final aki for im 2014
TRANSCRIPT
Approach to Acute Kidney Injury
Anna Jin, M.D.
LBVA/UCI7/21/2014
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.
> 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 <0.5 mL/kg/h for six hours
KDIGO Classification of AKI ( 2012 )
Stage Serum creatinine Urine output
1 1.5-1.9× baselineOR>0.3 mg/dL
<0.5 ml/kg/hr for 6-12 hrs
2 2-2.9× baseline<0.5 ml/kg/hr > 12 hrs
3 3 times baselineORincrease in Cr to ≥4.0 mg/dLOR Initiation of RRT
<0.3 ml/kg/hr > 24 hrsORAnuria > 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 < 400-500 mL/24 hours
Anuria – UOP < 100 mL/24 hours
Epidemiology
≈ 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 17:1135-1142, 2006
Chertow et al, JASN 16:3365-70; 2005
AKI and Mortality
Brigham and Womens, 9210 adults Multivariable Odds Ratio for Death
•AKI (Δ in SCr >0.5)
•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
<0.0001
<0.0001
<0.0001
<0.04
<0.0001
<0.001
<0.0001
<0.0001
Increase in Serum Creatinine from Baseline
Chertow GM et al. J Am Soc Nephrol 2005;16:3365
90 Day Mortality Rate in 2001
44.8% - AKI requiring dialysis
40.3% - AKI not requiring dialysis
12.1% - no AKI
JASN 17:1135-1142, 2006
Lai CF et al. Crit Care 2012
N=634
Ishani A et al. J Am Soc Nephrol 2009
N= 233.803
Acute kidney injury increases risk of ESRD among elderly
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
0
10
20
30
40
50
60
70
80
Prerenal Intrarenal Obstruct Idiopath
Outpatient
Inpatient
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
AcuteTubularNecrosis
AcuteInterstitialNephritis
AcuteGN
AcuteVascularSyndromes
IntratubularObstruction
Classification of the Etiologies of AKI
PrerenalAKI
PostrenalAKI
IntrinsicAKI
AcuteRenalInjury
Prerenal AKI
Intravascular volume depletion:
-bleeding, GI loss, Renal loss, Skin loss (burn), Third space loss, poor oral intake (NPO, AMS, anorexia)
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, CNI)
Prerenal Azotemia Tx In early stages can be rapidly corrected by
aggressive normalization of effective arterial volume.
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, indinavir,
acyclovir, foscarnet, oxalate in ethylene glycol toxicity)
Acute Tubular Necrosis (ATN)
Sepsis (48%)
Ischemia (32%) prolonged prerenal
azotemia Hypotension hypovolemic shock cardiopulmonary arrest cardiopulmonary bypass
Direct toxic Injury (20%)
Exogenous Radiocontrast Aminoglycosides Vancomycin Amphotericin B Cisplatin Acyclovir Calcineurin inhibitors HIV meds (tenofovir)
Endogenous (pigment nephropathy) Rhabdomyolysis Hemolysis
Laboratory Findings in Acute Kidney Injury Index Prerenal
Azotemia Oliguric AKI (ATN)
BUN/PCr Ratio >20:1 10-15:1
Urine sodium (UNa), meq/L
<20 >40
Urine osmolality, mosmol/L H2O
>500 <400
-Fractional excretion of sodium
-FEUrea
<1% <35%
>2%
>35%
Response to volume Cr improves with IVF Cr won’t improve much
Urinary Sediment Bland, Hyaline Muddy brown granular casts, cellular debris, tubular epithelial cells
Pitfalls: Fractional Excretion of NaPitfalls: Fractional Excretion of Na
Pre-existing CKD: FeNa 2-3 even without tubular injury
Poor sensitivity with diuretics use Picture might be muddied by fluid therapy
Etiologies of FeNa < 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:NephrolithiasisBlood clotPapillary
necrosisCancer
Extrinsic:
Retroperitoneal or pelvic malignancy
Endometriosis/Prolapsed uterus
Abdominal aortic aneurysm or Iliac artery aneurysm
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 bladder
Postrenal AKI tx Prompt recognition and relief of obstruction can
prevent the development of permanent structural damage.
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 2006;333;786-790
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 meds?
Any recent illnesses? Fever? Rashes?
Any recent surgery?
Cardiovascular instability?
Toxin exposure: new medications (Abx, NSAIDs)? IV contrast?
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
In’s/Out’s, 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
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 (>100-150 ml c/w voiding dysfunction)
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 cause
Optimization of hemodynamics to increase renal perfusion
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/O’s, 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, prophylaxis)
Nephrotoxic Drug Exposure
Minimizing nephrotoxinAvoid Aminoglycosides, Amphotericin,
Bactrim, Vancomycin, NSAIDs, IV contrast, Fleet’s 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
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!!!
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 doesn’t pee, then he’s either REALLY dry or in renal failure
Check UA, UCx, urine lytes
Consider Renal U/S if reasonable
THANK YOU!
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
<0.5 ml/kg/h for >6 h
2 2-3 times baseline <0.5 ml/kg/h for >12 h
3 3 times baseline OR0.5 mg/dl increase if baseline>4mg/dlORAny RRT given
<0.3 ml/kg/h for >24 hOR Anuria for >12 h
RIFLE2004
AKIN2007
LIMITATIONS STRENGTHS
KDIGO2012