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Acute Renal Failure

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Acute Renal Failure Diagnosis Staging with RIFLE Criteria Lab evaluation Clinical features Pathophysiology – PowerPoint PPT presentation

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Title: Acute Renal Failure


1
Acute Renal Failure
  • Diagnosis
  • Staging with RIFLE Criteria
  • Lab evaluation
  • Clinical features
  • Pathophysiology

2
Acute Renal Failure
  • Definition may depend on whom you ask
  • Surgeon - - low urine output
  • Intensivist-- severe acidemia
  • Nephrologist-- rising serum creatinine
  • Frequency - depends on clinical setting
  • 1 of all admissions to hospital
  • 2-5 of all individuals during a hospitalization
  • 4-15 during cardiopulmonary bypass
  • 10-30 of all admissions to ICU

3
Definition
  • a sudden and severe decrease in the glomerular
    filtration rate (GFR) sufficient to cause
    increases in BUN and Scr (azotemia), Na/H2O
    retention (edema), and development of acidemia
    and hyperkalemia
  • review of 27 studies showed no 2 used the same
    definition chronic renal confusion

4
Whats in a name?
  • lack of a universally recognized definition of
    ARF
  • 2004 consensus conference
  • proposed the term acute kidney injury (AKI) to
    reflect the entire spectrum of ARF recognizing
    that an acute decline in kidney function is often
    secondary to an injury that causes functional or
    structural changes in the kidneys

5
Newest Definition Mehta CritCare 2007
  • An abrupt (within 48 h) reduction in kidney
    function currently defined as
  • an absolute increase in serum creatinine of
    either gt 0.3 mg/dl,
  • or a percentage increase of gt 50 or a
    reduction in UOP (documented oliguria of lt 0.5
    ml/kg per h for gt 6)

6
The differential for any lab abnormality is
  • Lab error
  • Lab error
  • Lab error
  • Iatrogenic
  • Polypharmacy
  • Real disease
  • IN THIS ORDER!

7
Acute renal failure (ARF)
  • Differential for Lab abnormality Causes
  • A rise in the BUN level can occur without renal
    injury, such as in GI or mucosal bleeding,
    steroid use, or protein loading (such as IV
    nutrition)
  • A rise in the creatinine level can result from
    medications (eg, cimetidine, trimethoprim) that
    inhibit the kidneys tubular secretion, or an
    increase in creatinine production such as seen in
    Rhabdomyolysis. (muscle breakdown)
  • True Anuria is most commonly the result of an
    obstructed foley catheter, or an error in
    recording output. The worst cause of anuria is
    cortical necrosis.

8
Acute renal failure (ARF)
  • An abrupt or rapid decline in renal function
  • Marked by a rise in BUN (azotemia) or serum
    creatinine concentration
  • Immediately after a kidney injury, BUN or
    creatinine levels may be normal
  • The only sign of a kidney injury may be decreased
    urine production
  • Use RIFLE Criteria to evaluate Risk.

9
Acute Dialysis Quality Initiative
  • RIFLE Criteria Helps risk stratify patients with
    renal failure.
  • Increased mortality seen with increases in
    creatinine of 0.3 to 0.5 mg/dl (70 increase
    for all pts, 300 increase in cardiac surgery
    pts

10
RIFLE criteria
  • Risk low uop for 6 hours, creat up 1.5 to 2 times
    baseline
  • Injury creat up 2 to 3 times baseline, low uop
    for 12 hours
  • Failure Creat up gt 3 times baseline or over 4,
    anuria
  • Loss of Function Dialysis requiring for gt 4 weeks
  • ESRD Dialysis requiring for gt 3 months

11
(RIFLE Criteria for Acute Renal Failure)Bellomo R
- Crit Care Clin -APR-2005 21(2) 223-37
12
RIFLE estimate of Mortality
  • Two studies Uchino Hoste
  • No renal failure 4.4 5.5
  • Risk 15 8.8
  • Injury 29 11.4
  • Failure 53.9 26
  • Loss of Function
  • ESRD

Crit Care Med 2006 341913-7, Hoste CCM 2006
10R73
13
RIFLE criteria
  • When markers of severity of illness are looked at
    excluding renal data, no difference in groups is
    seen.

14
Acute renal failure (ARF)
  • History and Physical examination
  • Nephrotoxic drug ingestion
  • History of trauma or unaccustomed exertion
  • Blood loss or transfusions
  • Congestive heart failure
  • Exposure to toxic substances, such as ethyl
    alcohol or ethylene glycol

15
Acute renal failure (ARF)
  • History and Physical examination
  • Exposure to mercury vapors, lead, cadmium, or
    other heavy metals, which can be encountered in
    welders and miners
  • Hypotension
  • Volume contraction
  • Vomiting/Diarrhea/Sweating/Nursing Home
  • Evidence of connective tissue disorders or
    autoimmune diseases

16
Pathophysiology
  • ARF may occur in 3 clinical patterns

BUNCr gt 201
BUNCr 10-201
BUNCr gt 201
17
Pathophysiology
  • ARF may occur in 3 clinical patterns
  • Suggested by labwork

BUNCr gt 201 Pre-Renal or Post-Renal
BUNCr 10-201 Intra-Renal
BUNCr lt 101 Extrinsic Production of
Creatinine or a dialysis patient.
18
Acute renal failure (ARF)
  • Patients can have
  • Oliguria
  • Daily urine volume of less than 400 mL/d and has
    a worse prognosis, except in prerenal failure
  • Anuria is urine output of less than 100 mL/d and,
    if abrupt in onset, is suggestive of bilateral
    obstruction or catastrophic injury to both
    kidneys
  • Rapid or slow rise in creatinine levels
  • Differences in urine solute concentrations and
    cellular content

19
Prerenal ARF
  • Prerenal ARF represents the most common form of
    kidney injury and often leads to intrinsic ARF if
    it is not promptly corrected
  • From any form of extreme volume loss
  • GI, renal (diuretics, polyuria), cutaneous (eg,
    burns), and internal or external hemorrhage can
    result in this syndrome
  • Systemic vasodilation or decreased renal
    perfusion
  • Anesthetics
  • Drug overdose
  • Heart failure
  • Shock (eg, sepsis, anaphylaxis)

20
Prerenal ARF
  • Afferent Arteriolar vasoconstriction leading to
    prerenal ARF
  • Hypercalcemic states
  • Radiocontrast agents
  • NSAIDs
  • Amphotericin
  • Calcineurin inhibitors
  • Norepinephrine
  • Other pressor agents
  • Hepatorenal syndrome
  • Functional renal failure
  • develops from diffuse
  • vasoconstriction in vessels supplying the kidney.

21
Prerenal ARF
  • Efferent arteriolar vasodilation can induce
    prerenal ARF in volume-depleted states in the
    face of
  • ACE Inhibitors
  • ARBs
  • Otherwise safely tolerated and beneficial in most
    patients with chronic kidney disease
  • Both cause afferent and efferent dilation, but
    efferent more

22
Intrinsic ARF
  • Structural injury in the kidney
  • Most common form is acute tubular necrosis (ATN)
  • Either ischemic or cytotoxic 
  • Loss of brush borders
  • Flattening of the epithelium
  • Detachment of cells
  • Formation of intratubular casts
  • Dilatation of the lumen
  • Although these changes are observed
    predominantly in proximal tubules, injury to the
    distal nephron can also be demonstrated. The
    distal nephron may also be subjected to
    obstruction by desquamated cells and cellular
    debris. 

23
Intrinsic ARF
  • Intrarenal vasoconstriction is the dominant
    mechanism for the reduced glomerular filtration
    rate (GFR) in patients with ATN.
  • Tubular injury seems to be an important
    concomitant finding
  • Urine backflow and intratubular obstruction (from
    sloughed cells and debris) reduced net
    ultrafiltration.
  • Stressed renal microvasculature is more sensitive
    to potentially vasoconstrictive drugs and
    otherwise tolerated changes in systemic blood
    pressure.  
  • Injured kidney vasculature has an impaired
    vasodilatory response and loses its
    autoregulatory behavior
  • Dialysis may re-injure the kidneys as a result

24
Intrinsic ARF
  • Tubular
  • Cytotoxic
  • Crystals
  • Tumor lysis syndrome
  • Ethylene glycol poisoning
  • Megadose vitamin C
  • Acyclovir
  • Indinavir
  • Methotrexate
  • Drugs
  • Aminoglycosides
  • Lithium
  • Amphotericin B
  • Pentamidine
  • Cisplatin
  • Ifosfamide
  • Radiocontrast agents

25
A few words about markers of renal failure
26
Relationship Between GFR and Serum Creatinine in
ARF
120
80
GFR (mL/min)
40
0
6
Serum Creatinine (mg/dL)
4
2
0
0
7
14
21
28
Days
27
Serum Creatinine
  • Creatinine is more specific at assessing renal
    function than BUN but it corresponds only loosely
    to GFR 1315.
  • For example, a serum creatinine (SCrt)of 1.5
    mg/dL (133 mmol/L), at steady-state, corresponds
    to a GFR of approximately 36 mL/min in an
    80-year-old white woman, but approximately77
    mL/min in a 20-year-old black man.

28
Creatinine and the critically ill patient
  • Creatinine is formed from nonenzymatic
    dehydration of creatine in the liver 98 of the
    creatine pool is in muscle.
  • Critically ill patients may have abnormalities in
    liver function and markedly decreased muscle
    mass.
  • Additional factors that influence creatinine
    levels include conditions of increased production
    (eg, trauma, fever, immobilization) or conditions
    of decreased production (eg, liver disease,
    decreased muscle mass, aging).

29
Creatinine and the critically ill patient
  • In addition, tubular reabsorption (back-leak)
    may occur in conditions that are associated with
    decreased urine flow rate.
  • Finally, the volume of distribution (VD) for
    creatinine (total body water) influences SCrt and
    may be increased dramatically in critically ill
    patients in the short term, its concentration in
    plasma can be altered dramatically by rapid
    plasma volume expansion. The creatinine is
    diluted by extra volume.

30
Urine Output
  • commonly measured parameter of renal function in
    the ICU and is more sensitive to changes in renal
    hemodynamics than biochemical markers of solute
    clearance however, it is far less specific
    except when severely reduced or absent
  • severe ARF can exist despite normal urine output
    (ie, nonoliguric ARF) but changes in urine output
    often occur long before biochemical changes are
    apparent
  • nonoliguric ARF has a lower mortality rate than
    oliguric ARF, thus urine output is used to
    differentiate ARF conditions
  • Classically, oliguria is defined (approximately)
    as urine output of less than 5mL/kg/d or 0.5
    mL/kg/h however, no study exists to diagnose
    when oliguria is a true early marker of
    developing renal failure

31
Modification of Diet in Renal Disease (MDRD)
Calculation for GFR
Cockcroft Equation GFR 140 - AGE X Pt WT
X 0.85 Serum Creat 70
for female
The Cockcroft-Gault formula is calculated from
the patient's age, body weight, and serum
creatinine level. The MDRD uses the serum
creatinine level and age alone to estimate GFR,
with adjustments for sex and African American
race. (gt90 normal)
32
New markers for ARF
  • Creatinine is not very sensitive
  • Cystatin C may identify ARF 1.5 days earlier than
    creatinine
  • KI 2004 601115-1122
  • KIM-1 Kidney Integrelin Molecule
  • NGAL another Integrelin, which leaks into the
    urine after tubular cell death.

33
Acute Kidney Injury Network (AKIN)
34
Clinical Features of Acute Renal Failure
  • General Management
  • Pre-renal
  • Pathophysiology of ATN
  • Other Intrinsic Causes of ARF.

35
Reason for Nephrology Consultation
25
15
60
Ref Paller Sem Neph 1998, 18(5), 524.
36
Approach to ARF
  • Pre-Renal
  • Intra-Renal
  • Post- Renal
  • Pseudo-ARF
  • There are other things which can raise the BUN
    and Creatinine!

37
Approach to ARF
  • Pre-Renal
  • Most common
  • Due to NPO, Diuretics, ACE inhibitors, NSAIDS
  • Due to renal artery disease, CHF with poor EF.
  • Usually BUN / creat ratio over 20.
  • Usually creat lt 2.5

38
Approach to ARF
  • Intra-Renal
  • Most commonly pre-renal tipping over into true
    renal injury.
  • Acute Tubular Necrosis is result (70)
  • Tubulo-Interstitial Nephritis (20)
  • Acute vasculitis/GN rare (5-10 )

39
Intrinsic Renal Failure
  • Prerenal ARF
  • Intrinsic ARF
  • acute tubular necrosis
  • acute interstitial nephritis
  • acute glomerulonephritis
  • acute vascular syndromes
  • intratubular obstruction
  • Postrenal ARF

40
Instigating Factors for ARF in a Referral Hospital
11
5
30
30
12
12
Ref Paller Sem Neph 1998, 18(5), 524.
41
Approach to ARF
  • Post- Renal
  • Most commonly due to obstruction at bladder
    outlet
  • Prostate problems
  • Neurogenic bladder
  • Stone
  • Urethral stricture (esp after CABG)

42
Initial Treatment of ARF
  • Fluid Resuscitation
  • Always place Foley Catheter
  • Stop offending agents
  • NSAIDS, Contrast, ACE/ARB, potassium
  • Watch labs
  • Consider diuretics/Natrecor

43
Acute Renal Failure
  • Definitions
  • Azotemia - the accumulation of nitrogenous wastes
  • Uremia - symptomatic renal failure
  • Oliguria - urine output lt 400-500 mL/24 hours
  • Anuria - urine output lt 100 mL/24 hours

44
Acute Renal failure Cause
  • Acute renal failure is an abrupt renal
    impairment, presenting in a fall of GFR within
    hours or days.
  • The result is a severe imbalance of fluid and
    electrolyte homeostasis accompanied by
    accumulation of nitrogenous waste.
  • Occurs in response to a variety of insults
  • Hemodynamic
  • Immunological
  • Toxic
  • obstructive

45
Acute Renal failure
Causes of acute renal failure
Differentiation between Pre-renal, renal and
post-renal causes
Prerenal Intrinsic Renal Postrenal
Hypovolemia Decreased active blood volume Decreased cardiac output Renovascular obstruction Acute tubular necrosis Interstinal nephritis Glomerular disease (acute glomerulonephritis) Small vessel diease Intrarenal vasoconstriction (in sepsis) Tubular obstruction Bilateral ureteric obstruction Unilateral ureteric obstruction Bladder outflow obstruction
46
Acute Renal failure
Complications of acute renal failure
Hyperkalemia (? ECG abnormalities) Decreased
bicarbonate (acidosis) Elevated urea Elevated
creatinine Elevated uric acid Hypocalcemia Hype
rphosphatemia
47
In many cases kidney can recover from acute renal
failure The function may have to be temporarily
replaced by dialysis for 2 days to 2
weeks disturbed fluid or electrolyte
homeostasis must be balanced primary causes
like necrosis, drug toxicity or obstruction must
be treated
48
Manifestations of ARF
  • Azotemia progressing to uremia
  • Hyperkalemia
  • Metabolic acidosis
  • Volume overload
  • Hyperphosphatemia
  • Accumulation and toxicity of medications excreted
    by the kidney

49
Pathogenesis of Prerenal Azotemia
Renal Vasoconstriction
50
Prerenal Acute Renal Failure
  • BUNCreatinine ratio
  • gt 201
  • Urine indices
  • Oliguria
  • usually lt 500 mL/24 hours but may be
    non-oliguric
  • Elevated urine concentration
  • UOsm gt 700 mmol/L
  • specific gravity gt 1.020
  • Evidence of high renal sodium avidity
  • UNa lt 20 mmol/L
  • FENa lt 0.01
  • Inactive urine sediment

51
Classification of the Etiologies of Acute Renal
Failure
Acute Renal Failure
52
Intrinsic Acute Renal Failure
  • Acute tubular necrosis (ATN)
  • Acute interstitial nephritis (AIN)
  • Acute glomerulonephritis (AGN)
  • Acute vascular syndromes
  • Intratubular obstruction

53
Acute Tubular Necrosis
54
Acute Tubular Necrosis
  • Ischemic
  • prolonged prerenal azotemia
  • hypotension
  • hypovolemic shock
  • cardiopulmonary arrest
  • cardiopulmonary bypass
  • Sepsis
  • Nephrotoxic
  • drug-induced
  • radiocontrast agents
  • aminoglycosides
  • amphotericin B
  • cisplatinum
  • acetaminophen
  • pigment nephropathy
  • hemoglobin
  • myoglobin

55
Pathophysiology of ATN Tubular Epithelial Cell
Injury and Repair
Ischemia/ Reperfusion
Necrosis
Apoptosis
Loss of polarity
Normal Epithelium
Cell death
Differentiation Reestablishment of polarity
Sloughing of viable and dead cells with luminal
obstruction
Proliferation
Adhesion molecules
Na/K-ATPase
Migration , Dedifferentiation of Viable Cells
56
Pathophysiology of ATN
57
Pathophysiology of Acute Tubular Necrosis
  • Mechanisms of decreased renal function
  • Vasoconstriction
  • Tubular obstruction by sloughed debris
  • Backleak of glomerular filtrate across denuded
    tubular basement membrane

58
Acute Tubular Necrosis Urinary Findings
59
Acute Tubular Necrosis
  • Urine indices
  • Urine volume
  • may be oliguric or non-oliguric
  • Isosthenuric urine concentration
  • UOsm ? 300 mmol/L
  • specific gravity ? 1.010
  • Evidence of renal sodium wasting
  • UNa gt 40 mmol/L
  • FENa gt 0.02
  • Urine sediment
  • tubular epithelial cells
  • granular casts
  • BUN Creatinine ratio 101
  • Evidence of toxin exposure

60
Phases of Ischemic ATN
Prerenal
Initiation
GFR
Extension
Recovery
Maintenance
Time 2 days to 2 weeks typical
61
Prognosis of Acute Tubular Necrosis
  • Mortality dependent upon comorbid conditions
  • overall mortality 50
  • Recovery of renal function seen in 90 of
    patients who survive - although not necessarily
    back to prior baseline renal function

62
Time for a break
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