Download AKI

Dr. M. A. Al-Odat
Jordanian board of medicine
S.R. of ICU
KSMC
Definition
There is NO sharp definition of AKI.
Traditionally defined as:
Abrupt loss of kidney function that results in the retention of
urea and other nitrogenous waste products, and
dysregulation of extracellular volume and electrolytes.
AKI-RIFLE Criteria
GFR Criteria
Increased creatinine
x1.5 or GFR decrease >
25%
Risk
Injury
Failure
Urine Output Criteria
UO < .5ml/kg/h
x 6 hr
Increased creatinine x2
or GFR decrease > 50%
UO < .5ml/kg/h
x 12 hr
Increase creatinine x3
or GFR decrease
> 75%
UO < .3ml/kg/h
x 24 hr or
Anuria x 12 hrs
Loss
ESKD
Persistent ARF** = complete loss
of kidney function > 4 weeks
End Stage Kidney Disease
(> 3 months)
High
Sensitivity
High
Specificity
Limitations
The change in serum creatinine during acute renal failure
does not directly correlate with the actual change in
glomerular filtration rate, which alters the assignment of
that patient to a particular RIFLE level.
 Given these limitations, a modification of the RIFLE
criteria has been proposed by the Acute Kidney Injury
Network.
RIFLE and AKIN staging criteria for AKI
______________________________________________________________
RIFLE
AKIN
Serum Cr
Urine Output
Stage
Stage
Criteria
Criteria
______________________________________________________________
Risk
1
Increase in Scr of 1.5-2x
baseline or increase >0.3
< 0.5 ml/kg/hr
for 6 hrs
Injury
2
Increase in Scr of 2-3x
baseline
< 0.5 ml/kg/hr
for 12 hrs
Failure
3
Increase in Scr of more
than 3x baseline or Scr >4
with an acute rise of > 0.5
Loss
ESRD
Persistent renal failure > 4 wk
Persistent renal failure > 3 mo
< 0.3 ml/kg/hr
for 24 hr
or
anuria for 12 hr
Problems with Creatinine
 Serum creatinine does not accurately reflect the GFR
in a patient who is not in steady state.
 Creatinine is removed by dialysis. As a result, it is
usually not possible to assess kidney function by
measuring the serum creatinine once dialysis is
initiated.
 In the early stages of severe acute renal failure, the
serum creatinine may be low even though the actual
(not estimated) GFR is markedly reduced since there
may not have been sufficient time for the creatinine to
accumulate.
Abnormal BUN:Cr ratio
 BUN: Cr > 15
 BUN:Cr < 15
 High protein intake.
 Advanced liver disease.
 Catabolic states.
 Rhabdomyloysis.
 Tissue necrosis.
 Cimetidine.
 Corticosteroids.
 Ketones.
 Tetracyclines.
 Methyldopa.
 Sepsis.
 Barbiturates.
 Volume loss.
 Cotrimexazole
 Low cardiac output.
 Obstructive uropathy.
Renal:
1) Glomerular:
• Glomerulonephritis
Causes of AKI
2) Tubular:
• Ischaemic ATN
• Nephrotoxic ATN
• Myeloma cast
nephropathy
3) Tubulointerstesial:
• Drugs
• Myeloma
• Sarcoid
4) Vascular
Post Renal:
1) Urethral stricture
2) Prostatic hyperplasia/malignany
3) Kidney stones
4) Renal papillary necrosis
5) Retroperitoneal fibrosis
6) Carcinoma of cervix
Pre-Renal (reduced
renal perfusion):
1) hypovolaemia:
• hypotension
•Diarrhea/vomiting
•Blood loss
•Third space loss
•Inadequate intake
2) Reduced effective
circulating volume:
•Cardiac failure
•Septic shock
•Cirrhosis
3) Drugs:
•ACE-I
•NSAIDs
4) Renal artery stenosis
Of AKI
 67% of critical care patients have AKI
 12% class R
 27% class I
 28% class F
 More than half of patients with class R will progress
to either class I or F
 5% of patients in general intensive cares will require
RRT
 10-20% of surviving patients require ongoing RRT
beyond hospital discharge
Hoste et al Crit Care 2006
AKI and Mortality
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RIFLE class F have a mortality of 57%
RIFLE class I 45%
RIFLE class R 21 %
Compared to 8.4% of patients without AKI
Ostermann M, Chang RW: CCM 2007
Epidemiology of AKI in the ICU
Saudi Arabia
Clinical spectrum of acute renal failure Saudi Arabia.
Ghacha R, Sinha AK, Al-Khursani IA.
Saudi J Kidney Dis Transpl.
 Acute tubular necrosis (67.5%)
 Obstructive uropathy (30%)
 Mortality rate was 26%
Epidemiology of AKI in the ICU
Saudi Arabia
Epidemiology of acute renal failure in hospitalized patients:
experience from southern Saudi Arabia.
Al-Homrany M.
East Mediterr Health J. 2003
 Acute tubular necrosis 62%
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sepsis (24.7%)
ischemia (12.7%)
rhabdomyolysis (10.7%)
drugs (7.3%)
malaria and snake-bites (4.6%).
 Overall, 40% died
Clinical Picture
 The clinical picture of the cause.
 General signs/symptoms, including decreased or no urine
output, flank pain, edema, hypertension, discolored urine,
anorexia, vomiting, mental status changes or seizures.
 Many patients are asymptomatic and are noted on routine
examination to have an elevated plasma creatinine
concentration or an abnormal urinalysis.
 laboratory findings due to the renal injury.
Clinical Picture
Pre-Renal
 History and clinical picture of the cause.
 Tahycardia.
 Hypotension/Orthostatic hypotension.
 Dryness of mucocutaneous membranes.
 Oliguria ( < 400 ml/d).
 Anuria ( < 50 ml/d).
Clinical Picture
Pre-Renal
 Hypovolaemia:
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- blood loss
- Third space loss: pancreatitis, GIT obstruction,
hypoalbuminaemia.
Cardiovascular:
- infarction, tamponade, arrythmias, valvular diseases
Distributive:
- sepsis, cirrhosis, hepatorenal syndrome.
Local renal causes:
- renal artery stenosis, malignant hypertension.
Certain medications
Clinical Picture
Pre-Renal: Medications
 NSAIDs, ACE-I, Cocaine, Cyclosporines.
 Alteration of renal perfusion, and glomerular
haemodynamics.
 failure of glomerular pressure autoregulation.
 Predisposing factors:
- CHF
- liver cirrhosis
- nephrotic syndrome
- hypovolaemia
- atherosclerosis
- Age.
Clinical Picture
Pre-Renal: Medications

AKI associated with ACE-I
should prompt investigation to
rule out bilateral renal artery
stenosis.
Clinical Picture
Renal
 History and clinical picture of the cause.
 Acute glomerulonephritis: vasculitis, SLE, endocarditis,
cryoglobulinaemia, anti-glomerular basment membrane
disease.
 Acute interstitial nephritis: sarcoidosis, myeloprolifrative
disorders.
 Acute tubular necrosis: ischaemia, sepsis, nephrotoxins,
drugs, contrast, rhabdomyolysis, myoglobin/
haemoglobin.
Clinical Picture
Renal
 The most common cause of AKI in hospitalized patient is
intrinsic renal failure due to ATN.
 Polypharmacy is common among most patients with chronic
diseases and hospitalized patients.
 Allergic interstitial nephritis should be strongly considered in
all patients with AKI.
 Rhabdomyolysis .
 Contrast induced AKI.
Mechanisms of ATN
Medications causes of allergic interstitial
nephritis
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Penicillines
Cephasporines
Sulfonamides
Rifampin
Ciprofloxacin
NSAIDs
Thiazide diuretics
Loop diuretics
Cimetidine
Phenytoin
Allopurinol
Chinese herb
Pathophysiology of Rhabdomyolysis
Clinical Picture
Renal: contrast induced AKI
 Contrast induced AKI is predominantly via acute
vasoconstriction.
 Risk factors: GFR < 35 ml/min, diabetic nephropathy,
severe CHF, large volume of contrast, preexisting
hypotension/hypokalaemia.
Pathophysiology of contrast induced
acute kidney injury
Prevention of contrast induced AKI
 Administration of crystalloid(1-1.5mL/Kg/hr for 8-12 hours
before a procedure) remains the safest, most efficacious, and
cost-effective method of preventing contrast induced
nephropathy.
 Administration of acetylcysteine in two 600mg doses the day
along with saline infusion for patients with stable chronic renal
insufficiency(Cr~ 2.0mg/dL).
 Type of Contrast.
Clinical Picture
Post-Renal
 Total absence of urine (anuria) is primarily observed
with bilateral ureteral obstruction/ urethral
obstruction.
 Loin or flank pain.
 Prostatic hyperplasia/malignancy (male).
 Carcinoma of cervix (female).
Evaluation of AKI
Evaluation of AKI
 Intravascular volume status is the most important factor in the
evaluation of AKI. A decrease in urinary volume is often one of
the initial clinical findings in AKI.
 The most important laboratory test for a patient with AKI is urine
analysis.
 Both urinary sediment and urinary indices in combination with
serum values can often be extremely helpful in determining the
cause of AKI.
Urine analysis in AKI
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RBC, RBC cast, Protienuria:
- Glomerulonephritis – vasculitis
- thrombotic microangiopathy.
WBC, WBC casts:
- Pyelonephritis - Interstitial nephritis.
Eosinphilurea:
- Glomerulonephritis - Atheroemboli
- Allergic interstitial nephritis
Pigmented casts, renal tubular epithelium:
- ATN - Haemoglobinurea – myoglobinurea
Crystallurea:
- Uric Acid - Drugs - Toxins.
RBC cast
Hyaline cast
Granular cast
Granular cast
Granular cast
WBC cast
Oval fat body
and Hyaline cast
WBC cast
Urinary Sediment of ATN
GUIDELINE OF URINARY INDICES
Typical Urine Findings in Conditions
that cause AKI
Condition
Dipstick test
Sediment analysis
Uosmo
FENa
Pre-renal
Azotaemia
-ve, trace
few hyaline casts
>500
<1
Ischaemic
ATN
mild to mod.
proteinuria
Pigmented granular
cast
<350
>1
Nephrotoxins
mild-mod prot.
Pigmented gran. Cast
<350
>1
A. Interstitial
Nephritis
mild-mod prot,
hemoglobin, WBC
WBC, WBC casts, Eosin. <350
Eosin. Casts, RBC
>1
A. Glomerulo
Nephritis
mod-severe prot.
hemoglobin
RBC, RBC casts
>500
<1
Post-renal
Azotaemia
-ve, trace, WBC
hemoglobin
crystals, RBC
< 350
>1
Radiologic Studies :
 Ultrasonography is most common.
 Safe, easy to use, informative.
 Principally required to assess urinary tract obstruction,
kidney stones, renal cyst or mass.
 CT scan.
Renal Biopsy
 Indications : Isolated glomerular hematuria with proteinuria,
nephrotic syndrome, acute nephritic syndrome, unexplained
acute or rapidly progressive renal failure.
 Contraindications: Uncorrectable bleeding diathesis, Small
kidneys (indicative of chronic irreversible disease), Severe
hypertension, multiple, bilateral cysts or a renal tumor,
hydronephrosis, Active renal or perirenal infection,
uncooperative patient.
 Complications: Bleeding.
Biomarkers
 Neutrophil gelatinase–associated lipocalin (NGAL) is up-
regulated in proximal tubular cells immediately following
ischemic injury.
 Interleukin-18 (IL-18) is a proinflammatory cytokine that
is activated in proximal renal tubules following injury.
 Cystatin C is a better marker of GFR than serum
creatinine, and could identify the development of AKI 1 to
2 days before elevation in serum creatinine.
Management
 The goal of any focused evaluation of AKI is immediate
correction of its reversible causes.
 Recognition and relief of urinary outlet obstruction should
be given the highest priority, especially for patient with
anuria.
Management
 Support of renal perfusion with either volume infusion or
therapeutics that improve renal oxygen delivery should be
considered before any attempt to improve urinary flow.
 Urinary indices should be examined before diuretic
intervention.
Management
Renal Replacement therapy remains the cornerstone of
management of patients with severe AKI
Nephron Clin Pract 2009;112:c222-c229
Indications of RRT
 Anuria or Oliguria (UOP < 200 ml/12 hrs.)
 Hyperkalaemia (K > 6.5 mmol/L).
 Severe Acidaemia (pH < 7.1).
 Azotaemia ( Urea > 30 mmol/L).
 Clinically significant organ oedema (particularly Lungs).
 Uraemic: encephalopathy, pericarditis, neuropathy,
myopathy.
 Severe dysnatraenia (Na >160 or < 115 mmol/L)
 Drug over dose with dialysable product.
 Hyperthermia.
 Pharmacologic treatments under study:
 Dopamine: no benefit
 Atrial Natriuretic Peptide (ANP) or ANP-analogue
(Anaritide): promising
 Human Insulin like growth factor 1: no benefit
 Erythropoietin
 Intensive Insulin Therapy (IIT).
Case 1
 26 yo F is involved in a RTA, with multiple fractures, blunt
chest and abdominal trauma. She was briefly hypotensive on
arrival to ED, received 6L NS and normalized BP. Non contrast
CT showed small retroperitoneal hematoma. On day#2 her SCr
is 0.9 mg/dl, lipase is elevated and tense abdominal distension
is noted. US showed massive ascites. UOP drops to <20 cc/hr
despite of 10 L total IV intake. On day#3, SCr is 2.1mg/dl, CVP
is 17, UNa is 10 meq/L, with a bland sediment.
What is the cause of her AKI?
What bedside diagnostic test and therapeutic intervention is
indicated?
 Bladder pressure was 29 mmHg
 UOP and SCr improved with emergent paracenthesis.
 Dx: Abdominal Compartment Syndrome causing
decreased renal perfusion from increased renal vein pressure.
Case 2
 59 yo M, hx liver transplant in 2001 and acute on chronic
rejection, now decompensated ESLD, is admitted with
worsening ascites, hepatic encephalopathy and GI bleed (which
is now controlled). The only medications he has been receiving
are Lactulose and omeprazole. He has been hemodynamically
stable with average BP~100/70 mmHg. He had a 3.5 L
paracenthesis on day 2. His SCr has been slowly rising from 1.2
to 4.7 mg/dl within the 2nd to 4th day of admission and his UOP
has dropped to 150 cc/day. His daily FeNa is <1% despite of 2
L fluid challenge. His Urine sediment is blend. His renal US is
normal.
What is the cause of his AKI?
 Patient required HD.
 He had a second liver transplant and came
off HD after the surgery with stable SCr of
1.4 mg/dl.
 Dx: Hepatorenal Syndrome (HRS)
Case 3
 54 yo F with CAD, on statin, started a new exercise
program with intense weight training. She was
brought to ED with neck pain, and LL weakness. VS
stable, normal UOP, with dry mucosa. LL muscle
strength 2/5 bilaterally. BUN 40 mg/dl, creatinine=8
mg/dl. FeNa 1.5%. Renal US normal. UA: 1.010, 3+
blood, few RBCs, few granular casts.
What would be the next test to order?
What may be the cause of her AKI?
 Her CPK=57,700
 She was treated with IV NaHCO3 gtt to alkalinize
urine to PH>6.5 .
 Her UOP remained normal but she required HD for
uremia.
 Dx: ATN due to Rhabdomyolysis
Case 4
 72 yo M with DM, and prostate cancer metastatic to the bone,
on hormonal therapy. He is admitted with weakness,
progressive weight loss, and persistent nausea. His med list
also includes Diclofenac sodium daily for hip pain. BP=150/90,
350cc of urine collection immediately after foley placement,
and normal exam. BUN=107 mg/dl, creatinine=9.8 mg/dl (2.0
almost 6 months PTA), which remained unchanged with
hydration. Uric acid=8.2 mg/dl. UA: 1.010, 1+ protein, 1+
blood, few RBCs, no cast, no WBC. US showed 10-11 cm
kidneys, no hydronephrosis.
What seems to be the cause for his AKI?
 Patient was initiated on HD for uremia and remained
HD dependent for his symptomatic uremia.
 Patient and his family were concerned about his renal
recovery (outcome), so a renal Bx was done showing
severe chronic interstitial nephritis, with fibrosis and
glomerulosclerosis.
 Dx: ESRD due to chronic tubulo-interstitial
disease secondary to NSAIDs
Case 5
 59 yo F with prolonged HTN, kidney transplant in 2000, on
norvasc, prograf and prednisone was brought in for decreased
LOC. T=39, BP=95/60, HR=104, UOP=20 cc/hr, intubated for
airway protection, otherwise normal exam. BUN=80 mg/dl,
creatinine=6 mg/dl (normal baseline), K=6.5 meq/L, Hct=20%,
Plt=20000, FeNa 1%, urine eosinophil (-), UA: 2+ blood, no
protein, RBC > 50/hpf, no WBC, no cast.
What would be your next step?
What could be the reason for her AKI?
 Her PBS showed many schistocytes and fragmented
RBCs.
 Her Prograf was replaced with Sirolimus
 She underwent plasmapheresis, and required HD for
anuria, and persistent hyperkalemia. She came off HD
after 2.5 months with stable creatinine=1.2 mg/dl.
 Dx: TTP secondary to Prograf
Case 6
 72 yo F with depression and hypothyroidism, was found by
neighbors on the floor, unconscious, in respiratory distress.
Intubated for airway protection. VS stable, anuric, Lungs
crackles. BUN 50 mg/dl, Creatinine=4 mg/dl, with high anion
gap metabolic acidosis, and an osmolar gap of > 10. Lactic
acid=1.8, FeNa 1%, urine eosinophil (-), UA: 1.020, 1+ blood,
no protein, few RBCs, many oxalate crystals, few granular
casts. US showed normal sized kidneys with no
hydronephrosis.
What is your next step?
What seems to be the cause for her AKI?
 Her ethylene Glycol level came back after 2 days to
be 40 mg/dl.
 Pt was given Fomepizole and initiated on HD for
persistent acidemia. She remained HD dependent,
eventually extubated, started therapy for depression.
 Dx: Ethylene Glycol toxicity
Case 7
 38 yo M with post ERCP pancreatitis, is admitted to ICU,
intubated for hypoxic respiratory distress, is anuric, febrile, and
hypotensive, requiring massive volume resuscitation, on two
vasopressors. He has received 11 L of NS and other IV meds
within the last 8 hours and currently his CVP~12, has coarse
crackles, and 2+ edema. His Creatinine rose from 1.2 to 3.5 the
morning after the above event, FeNa > 1%, UNa 45 meq/L, UA:
1.010, no protein, no blood, moderate epithelial cells, many
muddy brown granular cell casts, moderate epithelial cell casts.
US showed normal sized kidneys with no hydronephrosis.
 What is the cause of his AKI?
 He was started on CVVH for volume control. Has had
a long hospital stay complicated with polymicrobial
bacteremia and VAP.
 Dx: ATN secondary to renal ischemia and
sepsis
Case 8
 45 yo M with CHF and Bipolar Disorder on Lithium for 10 years,
admitted for abdominal pain after a heavy meal, which turned out to
be due to acute cholecyctitis. He was kept NPO on D5 1/2NS 50
cc/hr. Next morning he felt well but thirsty and hungry, BP=120/80,
I/O=1200/4500. His SCr rose from 1.2 to 1.9 mg/dl. SNa 149 meq/L.
UNa 10 meq/L. UOsm 190 mOsm/Kg.
What is the cause of his AKI?
 Patients IVF was changed to ½ NS, replacing 80% of
UOP per hour. SCr and SNa improved to baseline in 2 days.
 Dx: Prerenal azotemia secondary to renal free water
loss in DI.
Case 9
 18 yo F with no PMH admitted with projectile
vomitting, fatigue, and low PO intake. Her
BP=200/110, normal UOP with dry mucosa, trace
edema, and otherwise normal exam. BUN=120
mg/dl, Creat=10 mg/dl which continued to rise on
the following days, Hct=25% without schistocytes
on PBS, UA: 3+ protein, 3+ blood, >50 RBC, many
RBC casts. FeNa 1%. US showed normal sized
kidneys.
What other tests do you order?
What may be the cause of her AKI?
 ANA (-), normal complements, cryo (-), serology for hepatitis B, and C (-),
P-ANCA (+), C-ANCA (-), anti-GBM (-), ASO (-), ESR 80.
 Her renal Bx showed crescentic glomerulonephritis, minimal non-specific
immune complex deposits, without chronic changes.
 She remained dialysis dependent despite of steroid, cyclophosphamide, and
10 plasmapheresis treatments.
 Dx: Crescentic Glomerulonephritis due to Wegner’s granulomatosis
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