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Acute Kidney Injury


Acute Kidney Injury AKI - an abrupt increase in serum creatinine of at least 0.3 mg /dl or 1.5 over baseline over 48 hours (based on AKI Network Consensus 2007) – PowerPoint PPT presentation

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Title: Acute Kidney Injury

Acute Kidney Injury
  • AKI - an abrupt increase in serum creatinine of
    at least 0.3 mg /dl or 1.5 over baseline over 48
    hours (based on AKI Network Consensus 2007)
  • stage 1 increase in creatinine 1.5-2 fold
  • stage 2 increase in creatinine gt2-3 fold
  • stage 3 increase in creatinine gt3 fold (or need
    for dialysis or a peak Cr gt4 mg/dl with at least
    a 0.5 mg/dl increase)
  • Increased morbidity and mortality with increasing


AKI - incidence and risks
  • Hospitalized patients 5 to 7.5
  • ICU 10 to 30
  • AKI associated with increased cost or length
    of hospital stay, risk of end-stage renal disease
  • AKI -increased risk of death with AKI and sepsis,
    trauma, cardiopulmonary bypass, burn injuries
    (despite correction for comorbidities and
    severity of illness) Crit Care Med 2010261
  • Hyperglycemia in hospital increases risk AKI

Creatinine interpretation
  • Increased BUN/creatinine ratio pre-renal, blood
    in gut, obstruction, steroids, tetracycline
  • Decreased BUN/creatinine ratio rhabdomyolysis,
    reduced protein intake
  • False elevations in creatinine ketones,
    trimethoprim, cimetidine
  • Rate of rise of creatinine when daily
    creatinine elevation starts to go down a clue
    that renal function starting to improve
  • eGFR can not be calculated if Cr not stable
  • Amputation - lower baseline creatinine
  • Indicator AKI relatively late need renal

Non -ICU
Diagnosis of prerenal azotemia
  • 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
  • Often remains a retrospective Dx made only after
    response to a fluid challenge

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Replacement fluids
  • Ringers lactate - since contains K do not give
    to oliguric patient
  • ½ NS avoid in hyponatremic patient
  • 0.9 NS resuscitation fluid of choice, but can
    worsen hyponatremia if SIADH
  • Hydroxyethyl starch increased incidence of AKI
    (osmotic nephrosis)
  • ½ NS 1 amp NaHCO3 if very acidotic

Colloid vs crystalloid
  • 7000 patients in medical and surgical ICUs in
    Saline vs Albumin Fluid Evaluation (SAFE) -
    randomized, double-blind trial comparing NS vs 4
    human albumin. Results - no difference in 28 day
    survival, days spent in the ICU, days on
    mechanical ventilator.
  • Hypoalbuminemic patients - small randomized trial
    in which IV albumin improved sequential organ
    failure assessment (SOFA) compared with NS.
  • Spontaneous bacterial peritonitis - randomized
    trial comparing antibiotics alone vs antibiotics
    plus IV albumin (1.5 gm/kg immediately on
    diagnosis then 1 gm kg on day 3). Results -
    decreased renal failure and improved survival.
    Current standard of care in SBP.

Early Goal Directed Therapy
  • Definition - in patients with septic shock early
    intervention within the first 6 hours in the ED
  • Goals - in first 6 hours MAPgt 65 mmHg, CVP 8-12,
    improvement in blood lactate, central venous 02
    satgt70, UOgt0.5 ml/kg/hour
  • ED patients transferred to ICU with SIRS mean
    creatinine 2.6 mg/dl sBPlt90 or lactategt4,
    central venous 02 sat lt50. Compared with control
    group the EGDT group received more fluids,
    transfusions, and dobutamine, but physiologic
    goals reached quicker hospital mortality
    reduced - 30 vs 45
  • Above protocol is the basis for Surviving Sepsis
    Guidelines Clin J Am Soc Neph 2010733

Fluid overload in AKI
  • 618 critically ill patients - Clin J Am Soc Neph
  • Prospective, multicenter, observational study
  • Examined the effect of fluid overload (gt10
    increase in body weight).
  • Those with fluid overload had more respiratory
    failure, mechanical ventilation, and sepsis.
  • Those with AKI and fluid overload had increased
    mortality at 30 and 60 days and at hospital
    discharge (corrected for severity of illness).

AKI fluid overload
  • 7000 patients with acute lung injury
  • Prospective randomized trial comparing
    conservative and liberal fluid management for 7
  • The conservative group received more furosemide
    and fewer fluid boluses, gained 7 kg less. No
    difference in mortality but conservative group
    less days on vent, less time in the ICU, and
    trend for lower need for dialysis.
  • the CVP in the aggressive group was 12 at the
    start of the study and remained 12 despite the 7
    kg weight gain whereas it went from 12 to 8 in
    the conservative group Clin J Am Soc Neph

AKI - use of dopamine or diuretics
  • Low dose dopamine does not reduce the incidence
    of AKI, the need for RRT or improve the outcome
    in AKI. Is associated with increased myocardial
    02 demand and increased incidence of atrial fib
  • Diuretics - can sometimes convert oliguric to
    non oliguric but no data that shorten duration of
    AKI, reduce need for RRT, or improve overall
    outcomes. But can help control volume overload.

Abdominal compartment syndrome
  • World Congress on ACS defined a normal
    intra-abdominal pressure (IAP) to be between 5-7
    mmHg in critically ill patients, elevated to be
    gt8 mmHg, and intra-abdominal hypertension to be
  • Abdominal compartment syndrome (ACS)
    intra-abdominal pressuregt20 mmHg associated with
    organ failure in one or more organs
  • The renal insufficiency results from decreased
    renal perfusion and correlates with the severity
    of the increased intra-abdominal pressure and a
    decreased abdominal perfusion pressure (Mean
    arterial pressure intra-abdominal pressure)

Measurement of intra-abdominal pressure
  • Clamp drainage tube of Foley catheter
  • Instill 50 mL of sterile water into the bladder
    via the aspiration port
  • Measure pressure using a transducer attached to
    an 18 gauge needle inserted into the aspiration
    port (transducer should be zeroed at the level of
    the pubic symphysis)

Abdominal compartment syndrome systemic effects
  • Cardiac - decreased cardiac output, increased
  • Pulmonary increased intra-thoracic and airway
    pressures, decreased pa02, increased paCO2
  • GI decreased splanchnic perfusion
  • Renal - reduced renal perfusion, GFR and urine

ACS - causes and treatment
  • Settings - trauma patient who requires massive
    volume resuscitation mechanical limitations of
    the abdominal wall (tight surgical closures or
    scarring after burn injuries) intra-abdominal
    inflammation with fluid sequestration (eg. bowel
    obstruction, pancreatitis, and peritonitis).
  • Treatment - Abdominal decompression Paracentesis
    if massive ascites, surgical decompression may be

Cardio-renal syndrome
  • As opposed to hepato-renal syndrome is not renal
    dysfunction due to cardiac disease but includes
    vice versa and also divides the responses into
    acute and chronic.
  • While creatinine is a better indicator of renal
    function the BUN in CHF correlates better with
  • The BUN also correlates much better with Na
    high BUN and low Na suggest pre renal state and
    stimulation of the renin-angiotensin system and
  • Many patients admitted with CHF are not very
    edematous. Average weight loss in CHF
    hospitalization is only several kgs with many
    patients not losing any weight. So the notion of
    all CHF admissions being due to fluid overload is
    simplistic. In many patients it seems to be more
    related to preceding increase in systemic BP or
    pulmonary hypertension

Acute decompensated HF (ADHF) and intra-abdominal
  • 40 consecutive patients admitted to CHF unit for
  • Age 59 /- 6
  • LVEF 19 /- 8
  • Baseline Cr 2 /- 0.8
  • Baseline IAP 8 /- 2 with 24 having high IAP
  • Elevated IAP associated with worsening renal
    function during that admission p0.0009
  • Intensive medical Rx improved hemodynamics and
    renal function in those with high IAP
  • Strong correlation between reduction in IAP and
    improved renal function seen in those with high
    IAP but neither changes in IAP or renal function
    correlated with hemodynamic changes
    JACC 2008300

ADHF response to reduction IAP
  • 9 consecutive pts that were volume overloaded
    with ADHF and elevated IAP refractory to
    intensive medical therapy
  • All had progressive elevation in serum creatinine
    and worsening in IAP with IV loop diuretics
  • Within 12 hours after paracentesis 5.3 L or UF 1.
    8 L there was a significant reduction in IAP from
    13 to 7 and improvement in Cr from 3.4 to 2.4 but
    no change in hemodynamics
    J Card Failure 2008508

  • Evaluation Study of CHF And Pulmonary artery
    catheterization Effectiveness
  • In 433 patients compared hemodynamic monitoring
    with PAC vs CVP in ADHF
  • Renal dysfunction (eGFR lt60) either baseline or
    worsening renal function (Cr increment gt0.3) both
    shown to be associated with adverse outcomes
    during treatment of CHF.
  • No correlation between baseline hemodynamics or
    change in hemodynamics and worse renal function -
    so poor forward flow does not account for
    development of worse renal function

Rx of edema with ultrafiltration
  • Aggressive diuresis causes aldosterone and renin
    to increase in the CHF patient
  • Renin and aldosterone may have negative effects
    on cardiac and vascular function counteracting
    the benefit of volume removal.
  • Ultrafiltration can remove significant volume in
    CHF and may not stimulate the renin angiotensin
    system as much as diuretics
  • High dose diuretics in retrospective studies in
    in acute Rx CHF associated with increased
    mortality JAMA 20022547

  • Peripheral line - double lumen 6 or 7 French
  • Blood pump and filter (CHF solutions device) with
    a blood flow of 40-50 cc/min
  • Medical floor not ICU
  • Disposables - very expensive
  • Systemic heparin
  • Remove up to 4-8 kg per day.
  • No change in concentration of BUN, creatinine,
    K, etc
  • UNLOAD - trial comparing UF vs IV diuretics in
    CHF UF removed more volume than furosemide,
    patients discharged a little sooner and less
    likely to be readmitted within 30 days (because
    their renin-angiotensin system had not been

Diagnostic criteria for hepatorenal syndrome
  • Chronic or acute hepatic disease with advanced
    hepatic failure and portal hypertension
  • Creatinine gt 1.5 mg/dL progressing over
  • The absence of other apparent causes for the
    renal disease - shock, bacterial infection,
    nephrotoxic drugs, and the absence of US evidence
    of obstruction or parenchymal renal disease.
  • Urine RBCs lt 50 cells/HPF and protein excretion
    less than 500 mg/day.
  • Lack of improvement in renal function after
    volume expansion with IV albumin (1 g/kg body
    weight per day up to 100 g/day) for at least 2
    days, DC of diuretics.
  • Urine Nalt10

Hepatorenal syndrome
  • Type 1 - doubling of serum creatinine to a level
    greater than 2.5 mg/dL or reduction of the
    creatinine clearance by 50 or more to a value lt
    20 mL/min over a duration of 2 weeks, usually in
    hospitalized patients, no inciting agent.
  • Type 2 - moderate and stable reduction in GFR,
    insidious onset and slow progression of renal
    insufficiency in the setting of refractory
    ascites, better prognosis than type 1
  • 5 randomized trials of splanchnic
    vasoconstricting agents (terlipressin or
    noradrenaline) plus albumin all demonstrated
    improved renal function and mortality benefit in
    responders. Crit Care Med 2010261

ATN causes
  • Nephrotoxic
    myoglobin, hemoglobin
  • Ischemic
    cardiopulmonary arrest
    profound hypotension
    unwitnessed arrhythmia
  • Septic often multifactorial

ATN - Recovery of renal function
  • 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.

Diagnosis of ATN
  • Urine sediment (in patient with high pre-test
    probability of ATN the presence of renal tubular
    epithelial cells or granular casts is
    confirmatory for ATN, but may be a relatively
    late sign) Clin J Am Soc Neph 20081615
  • UNa gt20 in ATN
  • U/Pcreat lt15 in ATN
  • FeNa gt1 in ATN
  • BUN/creat lt20

Contrast media
  • 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

Risk factors for contrast-induced nephropathy
  • Patient related pre-existing renal
    insufficiency, diabetes mellitus, intravascular
    volume depletion, reduced cardiac output, common
    nephrotoxins(especially NSAIDs)
  • Procedure related increased dose of
    radio-contrast, multiple procedures within 72
    hours, intra-arterial administration, type of

Prevention of contrast nephropathy
  • NS at a rate of 1 mL/kg per hour, begun at least
    2 and preferably 6-12 hrs prior to the procedure,
    and continuing for 6-12 hrs after contrast
  • Isotonic sodium bicarbonate may be as or more
    effective (conflicting meta-analyses)
    Acetylcysteine 600-1200 mg
    po BID, the day before and the day of the
    procedure, based upon its potential for benefit
    and low toxicity cost. (conflicting

Hemodialysis to prevent CIN
  • 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)
    AJKD 2006361
  • Extracorporeal blood purification therapies for
    prevention of radiocontrast-induced nephropathy
    a systematic review. Am J Kidney Dis 2006
  • Renal protection for coronary angiography in
    advanced renal failure patients by prophylactic
    hemodialysis. A randomized controlled trial. J Am
    Coll Cardiol 2007 501015.

Treatment of rhabdomyolysis
  • NS early hydration may prevent severe AKI.
    Must monitor for fluid overload
  • NaHCO3 to raise urine pH gt6.5 eg. I
    amp 1 L 1/2 NS monitor serum pH
  • Mannitol eg. 50 cc of 20 to each L of IV fluid
    to increase UO monitor osmolarity
  • Initial rate of IV fluid about 500-1000 cc/hour
    goal UO gt300.
  • All authorities agree with vigorous hydration but
    no consensus on the rate of IV fluids or the use
    of mannitol or NaHCO3

Indications for RRT
  • Refractory fluid overload
  • Hyperkalemia eg, K gt6.5 meq/L, rapidly rising
    levels, marked EKG changes espeically if patient
    oliguric or can not take kayexalate
  • Marked metabolic acidosis in which are limited in
    giving NAaHCO3 due to volume constraints
  • Signs of uremia, such as declining mental status,
    not eating, uremic pericarditis (rare)

CRRT vs intermittent hemodialysis
  • A number of meta-analyses have addressed this
    question. Current data do not support the
    superiority of either CRRT or IHD.
  • In Europe and Australia use of CRRT much higher
    than in US
  • Many patients during the course of AKI receive
    several modalities
  • Peritonal dialysis can be done also but may be
    difficult to give as much dialysis, no head to
    head trials showing that it is less effective

Timing of initiation of RRT
  • Initiation of dialysis prior to the development
    of symptoms and signs of renal failure due to AKI
    is recommended.
  • It is unproven whether initiation of earlier or
    prophylactic dialysis offers any clinical or
    survival benefit.
  • If do start RRT before symptoms is no concensus
    on what level of BUN or creatinine to start

AKI - obstructive uropathy
  • To cause AKI need bilateral obstruction or
    obstruction of sole kidney
  • Always consider in the hospitalized patient that
    the Cr elevation could be bladder dysfunction
    from meds, reduced LOC, bedridden patient.
  • Post-void residual by bladder scan
  • Renal US - a very sensitive test, false
    negatives retroperitoneal fibrosis, early
    obstruction, severe volume depletion

AKI - interstitial causes
  • Suspect if WBC casts, marked pyuria, on a med
    that commonly causes intersitial nephritis,
  • Acute interstitial nephritis - most commonly due
    to drugs esp antibiotics, PPI
  • Pyelonephritis
  • Acute urate nephropathy
  • Tumor lysis syndrome
  • hypercalcemia

AKI - acute glomerulonephritis
  • Suspect if patient has marked proteinuria, RBC
    casts, marked hematuria
  • If is AKI and GN indicates possible RPGN
  • Relatively urgent need for a renal biopsy since
    creatinine can go up daily and may not be
    completely reversible
  • If seriously suspect may start steroids before
    the biopsy is back

AKI vascular causes
  • Renal emboli suspect in patient with AF other
    embolic phenomenona, high LDH
  • Cholesterol emboli suspect if recent trauma or
    angio in elderly patient
  • Antiphospholipid syndrome
  • Renal vein thrombosis suspect if nephrotic
    levels of proteinuria

Acute tubular necrosis
  • Ischemic prolonged pre-renal azotemia,
    hypotension, hypovolemic shock, cardiac arrest,
    cardiopulmonary bypass
  • Nephrotoxic drug-induced (radiocontrast agents,
    aminoglycosides, amphotericin B, cis-platinum,
    acetaminophen). Pigment nephropathy (hemoglobin,
  • Sepsis

AKI causes
  • PRE RENAL - volume depletion, CHF, hepatorenal
    syndrome, abdominal compartment syndrome, drugs
    (ACEI, NSAIDs)

    acute tubular necrosis (ATN)

  • nephrotoxic (eg, contrast,
    aminoglycosides, rhabdomyolysis),
  • ischemic

  • sepsis
  • Interstitial - pyelonephritis, acute
    interstitial nephritis, myeloma,
  • hypercalcemia, hyperuricemia, tumor
    lysis syndrome, intratubular
  • obstuction - uric acid, myeloma
  • Glomerular - primary GN vs. secondary to a
    systemic disease
  • Vascular - renal emboli, cholesterol emboli,
  • anti-phospholipid syndrome, renal vein

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Prediction of AKI after renal insult
  • Coronary intervention - risk factors
    hypotension, IABP, CHF, agegt75, anemia, diabetes,
    contrast volume, and serum creatinine. If
    patient has a very low score likelihood of CIN
    -7.5 versus 57
  • Open heart surgery risk factors female, CHF,
    LVEF, preop IABP, COPD, IDDM, prior surgery,
    emergency surgery, prior creatinine elevation,
    valve surgery. Variation in need for dialysis
  • AKI after non cardiac surgery risk factors
    agegt59, BMIgt32, emergency surgery, high risk
    surgery, PVD, liver disease, COPD. Variation in
    risk of AKI 0.3 4.3

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Acute kidney injury
  • PRERENAL - volume depletion, CHF, hepatorenal
    syndrome, abdominal compartment syndrome, drugs
    (ACEI, NSAIDs)

  • acute tubular necrosis (ATN)

    nephrotoxic (especially contrast,
    aminoglycosides, rhabdomyolysis), ischemic

  • interstitial - pyelonephritis, acute interstitial
    nephritis, myeloma, hypercalcemia, hyperuricemia,
    tumor lysis syndrome, intratubular obstuction -
    uric acid, myeloma
  • glomerular - primary GN vs. secondary to a
    systemic disease
  • vascular - renal emboli, cholesterol emboli,
    anti-phospholipid syndrome, renal vein thrombosis

Treatment of hepato-renal syndrome
  • Management of underlying cause
  • Stop diuretics
  • Low salt diet and free water restriction if
  • Midodrine Octreotide Albumin
  • Terlipressin Albumin
  • RRT
  • TIPS

  • 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 .

Nephrotoxic ATN
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Pre renal disease
  • Predisposing factors
  • Advanced cardiac failure with low mean arterial
  • 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

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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

Testing in acute renal failure to try to narrow
down cause
  • Urinalysis RBC or WBC casts
  • Urine Na or fractional Na excretion
  • Urine eosinophils
  • Urine protein/creatinine ratio
  • BUN/creatinine ratio
  • Serum LDH, uric acid, anion gap, BNP,CPK
  • Bladder scanner
  • Foley change or irrigate
  • Renal US
  • Abdominal CT
  • Renal Scan

RR 2.4
RR 4.15
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hepatorenal syndrome
  • type 1 - doubling of serum creatinine to a level
    gt 2.5 mg/dl or a reduction in creatinine
    clearance by 50 or more or to a value lt 20
    over 2 weeks
  • tye 2 - moderate and stable reduction in ranal