Acute Renal Failure * 3 categories based on the - PowerPoint PPT Presentation

Loading...

PPT – Acute Renal Failure * 3 categories based on the PowerPoint presentation | free to download - id: 3ba388-Y2NjZ



Loading


The Adobe Flash plugin is needed to view this content

Get the plugin now

View by Category
About This Presentation
Title:

Acute Renal Failure * 3 categories based on the

Description:

Acute Renal Failure * 3 categories based on the pathophysiology * Exceeds community acquired ARF by 5-10 times 35000 in79 to 650000 in2002, 13% /year * 5-20% of ... – PowerPoint PPT presentation

Number of Views:304
Avg rating:3.0/5.0
Slides: 130
Provided by: casemedic
Learn more at: http://www.casemedicine.com
Category:

less

Write a Comment
User Comments (0)
Transcript and Presenter's Notes

Title: Acute Renal Failure * 3 categories based on the


1
Acute Renal Failure
2
  • Definition and Classification
  • Epidemiology
  • Pathophysiology and Etiology
  • Prerenal ARF
  • Intrinisic ARF
  • Postrenal ARF
  • Pharmacologic Management of ARF
  • RRT in ARF

3
Definition
4
(No Transcript)
5
  • MDRD
  • eGFR 186 x Screat ¹?¹54 X Age ?²³ X 1.21
    if black X o.74 if female
  • Undersetimates GFR in healthy people (when GFR
    gt60 ml/min)
  • Cockcroft-Gault formula
  • (140-Age) X Mass (In KG) X o.85 if female/72 X
    Serum Creat
  • The non-steady-state conditions that prevail in
    ARF preclude estimation of GFR using standard
    formulae derived from patients with chronic
    kidney disease.

6
RR 2.4
RR 4.15
RR6.37
7
Shortcomings
  • The assignement of corresponding changes in serum
    creat and changes in urine output to the same
    strata is not based on evidence. The criteria
    that results in the least favorable rifle strata
    to be used.
  • The patient would progress from "risk" on day one
    to "injury" on day two and "failure" on day
    three, even though the actual GFR has been lt10
    mL/min over the entire period.
  • It is impossible to calculate the change in serum
    creatinine in patients who present with ARF but
    without a baseline measurement of the serum
    creat. The authors of the RIFLE criteria suggest
    back-calculating an estimated baseline creat
    using the four-variable MDRD equation, assuming a
    baseline GFR of 75 mL/min per 1.73 m2 .

8
Diagnostic criteria
  • Abrupt (within 48 hours) absolute increase in the
    serum creatinine concentration of 0.3 mg/dL
    (26.4 micromol/L) from baseline.
  • Or a percentage increase in the serum creatinine
    concentration of 50 percent.
  • Or oliguria of less than 0.5 mL/kg per hour for
    more than six hours.
  • The diagnostic criteria could be applied only
    after volume status had been optimized
  • Urinary tract obstruction needed to be excluded
    if oliguria was used as the sole diagnostic
    criteria

9
(No Transcript)
10

11
Epidemiology of ARF
12
  • The observed incidence, etiology, and outcomes of
    ARF are highly dependent upon the populations
    studied and the definition of ARF employed.
  • The absence of centralized registries to track
    the incidence and outcomes of patients with ARF
    has hindered our understanding of its
    epidemiology.

13
The changing epidemiology of acute renal failure
  • Nature Clinical Practice Nephrology (2006)
    2,364-377

14
(No Transcript)
15
(No Transcript)
16
(No Transcript)
17
Non -ICU
ICU
18
Key Points
  • The absolute incidence of acute renal failure
    (ARF) has increased in the past two decades,
    while the mortality rate has remained relatively
    static
  • The lack of a standard definition of ARF
    complicates the process of identifying the
    factors that underlie changes in epidemiology of
    this condition.
  • Despite the use of different definitions in
    different studies, various factors that have
    contributed to altered epidemiology of ARF in the
    past few decades have been identified
  • These factors include geographical site of
    disease onset (developed vs developing countries
    community vs hospital vs intensive care unit),
    patient age, infections (HIV, malaria,
    leptospirosis and hantavirus), concomitant
    illnesses (cardiopulmonary failure,
    hematooncological disease), and interventions
    (hematopoietic progenitor cell and solid organ
    transplantation)

19
Prerenal Acute Renal Failure
20
  • GFR is reduced as a result of hemodynamic
    disturbances that decrease glomerular perfusion.
  • The defining feature of prerenal ARF is the
    absence of cellular injury and the normalization
    of renal function with reversal of the altered
    hemodynamic factors.

21
(No Transcript)
22
Pathophsiology
  • Of Prerenal ARF

23
(No Transcript)
24
(No Transcript)
25
(No Transcript)
26
(No Transcript)
27
Diagnosis of Prerenal ARF
  • Hx
  • P/E
  • Urine sediment (usually normal, without cellular
    elements or abnormal casts, unless chronic kidney
    disease is present)
  • UNalt 15 meq/L (gt20 in ATN)
  • U/Pcreatgt 20 (lt15 in ATN)
  • FeNa lt1 (gt1 in ATN)
  • UNa/K lt1/4
  • BUN/creat gt20

28
  • BUN/CREAT of gt20 is typical, BUT is not specific
    to prerenal ARF and may also be seen
  • Obstructive uropathy
  • Gastrointestinal bleeding
  • Other states associated with increased urea
    production.

29
FE Urea
  • Patients on diuretics
  • Prerenal azotemia due to vomiting on NG
    suctioning.
  • FE Na may be low is sepsis, RCN, myoglobinuria,
    nonoliguric ATN, acute GN, urinary tract
    obstruction and renal allograft rejection

30
Significance of the fractional
excretion of urea in thedifferential diagnosis
of acute renal failure
  • 102 patients were divided into three groups
  • Prerenal azotemia (N 50)
  • Prerenal azotemia treated with diuretics (N 27)
  • ATN (N 25)
  • Kidney International, Vol. 62 (2002),
    pp. 22232229

31
  • FENa was low only in the patients with untreated
    plain prerenal azotemia while it was high in both
    the prerenal with diuretics and the ATN groups.
  • FEUN was essentially identical in the two
    pre-renal groups (27.9 2.4 vs. 24.5 2.3), and
    very different from the FEUN found in ATN (58.6
    3.6, P lt 0.0001).
  • 92 of the patients with prerenal azotemia had
    FENa lt1.
  • 48 of those patients with prerenal and diuretic
    therapy had FENa lt1
  • 89 of patients with prerenal azotemia and on
    diuretics had a FEUNlt 35.

32
FE UREA
  • Low FE urea lt35 is a more sensitive and
    specific index than FE Na in differentiating
    between ARF due to prerenal azotemia and that due
    to ATN, especially if diuretics have been
    administered.

33
ARF Associated with ACE Inhibitors and
Angiotensin Receptor Blockers
34
(No Transcript)
35
  • Acute renal failure can develop acutely, when
    ACEI or ARB therapy is initiated, or in patients
    receiving chronic therapy, especially in patients
    with underlying CHF

36
  • Predisposing factors
  • Advanced cardiac failure with low mean arterial
    pressure
  • Volume depletion due to diuretic therapy
  • The presence of renal vascular disease
  • The concomitant use agents with vasoconstrictor
    effects (NSAIDs, cyclooxygenase-2 inhibitors,
    cyclosporine, and tacrolimus)
  • CKD The risk of ARF is higher in patients with
    chronic kidney disease of any cause than in
    patients with normal renal function

37
  • Serum creatinine and electrolyte concentrations
    should be measured before and 1 wk after
    initiating or changing the dose of therapy
  • An increase in serum creatinine of gt0.5 mg/dl if
    the initial serum creatinine is lt2.0 mg/dl, or a
    rise of gt1.0 mg/dl if the baseline serum
    creatinine is gt2.0 mg/dl, has been suggested as a
    threshold for discontinuation of therapy

38
  • The development of ARF should prompt an
    evaluation for cardiac failure, hypotension,
    volume depletion, use of a concomitant
    vasoconstrictive agent, or renovascular disease.

39
Acute Renal Failure Associated with NSAIDS
40
  • Nonsteroidal anti-inflammatory drugs (NSAID)
    agents inhibit the synthesis of vasodilatory
    prostaglandins in the kidney.

41
(No Transcript)
42
  • Risk factors
  • Severe CHF
  • Advanced liver disease
  • Severe atherosclerotic vascular disease
  • CKD

43
  • Elderly patients are at increased risk due to the
    increased prevalence of cardiac dysfunction,
    occult renal vascular disease, and subclinical
    chronic kidney disease.

44
Abdominal Compartment Syndrome
45
  • Unusual cause of decreased renal perfusion
    associated with increased intra-abdominal
    pressure
  • Trauma patients who require massive volume
    resuscitation
  • Mechanical limitations of the abdominal wall
    (tight surgical closures or scarring after burn
    injuries)
  • Medical etiologies that are characterized by
    intraabdominal inflammation with fluid
    sequestration, such as bowel obstruction,
    pancreatitis, and peritonitis.

46
Clinical manifestations
  • Respiratory compromise
  • Decreased cardiac output
  • Intestinal ischemia
  • Hepatic dysfunction
  • Oliguric renal failure

47
  • The renal insufficiency results from decreased
    renal perfusion and correlates with the severity
    of the increased intraabdominal pressure.
  • Oliguria develops when the intraabdominal
    pressure exceeds 15 mmHg, with anuria developing
    at pressures gt30 mmHg.

48
Diagnosis
  • The diagnosis should be suspected in patients
    with a tensely distended abdomen and progressive
    oliguria.
  • Measurement of intraabdominal bladder pressure.
  • Abdominal compartment syndrome can be excluded
    when the bladder pressure is lt10 mmHg and is
    virtually always present if the pressure is gt25
    mmHg.

49
Treatment
  • Abdominal decompression
  • Paracentesis if massive ascites.
  • Surgical decompression is required in the
    majority of patients.
  • Renal failure usually recovers promptly after
    relief of the increased intraabdominal pressure

50
Postrenal Acute Renal Failure
51
(No Transcript)
52
Intrinsic
Extrinsic
Lower tract obstruction
53
Urine output?
  • The obstruction
  • Complete Anuria

InComplete
54
Pathophysiology
  • After the acute onset of obstruction, GFR
    declines progressively, but it does not fall to
    zero.
  • Factors that maintain GFR include continued salt
    and water reabsorption along the nephron,
    dilatation of the collecting system, and
    alterations in renal hemodynamics.
  • Intratubular pressure rises acutely, but it
    begins to decline within the first 4 to 8 h,
    returning to nearly normal by 24 h.

55
(No Transcript)
56
Complete obstruction
  • Recovery after relief of obstruction depends on
  • Severity
  • Duration
  • Less than 1 wk duration, recovery complete.
  • Little or no recovery after 12 wk.

57
Partial obstruction
  • The course after relief of partial obstruction is
    less predictable
  • Depends on
  • Severity
  • Duration
  • Presence of infection or preexisting renal
    disease.

58
  • Relief of obstruction may be accompanied by a
    post-obstructive diuresis
  • Excretion of salt and water retained during the
    obstruction.
  • Persistent salt-wasting and impaired urinary
    concentrating ability .

59
Diagnosis
  • Elderly male patients
  • Measurement of a post-voiding residual bladder
    volume, either by an bedside ultrasound bladder
    scan or by placement of an indwelling bladder
    catheter.

60
Diagnosis
  • Ultrasonography
  • Sensitivity and specificity are high
  • Non diagnostic
  • Early in the course of postrenal ARF.
  • Severe volume depletion.
  • Obstruction is due to retroperitoneal disease
    (e.g., retroperitoneal fibrosis, tumors,
    adenopathy) encasing the ureter and preventing
    dilatation

61
Diagnosis
  • Computed tomography
  • Non-contrasted CT scanning may be particularly
    useful for the identification of obstructing
    kidney stones

62
Intrinsic ARF
63
Etiology of Intrinsic ARF
64
(No Transcript)
65
(No Transcript)
66
(No Transcript)
67
  • atn

68
  • Acute tubular necrosis is the most common form of
    intrinsic ARF (85 )
  • Tubular injury
  • Nephrotoxic (35)
  • Ischemic (50)
  • Multifactorial.
  • Profound ischemic injury may result in bilateral
    cortical necrosis.

69
(No Transcript)
70
(No Transcript)
71
Nephrotoxic ATN
72
Clinical course
73
Pathogenesis of ATN
74
(No Transcript)
75
(No Transcript)
76
Recovery from Ischemic Injury
  • In contrast to the heart and brain, where
    ischemic injury results in permanent cell loss,
    the kidney is able to completely restore its
    structure and function after acute ischemic or
    toxic injury.
  • The recovery from tubular necrosis involves the
    dedifferentiation and proliferation of remaining
    viable tubular epithelial cells followed by
    reestablishment of cellular polarity, normal
    histologic appearance, and physiologic function.

77
  • Under normal circumstances, renal tubular cells
    in vivo are quiescent and do not divide in
    response to growth factors.
  • After ischemic or toxic injury, alterations in
    gene expression are observed that are similar to
    those induced in vitro by growth factors.
  • Multiple growth factors, including (IGF-1),
    (EGF), and (HGF), and their receptors are
    upregulated during the regenerative process after
    renal injury
  • Administration of exogenous IGF-1, EGF, or HGF to
    experimental animals after ischemic or toxic
    renal injury accelerates renal regeneration.
  • Concern has been raised, that growth factors may
    also have a deleterious effect, augmenting
    tubulointerstitial injury and fibrosis.

78
Short-term Outcomes
  • The outcome of ATN is highly dependent on the
    severity of comorbid conditions.
  • Uncomplicated ATN is associated with mortality
    rates of 7 to 23
  • Mortality of ATN in postoperative or critically
    ill patients with multisystem organ failure is
    high as 50 to 80.
  • Mortality rates increases with the number of
    failed organ systems

79
Long-term Outcomes
  • Long-term outcomes of patients who survive are
    good.
  • Of a population of 979 critically ill patients
    with ARF who required RRT (predominately patients
    with ATN), in-hospital mortality was 69.
  • Patients who survived to hospital discharge, 6-mo
    survival was 77, 1-yr survival was 69, and 5-yr
    survival was 50
  • 59 of surviving patients had no residual renal
    insufficiency, and only 10 required chronic
    dialysis therapy.

80
Radiocontratst Nephropathy
81
  • Contrast media induced nephropathy (CMIN) is the
    third highest cause of hospital-acquired acute
    renal failure.
  • In nearly half of these patients, CMIN occurred
    during cardiac diagnostic or interventional
    procedures such as percutaneous coronary
    intervention.

82
(No Transcript)
83
(No Transcript)
84
ARFincrease in serum creat ofgt50 above
baseline or gt1 mg/dl if baselinegt2 mg/dl
  • Normal baseline creat negilgible risk
  • Mild to moderate CKD 5-10 risk
  • Mild to moderate CKD DM 10- 40
  • Advanced renal insufficiency gt50 risk





85
Pathogenesis
  • Haemodynamic alterations and tubuloglomerular
    feedback
  • The injection of CM induces early, rapid renal
    vasodilatation followed by prolonged
    vasoconstriction, with an increase in intrarenal
    vascular resistances, a reduction of total renal
    blood flow (RBF) and a decrease in glomerular
    filtration rate (GFR).
  • Conversely, the effect on the extrarenal
    vasculature is transient vasoconstriction that
    precedes a stable decrease in vascular peripheral
    resistances.
  • The resulting renal ischaemia due to these
    haemodynamic effects is, in part, responsible for
    nephropathy

86
(No Transcript)
87
  • Endothelial dysfunction
  • Vasoactive mediators
  • Free radicals and reperfusion damage
  • Haemorheological factors
  • Tubular toxicity and immunological mechanisms

88
Treatment
  • The best treatment of contrast-induced renal
    failure is prevention.
  • The use, if clinically possible, of
    ultrasonography, magnetic resonance imaging or CT
    scanning without radiocontrast agents,
    particularly in high-risk patients.
  • The use of lower doses of contrast and avoidance
    of repetitive studies that are closely spaced
    (within 48 to 72 hours).
  • Avoidance of volume depletion or nonsteroidal
    antiinflammatory drugs, both of which can
    increase renal vasoconstriction.
  • The use of low or iso-osmolal nonionic contrast
    agents.

89
Treatment
  • The administration of Intravenous Saline.
  • Isotonic saline at a rate of 1 mL/kg per hour,
    begun at least two and preferably 6 to 12 hours
    prior to the procedure, and continuing for 6 to
    12 hours after contrast administration.
  • The administration of the antioxidant
    Acetylcysteine.
  • Dose of 600 to 1200 mg orally twice daily,
    administered the day before and the day of the
    procedure, based upon its potential for benefit
    and low toxicity and cost.

90
Treatment
  • Routine hemofiltration or hemodialysis for the
    prevention of contrast nephropathy in patients
    with stage 3 and 4 CKD is not recommended.
  • More data are needed in stage 5 CKD
    (Prophylactic use of hemodialysis in patients
    with stage 5 CKD, can be considered,provided that
    a functioning access is already available)
  • Extracorporeal blood purification therapies for
    prevention of radiocontrast-induced nephropathy
    a systematic review. Am J Kidney Dis 2006
    48361.
  • Renal protection for coronary angiography in
    advanced renal failure patients by prophylactic
    hemodialysis. A randomized controlled trial. J Am
    Coll Cardiol 2007 501015.

91
Treatment
  • There is no indication for prophylactic dialysis
    for the prevention of volume overload in
    dialysis-dependent patients.

92
Treatment
  • Therapies with Limited Evidence
  • Calcium Channel Blockers
  • Diuretics
  • Atrial Natriuretic Peptide (ANP)
  • Endothelin (ET) Antagonists
  • Prostaglandin E1
  • ACE Inhibitors

93
  • The high-osmolal contrast media (osmolality
    15001800 mOsm/kg) are first generation agents.
  • Low-osmolal contrast media still have an
    increased osmolality compared with plasma
    (600850 mOsm/kg),
  • The newest nonionic radiocontrast agents have a
    lower osmolality, 290 mOsm/kg, iso-osmolal to
    plasma

94
  • In high-risk patient populations (patientswith
    underlying renal insufficiency and diabetes),
    both low-osmolar and iso-osmolar contrasts tend
    to reduce the risk of contrast nephropathy as
    compared to the high-osmolar compounds.

95
  • The volume of contrast administered to the patien
    also appears to correlate with the incidence of
    nephrotoxicity.
  • In patients who undergo only diagnostic coronary
    procedures, the volume of dye (approximately 100
    mL) is considerably less than in patients who
    undergo interventional procedures (approximately
    250-300 mL).

96
Heme pigment-induced acute tubular necrosis
  • Myoglobinuria rhabdomyolysis.
  • Hemoglobinuria intravascular hemolysis.

97
Rhabdomyolysis
  • The release of muscle cell contents as the result
    of traumatic or nontraumatic injury of skeletal
    muscle
  • Physical findings may consist of
  • Tender, doughy muscles
  • Edema
  • weakness
  • Compartmental compression symptoms with signs and
    symptoms of neurovascular compromise may develop,
    necessitating the need for emergent fasciotomy.

98
The majority of cases of rhabdomyolysis are
nontraumatic
99
Hemolysis
  • Transfusion reactions due to ABO incompatible
    blood are probably the most frequently
    encountered hemolytic processes that can lead to
    acute renal failure.
  • Severe acute hemolytic episodes in patients with
    glucose-6-phosphate dehydrogenase deficiency.

100
Laboratory abnormalities
Ph K CK SGOT Uric
acid LDH
CA
Hypovolemia and High AG acidosis
101
  • The urine may have a low FENa despite tubular
    injury.
  • Positive dipstick test for heme pigment without
    red blood cells on microscopic exam should
    suggest myoglobinuria.
  • Heme-pigmented granular casts.
  • Plasma is normal color in myoglobinuria and red
    brown in hemoglobinuria

102
Treatment
  • IVF
  • Isotonic saline at 1 to 2 liters per hour
  • Fluids are titrated to maintain a urine output of
    200 to 300 mL/hour
  • Continue until the urine discoloration clears,
    and plasma creatine kinase decreases to less than
    5,000 to 10,000 U/L (or there is cessation of
    hemolysis), or symptomatic fluid overload
    develops.

103
Treatment
  • Alkalinization.
  • Mannitol diuresis.

104
Acute Interstitial Nephritis
  • Acute interstitial nephritis (AIN) is a syndrome
    of ARF associated with an inflammatory infiltrate
    involving the renal interstitium

105
Drug hypersensitivity
  • Penicillin
  • Cephalosporin
  • Sulfonamide
  • Fluoroquinolone
  • Rifampin
  • NSAIDs
  • Phenytoin
  • Furosemide
  • Thiazide diuretics
  • Allopurinol
  • Alpha interferon
  • Cimetidine
  • Omeprazole

106
Others
107
Methicillin induced AIN
  • Renal symptoms typically develop 2 to 3 weeks
    after the initiation of treatment
  • Hematuria
  • Pyuria with white blood cell casts
  • Proteinuria lt 1g/d (can be nephrotic with NSAIDs)
  • Renal failure in 50 of patients
  • Extrarenal manifestations
  • Fever in 80
  • Eosinophilia in 80
  • Rash in 25

108
Other kinetics
  • Within 2 to 3 days after rechallenge with a drug
    with previous sensitisation
  • De novo in response to a med previoulsy tolerated
    medication

109
  • Renal failure is the most prominent feature
  • Develops within 3 wk of initiation of drug
    therapy in 80
  • Hematuria and pyuria each are present in only 50
    of patients.
  • Extrarenal manifestations, including fever,
    maculo-papular rash, arthralgias, and
    eosinophilia are each present in fewer than 50
  • All of them together in lt5

110
Eosinophiluria
  • Diagnostic value is poor.
  • Other conditions associated with Eosinophiluria
  • Prostatitis
  • RPGN
  • Bladder Cancer
  • Renal Atheroembolic disease

111
Eosinophiluria
  • PPV for AIN of only 50 .
  • NPV of 90?
  • Thus, the presence of eosinophiluria is not
    strongly predictive of a diagnosis of AIN
    however, its absence is useful in excluding the
    diagnosis.

112
Renal biopsy
  • Failure to improve after discontinuation of
    potential offending drug
  • If the potential offending drug is critical for
    therapy
  • If immunosupressive therapy is considered

113
Treatment
  • Supportive
  • Dicontinue offending drug
  • Prednisone 1mg/kg/d for 4 weeks
  • Controversial
  • Rcommended if biopsy proven AIN and who have
    persistent renal failure 1 week after DC the
    offending medication
  • ?adjunct cyclophosphamide

114
Hepatorenal syndrome
  • ARF in HRS results from profound renal
    vasoconstriction in the setting of histologically
    normal kidneys.
  • Although many of the features of HRS resemble
    prerenal azotemia, the defining feature is a lack
    of improvement in renal function with volume
    expansion.
  • Recovery of renal function is usually observed
    after restoration of hepatic function after liver
    transplantation

115
(No Transcript)
116
(No Transcript)
117
Diagnostic criteria
  • Chronic or acute hepatic disease with advanced
    hepatic failure and portal hypertension
  • A plasma creatinine concentration above 1.5 mg/dL
    (133 µmol/L) that progresses over days to weeks.
  • The absence of any other apparent cause for the
    renal disease, including shock, ongoing bacterial
    infection, current or recent treatment with
    nephrotoxic drugs, and the absence of
    ultrasonographic evidence of obstruction or
    parenchymal renal disease.
  • Urine red cell excretion of less than 50
    cells/HPF and protein excretion less than 500
    mg/day.
  • Lack of improvement in renal function after
    volume expansion with intravenous albumin (1 g/kg
    of body weight per day up to 100 g/day) for at
    least two days and withdrawal of diuretics.
  • Urine Nalt10

118
Treatment
  • Management of underlying cause
  • Stop diuretics
  • Low salt diet and free water restriction if
    hyponatremia
  • Midodrine Octreotide Albumin
  • Terlipressin Albumin
  • RRT
  • TIPS

119
  •  The management of patients with acute renal
    failure or acute kidney injury (AKI) is
    principally supportive, with renal replacement
    therapy (RRT) indicated in patients with severe
    kidney injury.

120
Treatment of ARF
121
Prevention
  • Renal hypoperfusion is a predisposing factor to
    the development of renal failure.
  • Optimizing vascular hemodynamics to ensure
    adequate renal perfusion is a fundamental
    principle in avoiding renal failure.
  • Avoidance or discontinuation of drugs that
    increase renal vaso-constriction, such as NSAID
    and selective COX-2 inhibitors.
  • Potentially nephrotoxic medications should be
    avoided, particularly in high-risk patients,
    whenever possible.
  • Using alternative imaging techniques such as MRI
    scanning should be considered in patients at high
    risk for contrast .

122
Pharmacologic Treatment of Acute Renal Failure
  • Dopamine
  • Loop diuretics
  • ANP
  • Thyroxine
  • IGF-1

123
Indications for RRT
  • Refractory fluid overload
  • Hyperkalemia (plasma potassium concentration gt6.5
    meq/L) or rapidly rising potassium levels
  • Metabolic acidosis (pH less than 7.1)
  • Signs of uremia, such as pericarditis,
    neuropathy, or an otherwise unexplained decline
    in mental status

124
Timing of initiation of RRT
  • It is not possible to specify a specific duration
    of renal injury or level of azotemia at which RRT
    should be optimally initiated.
  • It is unproven whether initiation of earlier or
    prophylactic dialysis offers any clinical or
    survival benefit.

125
  • The optimal timing for initiation of RRT in
    patients with AKI will require an adequately
    powered prospective randomized trial.
  • Adequate design of such a trial is limited by the
    current inability to quickly prospectively
    identify patients with early AKI who will have
    protracted renal injury and eventually require
    RRT.

126
  • Initiation of dialysis prior to the development
    of symptoms and signs of renal failure due to AKI
    is recommended.

127
  • Current data do not support the superiority of
    either CRRT or IHD.

128
Learning objectives
  • Understanding the limitations of serum creat
  • Formulation of a DDx
  • Understanding of the pathophysiology of ARF
  • Prevention of ARF

129
  • Thank you
About PowerShow.com