This document provides an overview of acute renal failure in children. It defines acute renal failure, discusses causes (pre-renal, intrinsic renal, post-renal), pathogenesis, laboratory findings, biomarkers, management including fluid resuscitation, diuretics, electrolyte abnormalities, nutrition, and indications for dialysis. Management is aimed at treating the underlying cause and maintaining fluid, electrolyte and acid-base balance until renal function recovers.

1. Acute Renal failure
Dr. Abhijeet Deshmukh
Dept. of Pediatrics
Pushpagiri Medical College & RC
Tiruvalla, Kerala

2. Definition
• A clinical syndrome in which a sudden
deterioration in renal function results in the
inability of the kidneys to maintain fluid and
electrolyte homeostasis.
• Also k/a Acute renal insufficiency
• 2-3% of children admitted to pediatric tertiary
care centres
• 8% of infants in neonatal ICU.

3. pRIFLE criteria

4. Pathogenesis
PRERENAL
INTRINSIC RENAL
POSTRENAL
Dehydration
Glomerulonephritis
Posterior urethral valves
Hemorrhage
•Postinfectious
•poststreptococcal
Ureteropelvic junction
obstruction
Sepsis
•Lupus erythematosus
Ureterovesicular junction
Hypoalbuminemia
•Henoch-Schönlein purpura
obstruction
Cardiac failure
•Membranoproliferative
Ureterocele
•Anti-glomerular basement
membrane
Tumor
Urolithiasis
Hemolytic-uremic syndrome Hemorrhagic cystitis
Acute tubular necrosis
Cortical necrosis
Renal vein thrombosis
Rhabdomyolysis
Acute interstitial nephritis
Tumor infiltration
Neurogenic bladder

5. Lab Findings
 Anemia : Dilutional or hemolytic eg. SLE, renal
vein thrombosis, HUS
 Leukopenia : SLE, sepsis
 Thrombocytopenia :SLE, renal vein
thrombosis, sepsis, HUS
 Hyponatremia : dilutional
 Metabolic acidosis
 Elevated BUN, creatinine, uric acid, potassium,
and phosphate (diminished renal function); and
hypocalcemia (hyperphosphatemia).

6. • Decreased serum C3 level :
- Postinfectious glomerulonephritis, SLE,
MPGN,
• Antibodies :
- Streptococcal : PSGN
- Nuclear : SLE
- Neutrophil cytoplasmic : Wegener
granulomatosis, microscopic polyarteritis
- GBM :Goodpasture disease

8. • Sensitivity and specificity of urine Na of <20
in differentiating prerenal azotemia from
acute tubular necrosis are 90% and 82%,
respectively.
• Fractional excretion of sodium
= urine:plasma (U/P) ratio of sodium divided
by U/P of creatinine × 100.
(sensitivity and specificity of fractional excretion of
sodium of <1% in differentiating prerenal
azotemia from acute tubular necrosis are 96%
and 95%, respectively)

9. • CXR : cardiomegaly, pulmonary
congestion (fluid overload) or pleural
effusions.
• Renal USG :
hydronephrosis /hydroureter,
Nephromegaly- s/o intrinsic renal disease.
• Renal biopsy : who do not have clearly
defined prerenal or postrenal ARF

10. • Other biomarkers:
- changes in plasma neutrophil
gelatinase-associated lipocalin (NGAL)
and cystatin C levels
- urinary changes in NGAL, interleukin18 (IL-18), and kidney injury molecule-1
(KIM-1).

11. Management
• Catheterization - in newborn with
suspected posterior ureteral valves &
nonambulatory older children.

12. If there is no evidence of volume
overload or cardiac failure, intravenous
administration of isotonic saline, 20 mL/kg
over 30 min.

13. hypovolemic patients generally void
within 2 hr after bolus; failure points to
intrinsic or postrenal ARF.
Hypotension due to sepsis - vigorous
fluid resuscitation f/b continuous infusion
of norepinephrine.

14. • Diuretic therapy :
 only after the adequate hydration.
 Mannitol (0.5 g/kg) and furosemide (2-4 mg/kg) - as a
single IV dose. [Mannitol - effective in pigment
(myoglobin, hemoglobin)-induced renal failure.]
 Bumetanide (0.1 mg/kg)- an alternative to furosemide.
If urine output is not improved - continuous diuretic
infusion may be considered.
 Consider Dopamine (2-3 µg/kg/min) in conjunction
with diuretic therapy.
 There is little evidence that diuretics or dopamine can
prevent ARF or hasten recovery.

15. • Hyperkalemia
• Sr K >6 mEq/L - cardiac arrhythmia, cardiac arrest, and death.
• Earliest ECG change - peaked T waves f/b widening of the QRS
intervals, ST segment depression, ventricular arrhythmias, and
cardiac arrest.
• Exogenous sources of K : dietary, intravenous fluids, total parenteral
nutrition) should be eliminated.
• Sodium polystyrene sulfonate resin (Kayexalate) : (1 g/kg) - orally or
by retention enema when Sr K>6 mEq/L
- exchanges sodium for potassium
- can take several hours to take effect. A single dose of 1 g/kg
can lower the sr K level by about 1 mEq/L.
- Resin therapy may be repeated every 2 hr, the frequency
being limited primarily by the risk of sodium overload.

16. • If Sr K >7 mEq/L : emergency measures in
addition to Kayexalate.
 Calcium gluconate 10% solution :
1.0 mL/kg IV, over 3-5 min
 Sodium bicarbonate :1-2 mEq/kg IV, over
5-10 min
 Regular insulin : 0.1 U/kg, with glucose
50% solution, 1 mL/kg, over 1 hr

17. • Mild metabolic acidosis:
common in ARF - rarely requires
treatment.
If severe (arterial pH < 7.15; serum
bicarbonate < 8 mEq/L) or contributes to
hyperkalemia it should be corrected.

18. • Hypocalcemia :
- Primarily treated by lowering the serum
phosphorus level.
- Calcium should not be given IV except
in cases of tetany, to avoid deposition of
calcium salts into tissues.
- Follow a low-phosphorus diet,

19. • Hyponatremia
- most commonly a dilutional
- must be corrected by fluid restriction.
- hypertonic (3%) saline - limited to
symptomatic hyponatremia
(seizures, lethargy) or those with a serum
sodium level <120 mEq/L.

20. • GI bleeding
 because of uremic platelet
dysfunction, increased stress, and heparin
exposure in hemodialysis.
 Oral or intravenous H2 blockerRanitidine.

21. • Hypertension

Common in ARF patients with acute
glomerulonephritis or HUS.
 Salt and water restriction, diuretics
 Isradipine (0.05-0.15 mg/kg/dose,
amlodipine, 0.1-0.6 mg/kg/24 hr qd or divided bid
propranolol, 0.5-8 mg/kg/24 hr divided bid or tid;
labetalol, 4-40 mg/kg/24 hr divided bid or tid
 severe symptomatic hypertension - continuous
infusions of sodium nitroprusside or esmolol

22. • Neurologic symptoms
 Headache, seizures, lethargy, and confusion
(encephalopathy).
 Potential etiologic factors - hyponatremia,
hypocalcemia, hypertension, cerebral
hemorrhage, cerebral vasculitis, and the
uremic state.
 Diazepam - most effective in controlling
seizures,
 Treat the underlying cause.

23. • Anemia of ARF
 generally mild
packed red blood cells if Hb < 7 g/dL
Slow (4-6 hr) transfusion with packed red
blood cells (10 mL/kg) diminishes the risk
of hypervolemia.

24. • Nutrition
 In most cases, sodium, potassium, and
phosphorus should be restricted.
Protein – restricted & caloric intake
maximised to minimize the accumulation
of nitrogenous wastes.
Critically ill patients with ARF - parenteral
essential amino acids given

25. • Protein :
 enough protein for growth - limiting high protein intake.
 Protein needs increase on dialysis.
 Foods with protein include
eggs
milk
cheese
chicken
fish
red meats
beans
yogurt
cottage cheese

26. • Sodium.
 Depend on stage of their kidney disease, their
age, and sometimes other factors.
 Foods high in sodium include
• canned foods
• some frozen foods
• most processed foods
• some snack foods, such as chips

27. Potassium.
Low-potassium
High-potassium
- apples
––cranberries
––strawberries
––blueberries
––raspberries
––pineapple
––cabbage
––boiled cauliflower
––mustard greens
- oranges
––melons
––apricots
––bananas
––potatoes
––tomatoes
––sweet potatoes
––cooked spinach

28. Health care team
•
•
•
•
•
•
•
•
pediatrician
nephrologist
dialysis nurse
transplant coordinator
transplant surgeon
social worker
financial counselor
dietitian

29. Dialysis
• Indications
 Volume overload with evidence of hypertension
and/or pulmonary edema refractory to diuretic therapy
 Persistent hyperkalemia
 Severe metabolic acidosis unresponsive to medical
management
 Neurologic symptoms (altered mental status, seizures)
 Blood urea nitrogen >100-150 mg/dL (or lower if
rapidly rising)
 Calcium:phosphorus imbalance, with hypocalcemic
tetany

30. Thank You !

31. Referances
• Nelson Textbook of pediatrics 19 th edition
• Treatment Methods for Kidney Failure in
Children (National instt. of Diabetes & Kidney
disease)