Seminar Presentation on Acute

Kidney Injury
Presenters:Temesgen Getachew
Yared Legesse
Yonas Kasahun
Yonas Zewudu

Moderator: Dr MULUKEN( MD, PEDIATRICIAN )

 Outline
• Epidemiology
• Definition
• Causes
• Pathogenesis
• Clinical Presentation
• Lab finding
• Treatment
 Objectives
After this seminar we are expected to
understand
• Definition and etiologies of AKI
• Clinical presentation and diagnosis
• Treatment principle of AKI
 Definitions

• Acute kidney injury - is a clinical syndrome in

which a sudden deterioration in renal function

the inability of the kidneys to maintain fluid and

electrolyte homeostasis.

accumulation of nitrogenous wastes in the body

occurring over days to weeks.

01/07/2024
 Definition
• The AKIN definition

• An increase in serum Cr level by 0.3mg/dl or

Percentage in Cr level≥ 50% ( 1.5 x) with in 48hrs

• Reduction in UOP to less than 0.5ml/kg/hr

over 6hrs
 CONT’D…
• PEDIATRIC-MODIFIED RIFLE (PRIFLE) CRITERIA

CRITERIA ESTIMATED CCl URINE OUTPUT

Risk eCCl decrease by 25% <0.5 mL/kg/hr for 8 hr

<0.5 mL/kg/hr for
Injury eCCl decrease by 50%
16 hr
<0.3 mL/kg/hr for
eCCl decrease by 75% or eCCl
Failure 24 hr or anuric for
<35 ml/min/1.73 m2
12 hr
Loss Persistent failure >4 wk
End-stage renal disease (persistent failure
End-stage
>3 mo)
eCCl, estimated
creatinine clearance
KIDGO modification to RIFLE and AKIN
 Classification
1. Clinical
– Prerenal
– Intrinsic renal
– Postrenal
2. Epidemiologic
– Community acquired
– Hospital acquired
3. Urine output
– Oliguric AKI
– Nonoliguric AKI
– Anuric
AKI 8
Etiology

9
Pre renal AKI

AKI 10
 Phases of ATN
• The Initiation phase
– Lasting hours to days
• Extension phase
– corticomedullary junction of the kidney
• Maintenance phase
– GFR 5-10ml/min
– Lasts 1-2 weeks
• Recovery phase
– polyuria

11
12
 Post renal AKI
obstructi on

Adapti ve
dilati on
hydro ureter/
hydronephrosis

Nephron
distructi on
 Sepsis-associated AKI
• AKI complicates more than 50% of cases of severe sepsis, and greatly increases
the risk of death

• Sepsis is the major cause of AKI in developing countries

• Mechanisms
– Generalized arterial vasodilation

– Neurohormonal activation

– Endothelial damage

– Microvascular thrombosis

– Activation of reactive oxygen species

14
 Hemolytic-uremic syndrome (HUS)

• HUS is a common cause of community acquired acute kidney injury

in young children.
Clinically it is classified as:
 D+HUS (diarrhea associated HUS) most common
 D-HUS (diarrhea negative HUS, might follow malignancy, HIV,
respiratory tract infection, SLE, malignant hypertension etc.,)

 D+HUS is caused by shigatoxin producing enterohemorrhagic

E.coli 0157:H7 (STEC) and S.dysenterie type I the commonest in
our case series.
 phatohsiology
Etiology Invasion of the gi Realse of toxin
E.Coli tact EHEC
shigella Shiga toxin

Anemia
Thrombocytopina HUS Toxin to the blood
stream
aki

Toxin attach to
Injury swollen
glomerular
Occluded
arteriolar
Platelet deposition
endothelium
 Diagnosis and Treatment

• Diagnosis
– CBC
– Peripheral blood smears
– U/A
• Treatment
– Supportive
• Fluid and electrolyte
• Control htn
– Transfusion
– Early dialysis
– Antibiotics are contraindicated
 Acute Post streptococcal Glomerulonephritis

• characterized by the sudden onset of:

– Gross hematuria
– Edema, subnephrotic proteinurea
– Hypertension, and
– Renal insufficiency
• It is one of the most common glomerular causes of gross
hematuria in children and is a major cause of morbidity
• 97% of cases occur in developing countries
 Pathogenesis

• Typical patient develops acute nephritic syndrome

• 1-2 wk after an antecedent strep. Pharyngitis or
• 3-6 wk after strep. Pyoderma
• Proposed mechanisms for the immunologic
glomerular injury include:
– Molecular mimicry
– in situ immune complex formation
– complement activation
Complications

• Hypertension (60%) ,hypertensive encephalopathy in 10% of

cases
• Heart failure
• Acute renal failure
• Hyperkalemia, hyperphosphatemia, hypocalcemia,
acidosis,seizures, and uremia
 CLINICAL PRESENTATION
Prerenal AKI patients present with symptoms of
hypovolemia

• Sweating • Thirst
• Hemorrhage • Burn
• Dizziness • Low fluid intake.
• Orthostatic • Decreased urine
hypotension. output
• Altered mental • Vomiting
status or • Polyuria
comatose .
 In intrinsic AKI patients present with:
• Hematuria • Recent blood transfusion
• Hypertension (hemolysis)
• Body swelling • Fever (sepsis).
• Proceeding skin or throat • Rash and arthralgia
infection • Exposure to certain
• Intoxication (recent exposure medication. (NSAIDS)
to radiologic agents, drug
• Chemotherapy and tumor.
overdose)
(Tumor lysis syndrome)
• Muscular pain, recent coma,
seizure, excessive exercise, • Hemoptysis; ANCA
and limb ischemia Vasculitis, Good pasture
(rhabdomyolysis) syndrome
In post renal AKI patients present with:
• Flank pain and hematuria. (Renal calculi)
• Weight loss, bleeding and signs of anemia
(Malignancy)
• Flank mass
• Trauma to lower abdomen region
• History of genitourinary surgery
• Use of drugs (acyclovir, methotrexate and
sulfonamides)
• Abdominal distension. (Neurogenic bladder
• Urgency, hesitancy and frequency of urination
 Laboratory Findings
1. CBC
• Infection
• Chronic anemia or acute blood loss
• Thrombosis.
2. Kidney function studies
• Elevated blood urea nitrogen and creatinine level.
• BUN to creatinine ratio > 2o: 1.
• Cystatin c
• Kidney injury molecule -1 (KIM -1).
3. Serum electrolyte
• Low Na, Ca and HCO3.
• High PO4, K, and uric acid.
3. Serologic tests
• ANCA, anti – GBM and ANA.
4. Urinalysis
5. Renal ultrasound
6. Renal biopsy
7. Complement testing
8. Aortorenal angiography
• Renal artery stenosis.
• Renal atheroembolic disease
9. Peripheral smear
• Hemolytic uremic syndrome.
• Thrombotic thrombocytopenic purpura.
10. Chest x-ray
11. Intravesical pressure
• Elevated if >25mmHg]
Urinary indices Pre-renal Intrincis Renal
specific gravity (>1.020 <1.010,
urine osmolality 500 mOsm/kg UOsm < 350 mOsm/kg
low urine sodium (Se/Sp - UNa < 20 mEq/L UNa > 40 mEq/L
90%/ 82%)

fractional <1% (<2.5% in neonates) >2% (>10% in neonates)

excretion of sodium (Se/Sp
- 96% and 95%)

FeNa = urine:plasma (U:P) ratio of sodium

×100
U:P of creatinine
 Treatment
• Specific treatment of the underlying cause
 General management principles
– Fluid management
– Electrolyte management
– Nutritional support
– Adjustment of drug dosing
– Renal replacement therapy
– Specific pharmacologic therapies
 Fluid management

based on volume status of the patient

• Hypovolemia
– IV NS bolus (10 to 20 mL/kg over 30 minutes,
repeated twice as needed)
– no change to urine output up to 2 hrs does not
increase and renal function fails to improve
with the restoration of intravascular volume 
bladder catheterization
Hypervolemia
• fluid removal and/or fluid restriction
• Diuretics
Monitor
Fluid intake
urine and stool output
body weight
serum chemistries
• Furosemide (2 to 5 mg/kg/dose) / Bumetanide (0.1 mg/kg)
and mannitol (0.5 g/kg) — induce a diuresis and convert AKI
from an oliguric to a nonoliguric form
– MoA: work on still functioning nephron. no effect on nonfunctioning
nephrons,  no effect on the course of the renal failure.
– Mannitol by prevention of pigment (myoglobin, hemoglobin)-
induced RF.
• If effective, LD: a continuous infusion of furosemide (0.1 to
0.3 mg/kg per hour)
• Discontinued: no response within two hours of bolus
administration.
• SE: The risk of ototoxicity and renal toxicity ,hypotension
 Electrolyte management

Oligo-anuric AKI
• Don’t give potassium or phosphorus.
• Sodium intake should be restricted to 2 to 3 mEq/kg per
day to prevent sodium and fluid retention with
resultant hypertension.

Poly-uric AKI ;are at risk for electrolyte losses

• Replace electrolyte
• Replace ongoing fluid loss
 Hyperkalemia

– most common electrolyte complication

– Occur due to impaired excretion
– often asymptomatic or symptomatic with malaise,
nausea, and muscle weakness.
– As a result, potassium levels need to be monitored
in anuric/oligo
– Dx- Serum K level, ECG
• ECG Changes of Hyperkalemia
– 5.5 – 6.5 mEq/L
• Tall, peaked T waves with a narrow base best seen on pericardial leads
• Shorted QT interval
• ST segment depression
– 6.5 – 8.0 mEq/L
• Peaked T waves
• Prolonged PR interval
• Decreased or disappearing P wave
• Widening of QRS
• Amplified R wave
– 8.0 mEq/L
• Absence of P wave
• Progressive QRS widening --- merges with T wave  form sign wave pattern
• Intraventricular /fascicular /bundle branch block
• Ventricular Fibrillation and asystole
 Metabolic acidosis
MA occur due to
 impaired renal excretion of acid,
 impaired reabsorption and regeneration of
bicarbonate.
 increase acid production high in critically-ill patients
due to shock or sepsis.
Mgt: - Hyperventilation
NaHCO3 in life threating situations
severe acidosis
contribute to hyperkalemia
Hyperphosphatemia and hypocalcemia

Hyperphosphatemia
 dietary restriction of phosphorus
 oral phosphate binders to decrease intestinal absorption of
phosphorus.
sevelamer (Renagel), calcium carbonate (Tums tablets or
Titralac suspension), and calcium acetate (PhosLo).
Aluminum-based binders,should be avoided because of
the risk of aluminum toxicity.
 Hypocalcemia
Occur due to binding
Asymptomatic or seizure, tetany
Manage by IV calcium gluconate should be
considered
 if hypocalcemia is severe and/or
 if bicarbonate therapy is required for severe acidosis
and hyperkalemia.
Tissue deposition
 Hyponatremia
most commonly a dilutional disturbance
corrected by fluid restriction.
Administration of hypertonic (3%) saline should be limited to
patients with
• 1. symptomatic hyponatremia (seizures, lethargy) or
• 2. Serum sodium level <120 mEq/L.
Acute correction of the serum sodium to 125 mEq/L (mmol/L) should
be accomplished using the following formula:

mEq sodium required = 0.6 * weight in kg × (125 − serum sodium in

mEq/L)
 GI bleeding:
Mechanism:
 uremic platelet dysfunction,
 increased stress, and
 heparin exposure if treated with hemodialysis or
CRRT
Oral or intravenous H2 blockers such as
ranitidine for prevention
 Hypertension
mechanism
• fluid overload and
• renin-mediated hypertension
• most common children with glomerulonephritis or
HUS.
management
Salt and water restriction is critical
diuretic administration may be useful.
Rapid reduction in blood pressure Ca channel blocker Isradipine (0.05-0.15 mg/kg/dose, maximum dose 5
mg qid)

Longer-acting agents such as Ca channel blockers amlodipine 0.1-0.6 mg/kg/24 hr qid or divided bid

β blockers propranolol, 0.5-8.0 mg/kg/24 hr divided bid or tid

labetalol, 4-40 mg/kg/24 hr divided bid or tid

hypertensive urgency or Ca channel blockers nicardipine continuous infusions/CI/ 0.5-5.0
emergency µg/kg/min

No sodium /CI/ 0.5-10.0 µg/kg/min

nitroprusside

β blockers labetalol /CI/ 0.25-3.0 mg/kg/hr

esmolol /CI/ 150-300 µg/kg/min
 Neurologic symptoms
• Potential etiologic factors;
 hypertensive encephalopathy,
 hyponatremia, hypocalcemia,
 cerebral hemorrhage,
 cerebral vasculitis, and the uremic state.
• Benzodiazepams- acutely controlling seizures
• subsequent therapy should be directed
toward the precipitating cause.
 Nutritional support
Aki associated with marked catabolism
• normal maintenance requirements and supplemental calories to
address the catabolic needs of the patient.
30 percent above the maintenance requirements
 infants should receive at least 120 Kcal/kg per day,
 older children, nutritional intake should be at least 150 percent of
maintenance needs.
• Tight glucose control is recommended
• Protein intake should be targeted to maintain blood
urea nitrogen (BUN) at the 40 to 80 mg/dL range as
an indication of positive nitrogen balance.
• If feasible, the enteral route is preferred over the
parenteral route for nutritional support.
• Because: it promotes gut mucosal integrity, restores
immune responses, prevents gut atrophy, reduces
the risk of nosocomial infection, and is more cost-
effective.
• Total parentral nutrition (TPN)
 Drug management
Avoidance of nephrotoxic drugs as they may
worsen the injury and delay recovery of
function.
 Dosing adjustment of renally excreted drugs.
 Dose reductions are generally necessary for
renally excreted drugs when GFR falls below
50 mL/min per 1.73 m2.
 Reference
• Nelson Text book of Pediatrics 21th Edition
• Uptodate 2018
• Medscape
THANK YOU