ACUTE KIDNEY INJURY (AKI)
ACUTE KIDNEY INJURY (AKI)
AKI is a common clinical problem defined by an
abrupt ( < 48 h) increase in serum creatinine resulting
from an insult that causes a functional or structural
change in the kidney, with or without oliguria.
Usually AKI is reversible although few cases may
progress to chronic kidney disease.
Mortality from AKI is reported to range from 10 to
60%.
ETIOLOGY
Causes are generally subdivided into three categories:
1. Prerenal (60%):
2. Renal (35%):
3. Postrenal (5%):
ETIOLOGY
Prerenal (60%):
Decreased True Intravascular Volume
• Gastrointestinal (GI) fluid losses: vomiting, diarrhea, and
dehydration.
• Renal losses: polyuria from excessive use of diuretics, salt-
wasting tubulopathy, diabetes insipidus, and diabetes
mellitus
• Blood losses: trauma, GI bleeding, and acute (hemorrhagic)
pancreatitis
• Increased insensible losses: hyperthermia, fever, and burns
ETIOLOGY
Prerenal (60%):
Decreased Effective Circulating Volume
• Capillary leak (sepsis, dengue hemorrhagic fever)
• Congestive heart failure
• Nephrotic syndrome
• Liver failure
• vascular lesions: renal artery thrombosis and renal vein
thrombosis
ETIOLOGY
Renal (35%):
1. acute tubular necrosis
2. Nephrotoxins
3. Acute cortical necrosis
4. Glomerulonephritis/ interstitial nephritis
5. Vascular (renal vein thrombosis, umbilical artery catheter)
6. DIC
7. Vasculitis
8. Hemoglobinuria/ myoglobinuria
ETIOLOGY
Postrenal (5%):
Obstruction of the urinary tract, commonly due to inherited
anatomic abnormalities
1. urethral obstruction( stricture, posterior urethral valve,
diverticulum)
2. ureteral obstruction (calculi, crystals, clot)
3. Ureterocele
4. Tumor
5. Neurogenic bladder
CLINICAL FEATURES
Clinical features either related to the causes or as a
consequence to renal injury.
History: vomiting, diarrhea (bloody), poor fluid intake,
history of trauma, muscle ache, arthalgia, rash, fever,
history of neurogenic bladder, recent infection and
medication history.
CLINICAL FEATURES
Physical exam:
Vital signs (fever, tachycardia, hypotension or
hypertension).
Weight (gain or loss).
Mucus membranes, skin rash, signs of heart
failure, abdominal distension (ascites, distended
bladder) and edema.
INVESTIGATION
Laboratory evaluation will depend on suspected underlying etiology.
CBC &blood film
Coagulation profile
Coombs’ test (positive in SLE, negative in HUS)
Serum urea and creatinine (diagnosis of AKI)
Serum electrolytes, glucose, albumin, proteins, uric acid,
CRP & ESR
Urine Analysis (Urine protein, blood, RBC casts, granular and epithelial
casts ,pyuria with WBC and granular casts
urine microscopy, and culture
C3 and C4
Renal ultrasound
Renal Biopsy.
PRIFLE CLASSIFICATIONS
Urine output GFR-based (eCCl) RIFLE
Stage
ml/kg/h × 8 h 0.5<
% GFR decrease ≥ 25 Risk
ml/kg/h × 16 h 0.5< % GFR decrease ≥ 50 Injury
ml/kg/h × 24 h 0.3<
GFR decrease ≥ 75%
or anuric for 12 h ,or <35 ml/min/1.73 m2 Failure
Persistent failure > 4 weeks Loss
)persistent failure >3 months(
End stage
ESRD
TREATMENT
• Treatment of the cause & its consequences.
• Restore fluid balance (input – output chart) &correct
according to situation (hypovolemia or fluid overload).
• Restore electrolyte balance(Na, K, Ca, Po4……
• Restore of acid base balance.
• Treatment of complications.
• Renal replacement therapy ( dialysis either peritoneal or
HD)
• There are no absolute blood values of
blood urea or serum creatinine that define
the need for dialysis; overall clinical picture
should be taken into consideration
INDICATIONS OF DIALYSIS
Hyperkalemia, either rapidly rising or stable at a dangerously high
level that is not response to treatment.
Volume-dependent hypertension or signs of CHF not responsive to
diuretics
Severe metabolic acidosis that cannot be treated with sodium
bicarbonate
Signs or symptoms of uremia (e.g., fatigue, encephalopathy,
anorexia, pruritus, cramps, bleeding, pericarditis)
Other severe electrolyte disturbances, including symptomatic
hyponatremia, hypocalcemia, and hyperphosphatemia
Need for a blood transfusion in the presence of oligo- or anuria .
LONG-TERM FOLLOW UP OF CHILDREN WITH AKI
• • After an episode of AKI, patients should be followed
periodically with urinalysis, renal function and BP
measurements.
• If there is no recovery of kidney function within three months,
the patient is considered to have developed chronic kidney
disease (CKD)
CHRONIC KIDNEY DISEASE (CKD)
• Definition:
Kidney damage for >3 months, as defined by
structural or functional abnormalities, with or
.without decreased GFR
• Classification:
Stage I: Injury with normal or increased GFR
Stage II: GFR 60–89 mL/min/1.73 m2
Stage III: GFR 30–59 mL/min/1.73 m2
Stage IV: GFR 15–29 mL/min/1.73 m2
Stage V: GFR <15 mL/min/1.73 m2 or dialysis.
CHILDREN
Structural malformations 40%
Glomerulonephritis 25%
Hereditary nephropathies 20%
Systemic diseases 10%
Miscellaneous/unknown 5%
CLINICAL FEATURES
Anorexia and lethargy
Failure to thrive/growth failure
CLINICAL FEATURES
Polydipsia and polyuria or oliguria and anuria.
Hypertension
Bony deformities from renal osteodystrophy
(renal rickets)
Unexplained normochromic, normocytic anemia
Bleeding tendency.
CLINICAL FEATURES
Acuteonchronic renal failure (precipitated
by infection or dehydration)
CNS manifestations (encephalopathy)
Incidental finding of abnormal kidney
function tests.
Others.
CLINICAL FEATURES
Chronic kidney disease presents with:
Anorexia and lethargy
Polydipsia and polyuria or oliguria and anuria.
Failure to thrive/growth failure
Bony deformities from renal osteodystrophy (renal rickets)
Hypertension
Acute on chronic renal failure (precipitated by infection or
dehydration)
Unexplained normochromic, normocytic anemia
Bleeding tendency.
CNS manifestations (encephalopathy)
Incidental finding of abnormal kidney function tests.
Others.
DIAGNOSIS
• Renal function testes
• Glomerular filtration rate can be estimated with the following formula:
eGFR (mL/min/1.73 m2) = k × height (cm)/creat (µmol/L)
Where k=0.413
K = 0.33 for LBW infant
= 0.45 for Full term infant
= 0.55 for child or adolescent girl
= 0.7 for adolescent boy (13-18 years old)
DIAGNOSIS
• Renal ultrasound.
• DMSA scan show shrunken kidneys.
• Others:
- CBC.
- Echocardiography .
- [Link].
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- parathromone.
- Bone X-ray to detect renal osteodystrophy.
TREATMENT
Conservative treatment for :
• Balanced diet and nutritional status evaluation.
• Fluid and electrolytes balance.
• Anemia= erythropoietin , iron, folic acid
• Hypertension =antihypertensive
• Renal osteodystrophy= vit.D, calcium, restricted phosphate&
phosphate binder
• GIT disorders = antiacid
• Growth restriction= growth hormone
• Psychological support.
TREATMENT
Renal replacement therapy
Dialysis :
• Peritoneal dialysis
• Hemodialysis
Kidney transplantation
Thank you
