Acute Kidney Injury in the Critically Ill

1
Acute Kidney Injury in the Critically Ill

• Stephanie Davidson, ACNP-BC
• Vanderbilt University Medical Center
• Medical Intensive Care Unit

2
Objectives

• Brief pathophysiology review
• Name the 3 types of acute kidney injury
• Review contrast nephropathy and its treatments
• Discuss necessary diagnostic tests
• Discuss treatment modalities for the 3 types of
  acute kidney injury

3
Epidemiology

• Acute Kidney Injury (AKI) occurs in up to 20
  of ICU patients
• 25 will require RRT
• 5 of general hospital population
• AKI is usually multifactorial
• Sepsis
• Hypotension
• Drugs
• Mortality rate up to 80

4
Pathophysiology

• Blood flows from renal arteries and is delivered
  to the glomeruli
• Glomeruli form ultrafiltrate ? delivered to renal
  tubules
• Nearly free of protein and blood elements
• Tubules reabsorb and secrete solute and/or water
  from ultrafiltrate
• Final tubular fluid (urine) leaves kidneys and
  drains into renal pelvis to ureters, bladder,
  then urethra

5
Pathophysiology

• Urine volume indicated kidney perfusion
• Urine specific gravity and osmolality
  (concentrating ability) indicate tubular function

6
(No Transcript)
7
(No Transcript)
8
Definition

• Lack of consensus definition in the past
• Acute Dialysis Quality Initiative (ADQI) created
• RIFLE criteria
• Graded risks of injury
• Has been validated in variety of critically ill
  populations
• Acute Kidney Injury Network (AKIN)
• Modified RIFLE criteria
• Diagnostic and staging criteria for injury
• Acute Kidney Injury to describe all levels of
  injury

9
Bellomo et al.,Critical Care 2004, 8R204-R212 
10
RIFLE Criteria
Creatinine/GFR UOP
Risk 1.5-fold ? in Cr OR GFR ? by 25 lt 0.5 ml/kg/hr x 6 hrs
Injury 2-fold ? in Cr OR GFR ? by 50 lt 0.5 ml/kg/hr x 12 hrs
Failure 3-fold ? in Cr OR GFR ? by 75 lt 0.5 ml/kg/hr x 24 hrs OR Anuria x 12 hrs
Loss Complete loss of function gt 4 weeks (needs RRT)
ESRD Complete loss of function gt 3 months
OR
11
AKIN Criteria

• Based on abrupt (48 hr) increases
• ? Cr of 0.3 mg/dl from baseline OR
• ? in Cr of 50 OR
• Oliguria ( lt 0.5mg/kg/hr x 6 hrs or more)
• ??Exclude obstruction if UOP is basis for
  diagnosis
• ??Optimize volume status, then apply criteria

Mehta, R, et al. Crit Care, 2007 11R31
12
Risk Factors for AKI

• age gt 75 yrs
• chronic kidney disease (CKD, eGFR lt 60
  mls/min/1.73m2)
• Cardiac failure
• Atherosclerotic peripheral vascular disease
• Liver disease
• Diabetes mellitus
• Nephrotoxic medications

13
Complications of AKI
Metabolic CV Neuro Heme GI Infectious
Metabolic acidosis Fluid overload Neuropathy Anemia NV UTI
Hyper K HTN Dementia Coag anomalies GI bleeding IV catheter sepsis
Hypo Ca Arrhythmias Seizures Pneumonia
Hyperphos Pericarditis
hyper uremic
Marini, J Wheeler, A, Critical Care Medicine,
2010
14
Types of AKI

• Pre-renal
• Hypoperfusion (shock, cirrhosis, CHF)
• Volume depletion (GI bleed, dehydration)
• Intra-renal
• Acute interstitial nephritis (drug induced)
• Acute tubular necrosis
• Tumor Lysis Syndrome
• Post renal
• obstruction

15
Tests and Formulas

• FENa - fractional excretion of sodium
• Can help differentiate prerenal from ATN
• Measures percentage of filtered Na that is
  excreted
• If lt1 prerenal, if gt1 ATN
• Not accurate if pt has received diuretics
• (PCr x UNa)/ (PNa x UCr) x 100
• Na mEq/L Cr mg/dl
• Feurea fractional excretion of urea
• Better estimation if pt has had diuretics
• (serumCr x urineUrea)/ (serumUrea x urineCr) x
  100
• all units in mg/dl

16
Tests and Formulas

• Urine to plasma creatinine ratio
• Estimates tubular water resorption
• Creatinine in filtrate is equal to that of plasma
• Urine Cr increases as water, not Cr, is
  reabsorbed

17
Prerenal AKI Postrenal AKI ATN AIN
Etiology Dehydration, hypoperfusion Obstruction Ischemia, nephrotoxins Allergic rxn drug rxn
Serum BUNCr ratio gt 201 gt 201 lt 201 lt 201
Urine Na (mEq/L) lt 20 Variable gt 20 Variable
FeNa lt 1 Variable gt 1 Variable
Urine osms (mosm/kg) gt500 lt 400 250 - 300 Variable
Urinary sediment Hyaline casts Nml or red cells, white cells, or crystals Muddy brown casts, renal tubular casts White cells, white cell casts, /- eosinophils
18
Common Diagnostics

• Urinalysis
• Serum BUN/Cr
• Urine Na
• FENa or FEurea
• Urine osmolality
• Urine to plasma Cr ratio
• Urine volume

• Renal ultrasound
• Gold standard
• Will show obstructions, hydronephrosis, kidney
  size
• Consider CT abd/pelvis
• Consider 24 hr urine collection

19
Prerenal Failure

• R/T hypoperfusion and incomplete compensatory
  mechanisms
• Causes
• Hypovolemia dehydration, hemorrhage, diuretics,
  GI losses
• Edematous states cirrhosis, CHF
• Renal artery stenosis, hepatorenal syndrome,
  compartment syndrome with elevated intraabdominal
  pressures
• Results
• Kidney is normal glomeruli, tubules and
  interstitium intact
• Untreated can lead to ischemia
• Can occur is MAP lt60 for gt30minutes worse if
  patient is hypoxic

20
Compensatory Mechanisms
21
Prerenal Treatment

• Treat underlying problem
• GI losses
• CHF/cirrhosis (intravascularly dry)
• Attempt to reverse oliguria
• Fluid challenge
• Over 20-30 min repeat if needed ? monitor UOP
• Use crystalloid solution, 15-30ml/kg x1
• Avoid if pt has s/s volume overload
• Lasix challenge one dose of 1mg/kg
• Consider invasive monitoring
• CVP

22
Intrarenal Failure
Tubular Disorders
Interstitial Nephritis
Glomerulonephritis and small vessel vasculitis
23
ATN

• Sudden decline in GFR, accumulation of
  nitrogenous wastes, and dysregulation of
  electrolytes and acid-base balance
• Causes
• Prerenal if delayed treatment
• Hypotension
• Sepsis
• Tumor lysis syndrome
• Nephrotoxic substances
• Drugs aminoglycosides, amphotericin,
  cyclosporine, ACEi, NSAIDs
• Ethylene glycol/methanol

24
Prerenal AKI Postrenal AKI ATN AIN
Etiology Dehydration, hypoperfusion Obstruction Ischemia, nephrotoxins Allergic rxn drug rxn
Serum BUNCr ratio gt 201 gt 201 lt 201 lt 201
Urine Na (mEq/L) lt 20 Variable gt 20 Variable
FeNa lt 1 Variable gt 1 Variable
Urine osms (mosm/kg) gt500 lt 400 250 - 300 Variable
Urinary sediment Hyaline casts Nml or red cells, white cells, or crystals Muddy brown casts, renal tubular casts White cells, white cell casts, /- eosinophils
25
ATN Treatment

• Treat underlying cause
• Sepsis, hypotension, ischemia, drugs
• Avoid volume overload
• Nonoliguric renal failure has better outcomes
  than oliguric
• Monitor for hyperkalemia and treat
• Monitor acid-base status (BMP)

26
ATN Treatment

• Consult nephrology
• Courtesy and evaluate for possible RRT
• Monitor for AEIOU of HD
• A acidosis/alkalosis
• E electrolyte disturbances
• I Intoxications (methanol, ethylene glycol,
  salicylate)
• O overload (volume)
• U uremia
• If any of these exist or are refractory, pt may
  need dialysis

27
-Decision when to start hemodialysis is difficult
and cannot be guided by a single objective
measure -Delaying until patient is symptomatic
could increase risk of harm and/or death
Tattersall, J., et al, Neph. Dial. Transplant
(2011). 26(7)2082-2086
28
Contrast-Induced Nephropathy

• Evaluate risk vs. benefit of test
• Occurs within 72 hrs of contrast given
• Can resolve within 5 days
• Prevent with fluid
• 0.9 saline 1mL/kg x 12 hrs pre and post
  procedure
• Isotonic bicarb same dosing
• No consensus on which is better
• No evidence for NAC (mucomyst)
• Consider holding ACE-I/ARB and metformin prior to
  contrast

29
AIN

• Drug induced allergic reaction in the renal
  interstitium
• Common drugs PCN, cephalosporins, sulfonamides,
  quinolones, rifampin, thiazides, furosemide,
  NSAIDs, allopurinol, cimetidine
• Oliguria and rising serum creatinine often only
  indicators
• ¼ of patients will have eosinophilia
• ? of patients will have eosinophiluria
• Discontinue offending drug, consider steroids

Marini, J Wheeler, A, Critical Care Medicine,
2010
30
Prerenal AKI Postrenal AKI ATN AIN
Etiology Dehydration, hypoperfusion Obstruction Ischemia, nephrotoxins Allergic rxn drug rxn
Serum BUNCr ratio gt 201 gt 201 lt 201 lt 201
Urine Na (mEq/L) lt 20 Variable gt 20 Variable
FeNa lt 1 Variable gt 1 Variable
Urine osms (mosm/kg) gt500 lt 400 250 - 300 Variable
Urinary sediment Hyaline casts Nml or red cells, white cells, or crystals Muddy brown casts, renal tubular casts White cells, white cell casts, /- eosinophils
31
Post Renal Failure

• Less than 10 of AKI cases
• High suspicion if abrupt stop in flow or
  decreased UOP
• Causes
• Renal calculi/clots
• Prostatic hypertrophy
• Ureteral stone
• Rhabdomyolysis
• Check renal ultrasound- hydronephrosis, renal
  obstruction
• Consider CT of abd/pelvis
• Treat underlying cause

32
Prerenal AKI Postrenal AKI ATN AIN
Etiology Dehydration, hypoperfusion Obstruction Ischemia, nephrotoxins Allergic rxn drug rxn
Serum BUNCr ratio gt 201 gt 201 lt 201 lt 201
Urine Na (mEq/L) lt 20 Variable gt 20 Variable
FeNa lt 1 Variable gt 1 Variable
Urine osms (mosm/kg) gt500 lt 400 250 - 300 Variable
Urinary sediment Hyaline casts Nml or red cells, white cells, or crystals Muddy brown casts, renal tubular casts White cells, white cell casts, /- eosinophils
33
Outcomes and Prognosis

• AKI patients associated with
• Increased hospital and long term mortality
• Longer hospital LOS
• Increased costs
• AKI patients requiring HD
• Extremely high risk for CKD
• 10 may go on to develop ESRD
• Importance to have post-discharge follow up
  with nephrologist

Waikar, S. Bonventre, J., Harrisons Principles
of Internal Medicine, 2012.
34
References

• Bellomo, R, et al. Acute renal failure-definition,
  outcome measures, aminal models fluid therapy
  and information technology needs the Second
  International Consensus Conference of the Acute
  Dialysis Quality Initiative (ADQI) Group. Crit
  Care 2004 8R 204.
• Erdbruegger, U. and Okusa, M. (2012). Etiology
  and diagnosis of acute tubular necrosis and
  prerenal disease. Retrieved from
  www.uptodate.com.
• Esson, M. and Schrier, R. (2002). Diagnosis and
  Treatment of Acute Tubular Necrosis. Annals of
  Internal Medicine, 137 744-752
• Fink, M., Abraham, E., Vincent, J.L., and
  Kochanek, P. (2005). Textbook of Critical Care
  (5th ed.). Philadelphia, PA Elsevier Saunders.
  Levin, A, et al. Improving outcomes from acute
  kidney injury report of an initiative. Am J
  Kidney Dis. 2007 501.

35
References

• Lewington, A. and Kanagasundaram, S. (2011).
  Summary of clinical practice guidelines for
  acute kidney injury. Retrieved from
  www.renal.org/Clinical/GuidelinesSection/AcuteKid
  neyInjury.aspx
• McPhee, SJ and Papadakis M. (2008). Current
  Medical Diagnosis and Treatment. Tierney Jr,
  Lawrence (Ed.). New York, NY McGraw Hill
  Medical.
• Neesh, P., Nadim, M., An overview of drug-induced
  acute kidney injury. Critical Care Medicine,
  2008 36 No 4 (suppl).
• Palevsky, P. (2012). Definition of acute kidney
  injury (acute renal failure). Retrieved from
  www.uptodate.com.
• Post, T. and Rose, B. (2012). Diagnostic
  approach to the patient with acute or chronic
  kidney disease. Retrieved from www.uptodate.com.
  
• Ricci, A., Cruz, D., and Ronco, C. (2008). The
  RIFLE criteria and mortality in acute kidney
  injury A systematic review. Kidney
  International, 73, 538- 546

36
References

• Tattersall, J., et al. When to start dialysis
  updated guidance following publication of the
  Initiating Dialysis Early and Late (IDEAL)
  Study. Nephrol. Dial. Transplant (2011) 26(7).
  2082-2086.
• Waikar S.S., Bonventre J.V. (2012). Chapter 279.
  Acute Kidney Injury. In Longo D.L., Fauci A.S.,
  Kasper D.L., Hauser S.L., Jameson J, Loscalzo J
  (Eds), Harrison's Principles of Internal
  Medicine, 18e. Retrieved August 16, 2014
  fromhttp//accessmedicine.mhmedical.com/content.a
  spx?bookid331S ectio nid40727068.

37
(No Transcript)