Diagnostic studies-urine
Urinalysis for sediment, casts
Response to volume repletion with return to baseline SCr hr c/w prerenal event
Urine Na; FENa
FENa (%) = UNa x SCr x 100
SNa x UCr
FENa < 1%: Prerenal
FENa 1-2%: Mixed
FENa > 2%: ATN
Hansel’s stain

65. Classic Lab Findings in AKI
Causes
UNa
FeNa
*FeUrea
BUN/Cr
Prerenal
<10
<1%
<35%
>20
Renal
>2%
>50%
<15
Postrenal
>40
>4%
>15
Increased levels of BUN and creatinine are the hallmarks of renal failure, however the rate of rise is dependent on the degree of renal insult as well as on protein intake with respect to BUN.
The ratio of BUN to creatinine is an important finding, because the ratio can exceed 20:1 in conditions in which enhanced reabsorption of urea is favored (eg, in volume contraction); this suggests prerenal acute kidney injury (AKI).
*Unlike the FeNa, the FeUrea is not affectect by diuretics and metabolic alkalosis. It is thus the preferred calculations when a patient is on diuretics or has a metabolic alkalosis

66. Urine Patterns in Renal Disease
Urinary Pattern
Renal Disease
Hematuria with red cell casts, heavy proteinuria, or lipiduria
Glomerular disease or vasculitis
Granular and epithelial casts with free epithelial cells
Acute Tubular Necrosis
Pyuria with white cell and granular casts and no/mild proteinuria
Tubular or interstitial disease or obstruction
Hematuria and pyuria with no or variable casts(excluding red cell casts)
Acute interstitial nephritis, glomerular disease, vasculitis, obstruction, renal infarction
Pyuria alone
Usually infections, sterile pyuria suggests TB
This slide demonstrates the utility of microscopy. Urinary sediment analysis can be a powerful non-invasive diagnostic test.

67. 10-MANAGEMENT&GUIDELINE

68. Obtain a thorough history and physical; review the chart in detail
5 Key Steps in Evaluating Acute Renal Failure
Obtain a thorough history and physical; review the chart in detail
Do everything you can to accurately assess volume status
Always order a renal ultrasound
Look at the urine
Review urinary indices

69. Management
Importantly, manangement of AKI is varied and depends on the cause.  Given no effective pharmaceutical options, management of AKI is primarily supportive.
Prerenal azotemia is usually responsive to isotonic fluid repletion
 Managament of ATN includes discontinuation of nephrotoxic agents, optimization of hemodynamics, continued monitoring of renal function (acid/base status, electrolyte abnormalities).
Postrenal causes warrant removal of the obstruction.
Intravenous hydration and volume status assessment is a reasonable first step in managing prerenal causes.
Postrenal causes can be ruled out with imaging and Foley catheter placement.

70. Management of AKI in ICU
Maintain renal perfusion
Correct metabolic derangements
Provide adequate nutrition
? Role of diuretics

71. Maintaining renal perfusion
Human kidney has a compromised ability to autoregulate in AKI.
Maintaining haemodynamic stability and avoiding volume depletion are a priority in AKI.
Kelleher S, Robinette J, Conger J: Sympathetic nervous system in the loss of autoregulation in acute renal failure. American Journal of Physiology 1984; 246: F

72. Maintaining renal perfusion
Current studies do not include patients with established AKI.
The individual BP target depends on age, co-morbidities (HTN) and the current acute illness.
A generally accepted target remains MAP ≥ 65.
Bourgoin A, Leone M, Delmas A, et al.: Increasing mean arterial pressure in patients with septic shock: Effects on oxygen variables and renal function. Critical Care Medicine 2005; 33:

73. Volume resuscitation – which fluid?
SAFE study – no statistical difference between volume resuscitation with saline or albumin in survival rates or need for RRT.
Post – hoc analysis – albumin was associated with increased mortality in traumatic brain injury subgroup and improved survival in septic shock patients.
Finfer S, Bellomo R, Boyce N, et al.: A comparison of albumin and saline for fluid resuscitation in the intensive care unit. New England Journal of Medicine 2004; 350:

74. Which inotrope/vasopressor?
There is no evidence that from a renal protection standpoint, there is a vasopressor agent of choice to improve kidney outcome.
Dennen P, Douglas I, Anderson R,: Acute Kidney Injury in the Intensive Care Unit: An update and primer for the Intensivist. Critical Care Medicine 2010; 38:

75. KDIGO Clinical Practice Guideline for Acute Kidney Injury
3.5.1: We recommend not using low-dose dopamine to prevent or treat AKI.
3.5.2: We suggest not using fenoldopam to prevent or treat AKI.
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76. Renal vasodilators?
“Renal” dose dopamine doesn’t reduce the incidence of AKI, the need for RRT or improve outcomes in AKI.
It may worsen renal perfusion in critically ill adults with AKI.
Side effects of dopamine include increased myocardial oxygen demand, increased incidence of atrial fibrillation and negative immuno-modulating effects.
Lauschke A, Teichgraber U, Frei U, et al.: “Low-dose” dopamine worsens renal perfusion in patients with acute renal failure. Kidney 2006; 69:
Argalious M, Motta P, Khandwala F, et al.: “Renal dose” dopamine is associated with the risk of new onset atrial fibrillation after cardiac surgery. Critical Care Medicine 2005; 33:

77. KDIGO Clinical Practice Guideline for Acute Kidney Injury
3.4.1: We recommend not using diuretics to preventAKI.
3.4.2: We suggest not using diuretics to treat AKI, exceptin the management of volume overload VOL 2 | SUPPLEMENT 1 | MARCH 2012.

78. Management Cont. Things to do for patients with AKI
Renally dose medications
Avoid nephrotoxins
Monitor I/Os
Serial assessment of serum creatinine
Renal Replacement Therapy (i.e dialysis) is the central component of care for patients with severe AKI  
The generally accepted indications for renal replacement therapy in the setting of AKI include:
Acidosis
Electrolyte disturbance
Ingestion/Intoxication
Volume Overload
Overt Uremia
If the insult to the kidney is severe, it is best to consult nephrology sooner rather than later as dialysis may be indicated.
AEIUO is a mnemonic often used to remember indications for dialysis.

79. Acute Kidney Injury INDICATIONS FOR RENAL REPLACEMENT THERAPY
Consensus generally includes:
Refractory volume overload
Severe metabolic acidosis; HCO3 may be variable, but declining level of factor; also falling pH to
Hyperkalemia, with levels > 6.5, or documented rapid rise refractory to medical therapy
Major uremic target organ manifestations i.e. pericarditis, progressive neuropathy, seizure
Platelet dysfunction, bleeding diasthesis
AKI in setting of dialyzable drug/toxin

80. Guideline 8.6 – AKI : Vascular access for RRT
We recommend that subclavian access should be avoided in patients at risk of progressing to CKD stage 4 or 5 due to the risks of compromising future, permanent vascular access.

81. Guideline 8.7 – AKI : Vascular access for RRT
We suggest that non-dominant arm upper limb vasculature should be preserved as a contingency for future permanent access.

82. When to call nephrology
Any known dialysis patient admitted
Any known renal transplant patient admitted
Any case of AKI where cause not clear
Worsening AKI
Emergency dialysis indications
Suspect glomerulonephritis