Acute Kidney

Injury
Unit X
ACUTE KIDNEY INJURY (AKI)
● Acute renal failure (ARF)
● Clinical syndrome generally defined by an abrupt reduction in
kidney function as evidenced by changes in:
○ Serum creatinine (Scr)
○ Blood urea nitrogen (BUN)
○ Urine output.
Serum Creatinine
● standard laboratory marker for
the detection of kidney disease.
● CREATININE
○ Waste product of creatine and
creatine phosphate, a high-energy
compound found in skeletal muscle
tissue.
○ Excreted in the urine
Serum Creatinine
● standard laboratory marker for
the detection of kidney disease.
● CREATININE
○ Waste product of creatine and
creatine phosphate, a high-energy
compound found in skeletal muscle
tissue.
○ Excreted in the urine
Serum Creatinine
● serum creatinine concentration
alone is not an optimal measure
of kidney function, it is often used
as a marker for referral to a
nephrologist
● Normal:
○ Male: 0.8-1.2mg/dL
○ Females: 0.6-0.9 mg/dL
Serum or Blood Urea Nitrogen
● Measures the amount of urea
nitrogen in the blood or serum
● Predicts uremic syndrome in
patients with severe renal failure
● Normal: 7 to 20 mg/dL (2.5 to
7.1 mmol/L)
Serum or Blood Urea Nitrogen
❏ Uremia
❏ high levels of blood urea,
(traditional synonym for renal
failure) which literally means
“urine in the blood”.
❏ Azotemia
❏ high levels of nitrogenous
products (such as urea,
creatinine, various body waste
compounds, and other
nitrogen-rich compounds) in the
blood
Urine Output
 Glomerular Filtration Tubular
Secretion
Urine Output

Tubular
Reabsorption
● Normal: 800 to 2000
mL/day
● Oliguria: <500 mL/day
● Anuria: <100 mL/day
● Polyuria: >2.5 L/day
Excretion
Glomerular Filtration Rate
● Gold standard quantitative index of kidney function.
✓ Estimation of GFR is important for early recognition and monitoring
of patients with chronic kidney disease.
✓ Estimation of CrCL is important as a guide for drug dose adjustment
in the presence of renal impairment.
● GFR < 60 for ≥ 3 months,
or GFR:
mL/min/1.73m2
● GFR > 60 with kidney
damage (marked by high
levels of albumin in your
urine) indicates chronic
kidney disease.
Creatinine Clearance
● Volume of blood plasma
cleared of creatinine per unit
time.
● It is a rapid and cost-effective
method for the measurement
of renal function.
● Normal:
○ Male: 110-150 mL/min
○ Female: 100-130 mL/min
Classification of Acute Kidney Injury
1. Risk, Injury, Failure, Loss of Kidney Function, and End-Stage Kidney
Disease (RIFLE)
2. Acute Kidney Injury Network (AKIN)
3. Kidney Disease: Improving Global Outcomes (KDIGO)
Risk, Injury, Failure, Loss of Kidney Function, and End-Stage
Kidney Disease (RIFLE)
CATEGORY Scr and GFR CRITERIA URINE OUTPUT

Scr increase to 1.5-fold or GFR decrease >25% from <0.5 mL/kg/hr for ≥6 hours
RISK
baseline
Scr increase to 2-fold or GFR decrease >50% from <0.5 mL/kg/hr for ≥12 hours
INJURY
baseline
Scr increase to 3-fold or GFR decrease >75% from Anuria for ≥12 hours
FAILURE baseline, or Scr ≥4 mg/dL (354 μmol/L) with an acute
increase of at least 0.5 mg/dL (44 μmol/L)
LOSS Complete loss of function (RRT) for >4 weeks

ESRD RRT >3 months

Acute Kidney Injury Network (AKIN)

CATEGORY Scr CRITERIA URINE OUTPUT

Scr increase ≥0.3 mg/dL (27 μmol/L) or 1.5- to <0.5 mL/kg/hr for ≥6 hours
STAGE 1
2-fold from baseline
STAGE 2 Scr increase >2- to 3-fold from baseline <0.5 mL/kg/hr for ≥12 hours

Scr increase >3-fold from baseline, or Scr ≥4 <0.3 mL/kg/hr for ≥24 hours or
STAGE 3 mg/dL (354 μmol/L) with an acute increase of at anuria for ≥12 hours
least 0.5 mg/dL (44 μmol/L), or need for RRT
Kidney Disease: Improving Global Outcomes (KDIGO)

CATEGORY Scr CRITERIA URINE OUTPUT

Scr increase ≥0.3 mg/dL (27 μmol/L) or 1.5-1.9 <0.5 mL/kg/hr for 6-12 hours
STAGE 1
times from baseline
STAGE 2 Scr increase 2-2.9 times from baseline <0.5 mL/kg/hr for ≥12 hours

Scr increase three times from baseline, or Scr ≥4 Anuria for ≥12 hours
mg/dL (354 μmol/L), or need for RRT, or eGFRc
STAGE 3
<35 mL/min/1.73 m2 (0.34 mL/s/m2) in patients
<18 years
Categories of Acute Kidney Injury
● PRERENAL AKI
○ Prerenal Azotemia
○ Results from hypoperfusion of the
renal parenchyma, with or
without systemic arterial
hypotension.
● Compensatory Mechanisms:
○ Stimulate RAAS
■ Vasoconstriction
■ Na+ and Water retention
■ Stimulate sympathetic activity
○ Release antidiuretic hormone
○ *Afferent Arteriole Dilation
(prostaglandins, kinins, Kallikrein,
NO)
○ *Efferent Arteriole constriction
(Angiotensin II)
Categories of Acute Kidney Injury
● PRERENAL AKI
○ Prerenal Azotemia
○ Results from hypoperfusion of the
renal parenchyma, with or
without systemic arterial
❏ ↓CO
hypotension.
❏ Intravascular Volume depletion
(Hypovolemia)
❏ Hemorrhage, excessive GI losses,
dehydration, sepsis, extensive burns, and
diuretic therapy
❏ Hypotension
❏ Acute MI
❏ Systemic vasodilation
❏ NSAIDs, ACEi, ARBS
Categories of Acute Kidney Injury
● INTRINSIC AKI
○ Intrarenal AKI
○ Direct damage to the kidneys by
inflammation, toxins, drugs,
infection, or reduced blood supply
❏ Renal vascular damage
❏ Renal artery/vein thrombosis
❏ Atherothromboembolism
❏ Vasculitis
❏ Acute Tubular Necrosis (ATN)
Categories of Acute Kidney Injury
❏ Glomerular damage
❏ Glomerulonephritis
❏ Autoimmune diseases
❏ Tubular Damage
❏ Acute Tubular Necrosis
❏ Ischemia
❏ Nephrotoxins
❏ Interstitial damage
❏ Acute Interstitial nephritis
❏ Penicillin, ciprofloxacin, sulfonamide,
NSAIDs
❏ Infection
Categories of Acute Kidney Injury
● POSTRENAL AKI
○ May develop as the result of
obstruction at any level within the
urinary collection system
Categories of Acute Kidney Injury
❏ Bladder outlet obstruction
❏ BPH
❏ Malignancy
❏ Anticholinergic Drugs
❏ Displace urinary catheter
❏ Ureteral obstruction
❏ Malignancy
❏ Nephrolithiasis
❏ Renal pelvis/tubular obstruction
❏ Nephrolithiasis
❏ Drugs
Categories of Acute Kidney Injury
❏ Bladder outlet obstruction
❏ BPH
❏ Malignancy
❏ Anticholinergic Drugs
❏ Displace urinary catheter
❏ Ureteral obstruction
❏ Malignancy
❏ Nephrolithiasis
❏ Renal pelvis/tubular obstruction
❏ Nephrolithiasis
❏ Drugs
 Clinical
Presentation
 Acute anuria
Clinical Presentation ● Urinary obstruction
● Shock
Oliguria
● Change in Urinary character ● Prerenal azotemia
○ Decreased urine output Nonoliguric renal failure
● Acute intrinsic kidneyeinjury
○ Urine discoloration ● Incomplete urinary obstruction

Cola colored urine

● Acute
glomerulonephritis
Clinical Presentation
● Electrolyte imbalance
● Metabolic Acidosis
● Sudden weight gain
● Nausea
● Vomiting
● Fatigue
● Severe abdominal pain
● Flank pain
● Edema
Diagnosis
Diagnosis
● Serum Creatinine (Scr) ● CBC
○ Estimated Creatinine Clearance ● Differential test
○ Estimate GFR (eGFR) ● Serum electrolyte
● Blood Urea Nitrogen (BUN) ○ ↑↑ K+, Ca+2, P
● Urine Output
● Urinalysis
Diagnosis
Urinalysis: ● Protein or Albumin
● pH ○ Proteinuria or Albuminuria
■ Persistent over a period of 3 to 6
○ Normal: 4.5-7.8
months, is now considered the
● Specific gravity principal marker of kidney damage.
○ Prerenal: >1.018 ■ used to characterize the severity of
○ Intrinsic: <1.012 CKD and to monitor the rate of
● Glucose disease progression or regression.

○ Glucosuria - Occurs if patient’s

blood glucose >180 mg/dL
Diagnosis
● Computed Tomography
○ evaluation of obstruction, malignancy, and infections of the kidney.

● Renal Ultrasonography
○ abnormalities in structure, such as occurs with obstruction.

● Magnetic Resonance Imaging

○ assessment of obstruction, malignancy, and renovascular lesions.
Treatment
Desired Outcome
● Prevent AKI
● Minimizing the degree of insult to the kidney, reducing extrarenal
complications, and expediting the patient’s recovery of kidney
function.
● The ultimate goal is to have the patient’s kidney function restored to
pre-AKI baseline.
Risk Factors
● Advanced age
● Acute infection
● Pre-existing CKD
● Diabetes
● Chronic respiratory disease
● Cardiovascular Disease
● Liver disease
● Acute blood loss in trauma
● Uric acid nephropathy
● Decreased renal perfusion
secondary to abdominal or
coronary bypass surgery
Prevention of
AKI
Prevention of AKI
● Withdrawal and Avoidance of Nephrotoxic agents
○ ACEi
○ NSAIDs
○ Aminoglycoside
○ Radiocontrast media
■ patients require contrast dye and are at risk of contrast–induced AKI (CI-AKI) renal
perfusion should be maximized (NSS or sodium bicarbonate solutions and administration
of oral acetylcysteine 600 mg every 12 hours for four doses)
○ Diuretics are not recommended to treat or prevent AKI, except for
management of volume overload
Prevention of AKI
● Rapid correction of Fluid and Electrolyte Balance
○ Isotonic Crystalloid solutions:
■ Isotonic saline (0.9% NaCl)
○ Colloid-containing solutions: “Plasma expanders”
■ Albumin, Dextran, Gelofusine
■ Hyperoncotic hydroxyethyl starch (HES) - Should be avoided!
Prevention of AKI
● Glycemic Control
○ Guidelines from the American Diabetes Association and Surviving
Sepsis Campaign
○ Target glucose level: 140-180 mg/dL; <180 mg/dL (critically ill)
■ Significant decrease the risk of AKI
 Strategies for
Treatment of AKI
General Approach
● Prerenal AKI ● Avoidance of nephrotoxins
○ Hemodynamic support ● Managing comorbidities
○ Volume replacement
● Severe AKI
● Postrenal AKI ○ Renal replacement therapy (RRT)
○ Removing the cause of obstruction
Intravenous Fluid
● Maintain and restore effective intravascular volume to assure
adequate renal perfusion
● Monitor:
○ Fluid intake
○ Urine output (≥0.5 mL/kg/hr during initial resuscitation)
○ BP (mean arterial BP≥65 mmHg)
○ Peripheral and Pulmonary edema
Intravenous Fluid
● Isotonic crystalloid
○ Preferred in the absence of hemorrhagic
shock
● Albumin
○ Preferred for hypoalbuminemia
secondary to cirrhosis or nephrotic
syndrome
● Vasopressors (*norepinephrine,
vasopressin, dopamine) in
conjunction w/ fluids
○ Preferred in critically ill patients with
vasodilatory shock
Intravenous Fluid
● Anuria or Oliguria
○ Slower rehydration
■ 250 mL boluses or 100 mL/hr short-term infusions
of isotonic saline or a balanced crystalloid solution
Establishing and Maintaining Adequate Diuresis
● Loop Diuretics ● Furosemide
○ Management of fluid overload ● Bumetanide
○ Continuous infusion of loop diuretics > Intermittent
● Torsemide
boluses
● Ethacrynic acid
○ Initial IV loading dose equivalent to Furosemide 40-80
(reserved for
mg should be administered before starting a
continuous infusion (equivalent to furosemide 10-20 sulfa-allergic
mg/hr) patients)
○ +Thiazide or K sparing diuretics→ Synergistic
○ *Metolazone - produce effective diuresis at GFR <20
mL/min
Electrolyte Management
● Hypernatremia and Fluid
retention
○ Total daily Na intake should be
monitored (nmt 3 g)
○ Monitor unintended sodium intake
from IV drugs (ie, antibiotics) or
foods can contribute to diuretic
therapy failure.
● Hyperkalemia
○ Monitor K levels daily
○ Restrict daily K <3 g/day
○ Avoid:
■ oral phosphorous replacement powders
(eg, Neutra-Phos and Neutra-Phos-K)
and alkalinizers (Polycitra)
■ Medications that promote K retention
by the kidney
Electrolyte Management
● Mild Hyperkalemia
○ Polystyrene sulfonate
(Kayexalate)
■ PO, Rectally
■ Cationic exchange resin
■ Promote the exchange of potassium
for sodium in the gastrointestinal (GI)
system
● Severe Hyperkalemia
○ IV Calcium (10-30 mL of 10%
calcium gluconate)
■ provide a temporary physiological
antidote to the cardiotoxic effect.
■ In the absence of renal impairment
→ by infusion of up to 200 mmol of
sodium bicarbonate (depending on
the degree of acidosis)
Electrolyte Management
● Severe Hyperkalemia
○ Insulin (20 units) and glucose (50 g).
○ In non-diabetic patients the insulin may
not be needed.
○ Beta-adrenergic agonists may also be
used, e.g. nebulized or injected
salbutamol. The effect may be additive to
that of insulin and glucose.
■ Beta2-adrenergic agonists: Promote cellular
re-uptake of potassium
Acidosis
● Sodium bicarbonate
○ PO: 1-6 g/day in divided doses → Not appropriate for acute metabolic
acidosis
○ IV: Isotonic sodium bicarbonate 1.4% or 1.26%, 250-500 mL over 15-60
minutes
● Dialysis
○ Extreme acidosis
Renal Replacement Therapy (RRT)
Intermittent RRT
● Intermittent Hemodialysis
● Most frequently used RRT
● Advantage:
○ widespread availability, last only 3 to 4
hours, 3x a week
● Disadvantage:
○ Hypotension
○ Venous access for dialysis can be difficult
in hypotensive patients
Continuous RRT
● To manage hemodynamically unstable patients with AKI, especially
those who cannot tolerate rapid volume removal.
● Runs continuously 24 hours a day, providing a slower but more
consistent removal of solutes and fluid over time.
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