Acute

Kidney
Injury
SARAH ABIGAIL C. ONG SIU
Second Year Resident
 Acute Kidney Injury
● Previously known as acute renal failure
● Abrupt loss of kidney function 
● Rapid decline in GFR
● Accumulation of waste products (BUN, Crea)
● Dysregulation of extracellular volume and electrolytes
 Acute Kidney Injury
● KDIGO AKI Consensus Conference
 Prerenal AKI
● Reduced blood flow to the kidney
● Systemic hypoperfusion: hypovolemia / hypotension
● Renal hypoperfusion: renal artery stenosis
● Tubular and glomerular function stay normal
Prerenal AKI
 Intrinsic renal AKI
● Renal parenchymal damage
● Conditions that affect the glomerulus or tubule
● Acute tubular necrosis
● Acute interstitial nephritis
Intrinsic renal AKI
 Postrenal AKI
● Obstructive causes
● Unilateral obstruction may not always present as AKI
● Renal/ureteral calculi, tumors, blood clots, or any urethral
obstruction
● Most common: bladder outlet obstruction
 Clinical Manifestations and Diagnosis
● Carefully taken history is critical
● Determine etiology and timeline of progression
● History of hypovolemia or hypotension
● Diarrhea, nausea, vomiting
● NSAIDs or other nephrotoxins
● Co-morbids: cirrhosis and history of blood clots
 Physical Examination
● Thorough physical examination, with careful attention to
volume status
● Orthostatic vital signs: clue for hypovolemia
 Laboratory FIndings
● Anemia (dilutional or hemolytic): SLE, RVT, HUS
● Leukopenia: SLE, sepsis
● Thrombocytopenia: SLE, RVT, sepsis, HUS
● Hyponatremia (dilutional)
● Elevated serum BUN, creatinine, uric acid, K, and
phosphate (diminished renal function)
● Hypocalcemia (hyperphosphatemia)
 Laboratory Findings
● Low serum C3: PSGN, SLE, MPGN
● Serum antibodies to specific antigens:
● Streptococcal: PSGN
● Nuclear: SLE
● Neutrophil cytoplasmic: granulomatosis with
polyangiitis, microscopic polyarteritis
● Glomerular basement membrane (Goodpasture disease)
 Laboratory Findings
Hematuria, proteinuria, and red Intrinsic AKI (glomerular
blood cell or granular urinary casts disease, ATN)
White blood cells and white blood
cell casts with low-grade hematuria Tubulointerstitial disease
and proteinuria
Drug-induced tubulointerstitial
Urinary eosinophils
nephritis
Laboratory Findings
 Acute Kidney Injury
● Chest radiography
● Cardiomegaly
● Pulmonary congestion (fluid overload)
● Pleural effusions
● Renal ultrasonography
● Hydronephrosis and/or hydroureter: obstruction
● Nephromegaly: intrinsic renal disease
 Laboratory Findings
● Renal biopsy: determine precise cause of AKI
● Serum creatinine: insensitive
● Delayed measure of decreased kidney function
following AKI
 Medical Management
● Placement of bladder catheter
● Infants and children with obstruction
● Non-ambulatory older children
● Adequate drainage, monitor urine output
● Precautions to prevent iatrogenic infection
 Medical Management
● Diuretic therapy
● Furosemide (2-4 mg/kg) IV single dose
● Continuous diuretic infusion
● If no response to diuretic challenge  fluid restriction
 Medical Management
● Fluid restriction
● 400 mL/m2 /24 hr (insensible loss) + urine output
● Replace extrarenal (blood, GI tract) losses (ml/ml)
● Monitor fluid intake, urine and stool output, body weight,
and serum chemistries daily
 Medical Management
Hyperkalemia
● > 6 mEq/L)  cardiac arrhythmia, arrest, death
● Peaked T waves
● Widening of QRS intervals, ST segment depression,
ventricular arrhythmias, and cardiac arrest
● Eliminate exogenous sources of potassium
 Medical Management
Hyperkalemia
● Na polystyrene sulfonate resin (Kayexalate) 1 g/kg
● Exchanges sodium for potassium
● Lowers serum K level by about 1 mEq/L
● Repeated every 2 hr
 Medical Management
Hyperkalemia
● More severe elevations (>7 mEq/L)
● Calcium gluconate 10% solution
● Counteracts the potassium-induced increase in
myocardial irritability
● Does not lower the serum potassium level
 Medical Management
Hyperkalemia
● More severe elevations (>7 mEq/L)
● 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
● Dialysis: for persistent hyperkalemia
 Medical Management
Hyponatremia
● Dilutional, corrected by fluid restriction
● Hypertonic (3%) saline: for symptomatic hyponatremia
(seizures, lethargy) or < 120 mEq/L
● Acute correction to 125 mEq/L (mmol/L)
● mEq required = 0.6 x wt in kg (125 – serum Na)
 Medical Management
Hypertension
● Most common in acute glomerulonephritis or HUS
● Salt and water restriction
● Diuretic administration
● Isradipine (0.05-0.15 mg/kg/dose, max 5 mg qid): rapid
reduction
 Medical Management
Hypertension
● Longer-acting oral agents:
● Calcium channel blockers (amlodipine, 0.1-0.6
mg/kg/24 hr OD/BID)
● β blockers (labetalol, 4-40 mg/kg/24 hr BID/TID)
 Medical Management
Severe symptomatic hypertension (hypertensive urgency or
emergency): continuous infusions
● Nicardipine (0.5-5.0 μg/kg/min)
● Sodium nitroprusside (0.5-10.0 μg/kg/min)
● Labetalol (0.25-3.0 mg/kg/hr)
● Esmolol (150-300 μg/kg/min)
 Medical Management
Neurologic symptoms
● Headache, seizures, lethargy, and confusion
(encephalopathy)
● Etiologic factors: hypertensive encephalopathy,
hyponatremia, hypocalcemia, cerebral hemorrhage, cerebral
vasculitis, and the uremic state
● Benzodiazepines: control of seizures
 Medical Management
Anemia
● Generally mild (hemoglobin 9-10 g/dL)
● From volume expansion (hemodilution)
● HUS, SLE, active bleeding, or prolonged AKI
 Medical Management
Anemia
● Packed red blood cells transfusion if Hgb < 7 g/dL
● In hypervolemic patients, can precipitate hypertension,
heart failure, pulmonary edema
● Slow (4-6 hr) transfusion (10 mL/kg)
● Safely administered during dialysis or ultrafiltration
 Medical Management
Nutrition
● Restrict sodium, potassium, and phosphorus
● Protein intake should be moderately restricted
● Minimize accumulation of nitrogenous wastes
 Medical Management
Dialysis
● Anuria/oliguria
● Volume overload with evidence of hypertension and/or
pulmonary edema refractory to diuretic
● Persistent hyperkalemia
● Severe metabolic acidosis unresponsive to medical
management
 Medical Management
Dialysis
● Uremia (encephalopathy, pericarditis, neuropathy)
● Calcium:phosphorus imbalance, with hypocalcemic tetany
that cannot be controlled by other measures
● Inability to provide adequate nutritional intake because of
the need for severe fluid restriction
 Medical Management
Dialysis
● For days or for up to 12 wk (1-3 wk)
● Intermittent hemodialysis
● With relatively stable hemodynamic status
● Both fluid and electrolyte removal
● May be performed 3-7 times per week
 Medical Management
Dialysis
● Peritoneal dialysis
● Most common in neonates and infants
● Hyperosmolar dialysate is infused into the peritoneal
cavity via surgically or percutaneously placed
peritoneal dialysis catheter
 Medical Management
Dialysis
● Peritoneal dialysis
● Fluid is allowed to dwell for 45-60 min then drained
from the patient by gravity
● Repeated for 8-24 hr/day
● Anticoagulation is not necessary
● Contraindication: abdominal pathology
 Medical Management
Continuous renal replacement therapy (CRRT)
●In patients with an unstable hemodynamic status, concomitant
sepsis, or multiorgan failure
●Fluid, electrolytes, and small- and medium-size solutes
continuously removed from blood (24 hr/day)
 Prognosis
● Depends on nature of underlying disease process
● Postinfectious GN: very low mortality rate (<1%)
● Multiorgan failure: very high mortality rate (>50%)
● Recovery of renal function is likely after AKI resulting
from prerenal causes, ATN, acute interstitial nephritis, or
tumor lysis syndrome
 Prognosis
● Complete recovery is unusual in RPGN, bilateral RVT, or
bilateral cortical necrosis
● Medical management may be necessary for a prolonged
period to treat the sequelae of AKI: chronic renal
insufficiency, hypertension, renal tubular acidosis
 Prognosis
● Children with AKI are at long-term risk for developing
chronic kidney disease (CKD)
● Patients with moderate to severe AKI should be followed
annually to detect signs of CKD
(hypertension and proteinuria).
Thank you!