Approach to Acute Kidney Injury Anna Jin, M.D. LBVA/UCI 7/21/2014 - PowerPoint PPT Presentation


PPT – Approach to Acute Kidney Injury Anna Jin, M.D. LBVA/UCI 7/21/2014 PowerPoint presentation | free to download - id: 6d5882-MDgyM


The Adobe Flash plugin is needed to view this content

Get the plugin now

View by Category
About This Presentation

Approach to Acute Kidney Injury Anna Jin, M.D. LBVA/UCI 7/21/2014


Approach to Acute Kidney Injury Anna Jin, M.D. LBVA/UCI 7/21/2014 – PowerPoint PPT presentation

Number of Views:103
Avg rating:3.0/5.0
Slides: 46
Provided by: Admini501


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

Title: Approach to Acute Kidney Injury Anna Jin, M.D. LBVA/UCI 7/21/2014

Approach to Acute Kidney Injury Anna Jin,
M.D. LBVA/UCI 7/21/2014
Learning Objectives
  • Definitions and classification of AKI
  • Epidemiology and clinical outcome
  • Diagnosis and etiology
  • Approach and management of AKI
  • Risk factors and preventive strategies

Definition of AKI
  • a sudden, sustained, and usually
  • reversible decrease in the glomerular
  • filtration rate (GFR) occurring over a
  • period of hours to days.
  • gt 30 definitions used in published
  • studies

KDIGO Definition of AKI ( 2012 )
  • Defined by any of the following
  • Increase in SCr by 0.3 mg/dL within 48 hours
  • Increase in Scr by 1.5 times baseline, which is
    known or presumed to have occurred within the
    prior seven days
  • Urine volume lt0.5 mL/kg/h for six hours

KDIGO Classification of AKI ( 2012 )
Stage Serum creatinine Urine output
1 1.5-1.9 baseline OR gt0.3 mg/dL ? lt0.5 ml/kg/hr for 6-12 hrs
2 2-2.9 baseline lt0.5 ml/kg/hr gt 12 hrs
3 3 times baseline OR increase in Cr to 4.0 mg/dL OR Initiation of RRT lt0.3 ml/kg/hr gt 24 hrs OR Anuria gt 12 hrs
KDIGO Clinical Practice Guideline for AKI.
Kidney Int 2012
Definitions of Terminology
  • Azotemia - the accumulation of nitrogenous
    wastes (high BUN)
  • Uremia clinical manifestation (symptomatic
    renal failure)
  • Oliguria UOP lt 400-500 mL/24 hours
  • Anuria UOP lt 100 mL/24 hours

  • 5-10 in hospitalized pts
  • 70 in critically ill pts
  • 5-6 ICU pts require RRT
  • Once AKI occurred, the treatment is supportive,
    at an annual cost 10 billion in the US.

Incidence of Non-Dialysis AKI
Kidney Int 2007
Incidence of Dialysis-Requiring AKI
Kidney Int 2007
In-Hospital Mortality Rate 1992-2001
  • 33 - AKI requiring dialysis
  • 27.5 - AKI not requiring dialysis
  • 4.6 - no AKI
  • JASN 171135-1142, 2006

AKI and Mortality Brigham and Womens,
9210 adults Multivariable Odds Ratio for Death
AKI (? in SCr gt0.5) Age (per 10 yr) CKD CV dis. Respiratory dis GI dis. Cancer Infection 6.5 1.7 2.5 1.5 3 2.4 2.9 7.5 lt0.0001 lt0.0001 lt0.0001 lt0.04 lt0.0001 lt0.001 lt0.0001 lt0.0001
Increase in Serum Creatinine from Baseline
Chertow GM et al. J Am Soc Nephrol 2005163365
90 Day Mortality Rate in 2001
  • 44.8 - AKI requiring dialysis
  • 40.3 - AKI not requiring dialysis
  • 12.1 - no AKI
  • JASN 171135-1142, 2006

Lai CF et al. Crit Care 2012
Acute kidney injury increases risk of ESRD among
N 233.803
Ishani A et al. J Am Soc Nephrol 2009
Hou SH, Bushinsky DA, Wish JB. Am J Med 1983 74
243-8. Nash K, Hafeez A, Hou S. Am J Kidney Dis.
2002 39 930-6. Kaufman J, Dhakal M, Patel B, Et
al. Am J Kidney Dis 1991 17 191-8.
Etiology of AKI
ATN is the cause in more than 90. Sepsis is
the leading cause of ATN
To function properly kidneys require
  • Normal renal blood flow
  • Prerenal d/t renal hypoperfusion
  • Functioning glomeruli and tubules
  • Renal (Intrinsic)
  • Clear urinary outflow tract for drainage and
    elimination of formed urine
  • Post renal obstruction

Classification of the Etiologies of AKI
Acute Renal Injury
Prerenal AKI
  • Intravascular volume depletion
  • -bleeding, GI loss, Renal loss, Skin loss (burn),
    Third space loss, poor oral intake (NPO, AMS,
  • Decreased effective circulating volume
  • -congestive heart failure, cirrhosis, nephrotic
    syndrome, sepsis
  • Decreased flow through renal artery
  • -RAS or occlusion (compartment syndrome),
    hepatorenal syndrome, hypercalcemia
  • -pharmacologic impairment (RAAS blocker, NSAIDs,

Prerenal Azotemia Tx
  • In early stages can be rapidly corrected by
    aggressive normalization of effective arterial
  • Correction of volume deficits
  • Optimization of cardiac function
  • Discontinuation of antagonizing medications
  • NSAIDs/COX-2 inhibitors
  • Diuretics
  • RAAS blockers

Renal / Intrinsic AKI
  • Tubule ATN (sepsis, ischemic, toxins)
  • Interstitium AIN (Drug, infection, neoplasm)
  • Glomerulus AGN (primary, post-infectious,
  • rheumatologic,
    vasculitis, HUS/TTP)
  • Vasculature
  • Atheroembolic dz, renal artery thromboembolism,
    renal artery dissection, renal vein thrombosis
  • Intratubular Obstruction
  • myoglobin, hemoglobin, myeloma light chains,
  • uric acid, tumor lysis, drugs (bactrim,
  • acyclovir, foscarnet, oxalate in ethylene
    glycol toxicity)

Acute Tubular Necrosis (ATN)
  • Direct toxic Injury (20)
  • Exogenous
  • Radiocontrast
  • Aminoglycosides
  • Vancomycin
  • Amphotericin B
  • Cisplatin
  • Acyclovir
  • Calcineurin inhibitors
  • HIV meds (tenofovir)
  • Endogenous (pigment nephropathy)
  • Rhabdomyolysis
  • Hemolysis
  • Sepsis (48)
  • Ischemia (32)
  • prolonged prerenal azotemia
  • Hypotension
  • hypovolemic shock
  • cardiopulmonary arrest
  • cardiopulmonary bypass

Laboratory Findings in Acute Kidney Injury
Index Prerenal Azotemia Oliguric AKI (ATN)
BUN/PCr Ratio gt201 10-151
Urine sodium (UNa), meq/L lt20 gt40
Urine osmolality, mosmol/L H2O gt500 lt400
-Fractional excretion of sodium -FEUrea lt1 lt35 gt2 gt35
Response to volume Cr improves with IVF Cr wont improve much
Urinary Sediment Bland, Hyaline Muddy brown granular casts, cellular debris, tubular epithelial cells
Pitfalls Fractional Excretion of Na
  • Pre-existing CKD FeNa 2-3 even without tubular
  • Poor sensitivity with diuretics use
  • Picture might be muddied by fluid therapy
  • Etiologies of FeNa lt 1
  • hepatorenal syndrome
  • contrast nephropathy
  • rhabdomyolysis
  • acute glomerulonephritis
  • early obstructive uropathy

Postrenal AKI Classification
  • Level of obstruction
  • Upper tract (ureters)
  • Lower tract (bladder outlet or urethra)
  • Degree of obstruction
  • Partial vs. Complete
  • Type
  • Anatomic lesion (unilateral vs. bilateral)
  • Functional
  • Duration (Acute vs Chronic)
  • Cause (Congenital vs Acquired)

Etiologies Upper tract obstruction
  • Intrinsic
  • Nephrolithiasis
  • Blood clot
  • Papillary necrosis
  • Cancer
  • Extrinsic
  • Retroperitoneal or pelvic malignancy
  • Endometriosis/Prolapsed uterus
  • Abdominal aortic aneurysm or Iliac artery
  • Retroperitoneal fibrosis

Etiologies Lower tract obstruction
  • BPH or prostate cancer
  • Bladder cancer
  • Urethral strictures
  • Bladder stones
  • Blood clots
  • Functional obstruction as a result of neurogenic

Postrenal AKI tx
  • Prompt recognition and relief of obstruction can
    prevent the development of permanent structural
  • Lower tract obstruction (bladder catheter)
  • Upper tract obstruction
  • ureteral stents
  • percutaneous nephrostomies
  • Monitor for post-obstructive diuresis
  • Recovery of renal function dependent upon
    duration of obstruction.

How do we assess a pt with AKI?
  • Is this acute or chronic renal failure?
  • Establish baseline Cr and assess Cr trend
  • History and examination
  • Small kidneys on ultrasound (except for in
    -Diabetes, PCKD, Urinary Tract Obstruction)

Hilton et al, BMJ 2006333786-790
AKI Focused History
  • Prenal hx N/V/D? Oral intake? Diuretics?
    Hx of heart dz, liver dz, previous
    renal dz?
  • Post-renal sxs hesitancy, frequency, urgency,
    weak stream, dribbling, feeling of incomplete
    bladder emptying, flank pain. h/o kidney stones
    or BPH? Spinal cord injury? Anticholingergic
  • Any recent illnesses? Fever? Rashes?
  • Any recent surgery?
  • Cardiovascular instability?
  • Toxin exposure new medications (Abx, NSAIDs)? IV
  • Change in urination, any edema/SOB/Wt. gain?
  • Look for temporal link of exposure or risk factor
    to elevation of Cr or decline in UOP

  • How to assess volume?
  • History (intake, fluid loss, meds)
  • Postural blood pressure and pulse
  • Daily weights
  • Ins/Outs, fluid balance/fluid challenge
  • Signs of volume depletion
  • -Dry mouth, Increased thirst, Lightheadedness,
    Muscle cramps, extremities are cool to the touch,
    palpitations, reduced and dark urine, syncope
  • -PE Listlessness/AMS/LOC, tachycardic, weak
    rapid pulse, hypotensive (orthostatic vitals),
    tachypnic, increased Temp, poor capillary refill,
    decreased skin turgor, flattened neck veins,
    little or no urination for several hrs

Further work-up
  • U/A, Urine protein/Cr, Urine Eosinophilla
  • FeNa, FeUrea
  • CPK, uric acid
  • Urine microscopy
  • Muddy brown casts in ATN
  • WBC casts in AIN
  • RBC casts in AGN
  • Post-void residual (gt100-150 ml c/w voiding
  • bladder catheterization
  • renal ultrasound

Management of AKI general principle
  • No therapy to date have shown efficacy in
    treating AKI.
  • Identify the etiology and treat the underlying
  • Optimization of hemodynamics to increase renal
  • Lack of benefit low dose dopamine, loop
    diuretics only if markedly fluid overload
  • Identify and aggressively treat infection (early
    removal of foley catheters, and minimize
    indwelling lines)

Management of AKI treat complications
  • Correct fluid imbalances strict I/Os, daily
    wts. determine fluid balance goals daily, fluid
    selection or diuresis, readjust for UOP recovery,
    post diuresis or dialysis
  • Electrolyte imbalances (low K/phos diet, binder)
  • Metabolic acidosis (Bicarb deficit, mode and rate
    of replacement)
  • Nutrition adjust TPN/protein intake
  • Medication dosing adjustment for eGFR to avoid
    under or over dosing, timing for dialytic
    therapy, reassess dosing for renal recovery or
    dialysis modality)
  • Procedural considerations (prefer non-contrast
    CT, appropriate to delay contrast exposure,

Nephrotoxic Drug Exposure
  • Minimizing nephrotoxin
  • Avoid Aminoglycosides, Amphotericin, Bactrim,
    Vancomycin, NSAIDs, IV contrast, Fleets enemas
  • Renal dose medications especially antibiotics
    and monitor level
  • Cautious use (metformin, long acting oral
    hypoglycemic agents, insulin, gemfibrozil and
    statins, neurotin, colchicine/allopurinol,
    morphine/codeine, lmwh)

Ancient Chinese Medical Text
  • The inferior doctor treats actual illness.
  • The mediocre doctor attends to impending illness.
  • The superior doctor prevents illness.
  • 2600 BC - Huang Dee Nai-Chang

Best cure is to prevent!
  • Be aware of pts who are at risk for AKI
  • Volume depletion or Hypotension
  • Sepsis
  • Pre-existing renal, hepatic, or cardiac dz
  • Diabetes mellitus
  • Elderly
  • Exposure to nephrotoxins
  • Aminoglycosides, amphotericin, immunosuppressive
    agents, chemo., NSAIDs,, RAAS blockers,
    intravenous contrast media
  • Post cardiac or vascular Surgery pts or ICU pts
    with multiorgan failure

Take Home Messages AKI
  • AKI is increasingly common.
  • It involves high cost of management, carries a
    high morbidity and mortality risks.
  • The most common cause of in-hospital AKI is ATN
    that results from multiple acute insults (sepsis,
    ischemia, or nephrotoxin).
  • No drug treatment has been shown to limit the
    progression of, or speed up recovery from AKI.
  • Review medications and adjust dose
  • Recognize risk factors
  • The Best Treatment is PREVENTION and avoid
    further renal damage!!!

Doc, your pt hasnt peed in 5 hrs....what do you
want to do?
  • Examine pt BP? Dry? Septic (vasodilated)?
  • Flush foley (sediment can obstruct outflow)
  • Check I/Os (has he been drinking?)
  • Give IV BOLUS (250-500cc IVF), see if pt pees in
    next 30-60 min
  • If he pees, then he was dry
  • If he doesnt pee, then hes either REALLY dry or
    in renal failure
  • Check UA, UCx, urine lytes
  • Consider Renal U/S if reasonable

(No Transcript)
RIFLE Criteria for AKI (2005)
Definition of AKI based on AKIN Acute Kidney
Injury Network ( 2007 )
Stage Increase in Serum Creatinine Urine Output
1 1.5-2 times baseline OR 0.3 mg/dl increase from baseline lt0.5 ml/kg/h for gt6 h
2 2-3 times baseline lt0.5 ml/kg/h for gt12 h
3 3 times baseline OR 0.5 mg/dl increase if baselinegt4mg/dl OR Any RRT given lt0.3 ml/kg/h for gt24 h OR Anuria for gt12 h
RIFLE 2004
AKIN 2007
KDIGO 2012