AKI

By
Assist Prof.
Dr. Amin Turki
By
Assist Prof.
Dr. Amin Turki
L5: Acute Kidney Injury
Acute kidney injury (AKI) (formerly called acute renal failure) is a clinical syndrome in which there is sudden deterioration in renal function results in inability of the kidney to maintain fluid and electrolyte homeostasis.
Classification:
AKI is classified by pediatric-modified RIFLE criteria in to Risk of AKI, renal Injury, renal Failure, Loss of renal function and End stage renal disease according to reduction in the creatinine clearance and urine output as following:
CRITERIA
ESTIMATED CREATININ CLEARANCE
URINE OUTPUT
Risk
decrease by 25%
<0.5 mL/kg/hr for 8 hr
Injury
decrease by 50%
<0.5 mL/kg/hr for 16 hr
Failure
decrease by 75% or <35 ml\min\1.73 m2
<0.3 mL/kg/hr for 24 hr
or anuria for 12 hr
Loss
Persistent failure >4 wk


End-stage
End-stage renal disease
(persistent failure >3 mo)

** Other classification of AKI according to rise in serum creatinine:

stage 1: S. creatinine >150% of normal
stage II: S. creatinine >200% of normal
stage III: S. creatinine >300% of normal

Etiology and Pathogenesis: AKI classified according to its etiology into 3 categories:

1. Prerenal AKI, also called prerenal azotemia, is characterized by decreased effective circulating arterial volume, causing inadequate renal perfusion and a decreased GFR. Evidence of kidney damage is absent.
Causes:
Dehydration, sepsis, hemorrhage, severe hypoalbuminemia, and cardiac failure.
**If the underlying cause of renal hypoperfusion is reversed, renal function returns to normal. If hypoperfusion is persist, intrinsic renal parenchymal damage will develop

2. Intrinsic (Renal) AKI : characterized by renal parenchymal damage, most commonly due to ischemic/ hypoxic injury and nephrotoxic insults.
Causes:
Glomerulonephritis: postinfectious GN, SLE nephritis, HUS nephritis, membranoproliferative GN
Acute tubular necrosis and Cortical necrosis
Renal vein thrombosis
Acute interstitial nephritis (due to hypersensitivity to drugs or infectious agents)
Tumor infiltration
Tumor lysis syndrome.
3. Postrenal AKI characterized by obstruction of the urinary tract. In a patient with 2 functioning kidneys, obstruction must be bilateral to result in AKI. Relief of the obstruction usually results in recovery of renal function, except in patients with associated renal dysplasia or prolonged urinary tract obstruction.
Causes:
posterior urethral valves
bilateral ureteropelvic junction obstruction
urolithiasis (stones)
tumor (intra-abdominal or renal)
hemorrhagic cystitis
neurogenic bladder


CLINICAL MANIFESTATIONS:
A careful history and clinical examination are critical to identify the cause of AKI.
History:
infant with a history of vomiting and diarrhea most likely has prerenal AKI caused by dehydration, or hemolytic-uremic syndrome.
A neonate with a history of hydronephrosis on prenatal ultrasound and a palpable bladder most likely has congenital urinary tract obstruction, mostly due to posterior urethral valves.
child with a history of recent pharyngitis who presents with periorbital edema, hypertension, and gross hematuria most likely has intrinsic AKI related to acute postinfectious GN.
Physical examination:
Tachycardia, dry mucous membranes, and poor peripheral perfusion suggest hypovolemia and the possibility of prerenal AKI.
Hypertension, peripheral edema, rales, and a cardiac gallop suggest volume overload and the possibility of intrinsic AKI from GN or acute tubular necrosis.
The presence of a rash and arthritis might indicate SLE or Henoch-Schönlein purpura nephritis.
Palpable flank masses may be seen with renal vein thrombosis, tumors or cystic disease

Investigations:

Urinalysis (GUE) should be obtained in all children with AKI:
In prerenal azotemia, the GUE is unremarkable with a high specific gravity which indicate good renal retention of water in case of renal hypoperfusion.
The presence of hematuria, proteinuria, and RBC or granular urinary casts suggests intrinsic AKI, especially glomerular disease and ATN.
The presence of WBCs and WBC casts with low-grade hematuria and proteinuria suggests tubulointerstitial disease.
Urinary eosinophils may be present in drug-induced interstitial nephritis.
CBC: shows:
Anemia: dilutional or hemolytic, as in SLE, renal vein thrombosis, HUS
Leukopenia: in SLE, sepsis.
Thrombocytopenia: in SLE, renal vein thrombosis, sepsis, HUS
3. Other blood tests: hyponatremia (dilutional); metabolic acidosis; increased BUN, creatinine, uric acid, potassium, phosphate ( due to diminished renal function); and
hypocalcemia (due to hyperphosphatemia).
4. The serum C3 level may be decreased as in postinfectious GN, SLE, or membranoproliferative GN.
Chest XR may reveal cardiomegaly, pulmonary congestion or pleural effusions.
Renal ultrasonography can reveal hydronephrosis and/or hydroureter, which suggest urinary tract obstruction, or hydronephrosis.
Renal biopsy indicated in patients who do not have clearly defined prerenal or postrenal AKI.


Clinical and laboratory differentiation between 3 types of AKI
LABORATORY/
CLINICAL FEATURE
PRERENAL
RENAL
POSTRENAL
Urine output
Low
Low, normal, or high
Low or normal
Urinalysis
Normal
RBCs, WBCs, protein, casts
Variable
Urine Na+ (mEq/L)
Child <15
Neonate <20–30
Child >40
Neonate >50
Variable, may be >40
FENa (fractional Na excretion (%)
Child <1
Neonate <2.5
Child >2
Neonate >2.5
Variable, may be >2
Urine osmolality
(mOsm/L)
Child >500
Neonate >350
Child ∼300
Neonate ∼300
Variable, may be
<300
Renal ultrasound
Normal
Increased echogenicity, decreased
corticomedullary differentiation
Hydronephrosis


Treatment of AKI:
Bladder catheterization for patient with U.T. obstruction to ensure urinary drainage and for accurate monitoring of UOP.
Fluid and diuretics therapy:
Normal saline( bolus) 20ml\kg\30 min for plasma expansion in patients with decrease renal perfusion (hypovolemia) after exclusion of heart failure and fluid overload. It might repeated 2-3 times.
Hypovolemic patients usually pass urine within 2 hours after rehydration. Failure of passing urine suggest intrinsic or postrenal AKI.
Diuretic therapy is indicated in hypervolemic patients after establishment of adequate circulatory volume. It include:
Furosemide 2mg\kg with manitol 0.5g\kg as a single dose.
If the UOP not improved, continuous diuretic infusion may be indicated.
Dopamine 2-3Mg\kg\min PLUS furosemide to increase renal cortical perfusion.
There is little evidence that diuretics or dopamine can prevent AKI or facillate the recovery but manitol may be effective in prevention of pigment-induced AKI (myoglobin, hemoglobin)
If there is no response to diuretic therapy, it should be stopped and fluid daily intake should be limited to 400ml\m2\24 hr (insensible loss) Plus the urine output and extrarenal loss (blood and GIT).
Close monitoring of fluid intake, UOP, stool output, body weight and serum electrolytes.

Management of hyperkalemia:

Rapid development of hyperkalemia (S. K >6 mEq/L) can lead to cardiac arrhythmia, cardiac arrest, and death.
The earliest ECG change is peaked T waves. This may be followed by widening of the QRS, ST segment depression, ventricular arrhythmias, and cardiac arrest.
Treatment:
Eliminate exogenous K sources (dietary, IV fluids, total parenteral nutrition).
Sodium polystyrene sulfonate resin (Kayexalate), 1 g/kg, given orally or by retention enema. It exchanges sodium for potassium in the GIT enhancing its excretion but it take several hours to take its effect.
A single dose of 1 g/kg can lower the serum potassium level by about 1 mEq/L. It may be repeated every 2 hr. according to the severity of hyperkalemia.
More severe cases (S. K >7 mEq/L), especially if associated with ECG changes, require emergency treatment in addition to Kayexalate. This include:
Calcium gluconate 10% solution, 1 mL/kg IV, over 3-5 min. It counteracts the potassium-induced increase in myocardial irritability but does not lower the S. K
Sodium bicarbonate, 1-2 mEq/kg IV, over 5-10 min
Regular insulin, 0.1 units/kg, with glucose 50% solution, 1 mL/kg, over 1 hr
β-adrenergic agonists (Salbutamol) in adults, but it not proved in pediatrics.
Sodium bicarbonate, insulin, and glucose and β-adrenergic agonists lowers the S. K. level by shifting K from the extracellular to the intracellular compartment
Dialysis indicated in persistent hyperkalemia despite the previous treatments.


Treatment of severe metabolic abnormalities including metabolic acidosis, hypocalcemia, and hyponatremia.
Treatment of hypertension: by salt and water restriction, diuretics, Ca. channel blocker or B-blockers.
Treatment of anemia: It is usually mild dilutional anemia (Hb 9-10g\dl) but severe anemia (Hb < 7g\dl) might occur with SLE, HUS, active bleeding or prolong AKI required packed RBCs transfusion 10 ml\kg over 4-6 hr to avoid hypervolemia.
Nutritional therapy:
Restriction of Na, K, and Ph intake.
Protein intake moderately restricted to avoid accumulation of nitrogenous waste products.
Parenteral hyperalimenation with essential aminoacids in critically ill patients.
Dialysis: indicated in:
Anuria/oliguria
Volume overload with hypertension and/or pulmonary edema refractory to diuretic therapy
Persistent hyperkalemia
Severe metabolic acidosis unresponsive to medical management
Uremia (encephalopathy, pericarditis, neuropathy)
Blood urea nitrogen >100-150 mg/dL (or lower if rapidly rising)
Calcium: phosphorus imbalance, with hypocalcemic tetany refractory to other treatments.