Download - Acute kidney injury(AKI)
ACUTE KIDNEY INJURY
Acute kidney injury (AKI) is abrupt reduction in kidney
functions as evidence by changed in laboratory values; serum
creatinine, blood urea nitrogen(BUN)and urine output.
Acute kidney injury (AKI) is diagnosed if one of the
following criteria is met :
increase in serum creatinine (SCr) of at least 0.3 mg/dL
within 48 hours,
a 50% increase in baseline SCr within 7 days, or
a urine output of less than 0.5 mL/kg/hour for at least 6
hours.
EPIDEMIOLOGY AND ETIOLOGY
Between 5% and 7% of all hospitalized patients develop
AKI.
A greater prevalence of AKI is found in critically ill
patients ( ICU-Acquired AKI).
Despite improvements in the medical care of individuals
with AKI, mortality generally exceeds 50%.
CLASSIFICATION OF AKI
Criteria used for AKI classification
RIFLE: Risk, Injury, Failure, Loss of Kidney
Function and End Stage Renal Disease).
AKIN: Acute Kidney Injury Network
KDIGO: Kidney Disease Improving Global
Outcome
PATHOPHYSIOLOGY
There are typically three categories of AKI:
1-prerenal AKI
2- intrinsic AKI
3- Postrenal AKI
PRERENAL AKI
Prerenal AKI: is characterized by reduced blood delivery to the kidney.
A common causes are:
Volume depletion hemorrhage
dehydration
GI fluid losses.
Decrease effective circulatory blood volume Decrease cardiac output (CHF, MI, hypotension
Pulmonary hypertension
Liver failure
Sepsis
Functional ACEIs, NSAIDs, ARBs, Cyclosporine and tacrolimus
Prompt correction of volume depletion can restore kidney function to normal because no structural damage to the kidney has occurred.
INTRINSIC AKI
Damage is within the kidney (structure of the nephron,);
Vascular damage (renal thrombosis)
Glomerular damage (nephrotic/nephritic glomerulonephritis
Acute tubular necrosis(ATN)(it accounts for 50% of all cases of AKI)
Ischemia (hypotension, sepsis
Endogenous toxins(uric acid ,hemoglobin
Exogenous toxin
Aminoglycosides
contrast induced nephropathy (CIN)
amphotericin B
Acute interstitial nephritis NSAIDs
infections
Prerenal AKI can progress to intrinsic AKI if the underlying condition is not promptly corrected
POSTRENAL AKI
Postrenal AKI is due to obstruction of urinary
outflow
Bladder outlet obstruction
Benign prostatic hypertrophy
Prostate cancer
Anticholinergic drug
Ureteral obstruction Malignancy
Pelvic / renal obstruction
Postrenal AKI accounts for less than 10% of cases of
AKI
Rapid resolution of Postrenal AKI without structural
damage restore kidney function
By monitoring Scr on a routine basis, it can be
estimated whether kidney function is improving or
worsening.
Kidney function can also be evaluated based on urine
output. Oliguria and anuria
Oliguria is defined as urine outputs of less than 400 ml
over 24 hours
anuria is defined as urine output of less than 50 mL over
24 hours.
CLINICAL PRESENTATION AND DIAGNOSIS OF AKI
Peripheral edema
Weight gain
Nausea/vomiting/diarrhea/anorexia
Mental status changes
Fatigue
Shortness of breath
Pruritus
LABORATORY TESTS
Elevated Scr (normal range approximately 0.6-1.2
mg/dL [53 to 106 μmol/L])
Elevated BUN concentration (normal range
approximately 8 to 25 mg/dL [2.9-8.9 mmol/L])
Decreased CrCl (normal 90–120 mL/min)
BUN: creatinine ratio
greater than 20:1 in Prerenal AKI
Less than 20:1 in intrinsic or Postrenal AKI
Hyperkalemia
Metabolic acidosis
PREVENTION APPROACHES
Non-pharmacology for prevention
Hydration to prevent contrast induced nephrotoxicity
KDIGO guideline recommend using normal saline or
sodium bicarbonate infusion
Normal saline regimen: 1ml/kg/h for 12hours before
and after procedure.
Sodium bicarbonate regimen: 3ml/kg/hours for one
hour before procedure and 1ml/kg/hours for 6 hours
postcontrast.
PHARMACOLOGICAL THERAPY
For prevention of CIN
Ascorbic acid:3g orally pre and 2mg orally for two
doses postprocedure and N-acetylcysteine(600-1200mg
orally every 12 hours for 2-3 days, the first two doses
precontrast
Current KDIGO guideline suggest moderate control of
blood glucose to level of 110-149 mg/dl with insulin
prevent ICU-Acquired AKI
Goal of treatment:
Minimize the degree of kidney insult
Reduce extrarenal complication
Restoration of renal function to pre AKI is the
ultimate goal
TREATMENT APPROACHES
Currently, there is no definitive therapy for
AKI, supportive care is the mainstay of
management regardless of etiology.
SUPPORTIVE CARE IN AKI
Supportive care includes :
Adequate nutrition,
correction of electrolyte and acid-base abnormalities
(particularly hyperkalemia and metabolic acidosis)
Fluid management,
Correction of any hematologic abnormalities
Medical management of infections, cardiovascular and
GI conditions, and respiratory failure
all drugs should be reviewed, and dosage adjustments
made based on an estimate of the patient’s GFR.
NON-PHARMACOLOGICAL THERAPY
Maintenance of adequate cardiac output and blood pressure to optimize tissue perfusion
Discontinue medication associated with diminished renal blood flow
Initiate appropriate fluid and electrolyte
Renal replacement therapy RRT in sever AKI Hemodialysis
Peritoneal dialysis
Absolute indications for dialysis usually include: BUN greater than 100 mg/dL (35.7 mmol/L)
Potassium greater than 6 mEq/L (6 mmol/L)
Magnesium greater than 9.7 mg/dL (4.0 mmol/L)
Metabolic acidosis with a pH less than 7.15
Diuretic-resistant fluid overload.
PHARMACOLOGIC THERAPY
Loop diuretics : are effective to reduce fluid
overload.
it can worsen AKI.
Thiazide diuretics, when used as single agents, are
generally not effective for fluid removal.
Mannitol is also not recommended for treating volume
overload associated with AK.
Potassium sparing diuretics are not recommended.
low dose dopamine LDD is not indicated in treating the
AKI.
Equipotent dose of loop diuretics (Furosemide,
bumetanide, torsemide and ethacrinic acid ) all have
similar efficacy
Ethacrynic acid is reserved for sulfa-allergic patient
Continues infusion of loop diuretic overcome
diuretic resistance
associated with less adverse effect than intermittent bolus
Dose:
Initial iv loading dose equivalent to (40-60mg
furosemide )
Continuous infusion equivalent to 10-20mg/h
STRATEGY TO OVERCOME DIURETIC
RESISTANCE
Administration of agents from different
pharmacological classes, they act synergistically
Thiazide (works on: distal convoluted tubule)
loop diuretics (works on: ascending loop of Henle)
ELECTROLYTE MANAGEMENT
Serum electrolyte should be monitored
daily.
Hyperkalemia is the most common and serious
electrolyte abnormality in AKI
Hypernatremia and fluid retention commonly
occur …require daily calculation of sodium intake
Phosphorus and magnesium should be
monitored
PREVENTION OF ACUTE RENAL
FAILURE
Avoidance
The best preventive measure for AKI, especially in individuals at
high risk, is to avoid medications that are known to precipitate AKI.
Nephrotoxicity is a significant side effect of
aminoglycosides,
ACE inhibitors, angiotensin receptor
antagonists(ARBs),(what are the risk factors?)
Amphotericin B
NSAIDs
Cyclosporine, tacrolimus,
Radiographic contrast agents GFR less than 60 mL/min
, diabetes, dehydration, age more than 65 years,
How to reduce CI-AK?