pediatrics AKI

1. Acute Renal
failure
management
Moderator
Dr Sudha Rudrappa
Dr. Vinayaka hegde

5. Clinical Approach to AKI:
Pre-, Intra-, and Post-Renal
History
Volume status
Ultrasound
Urinalysis US shows
Hydronephrosis
Post-Renal
Urinalysis Normal
Urinalysis
Abnormal
Tubulointerstial
Disorders
Glomerular and
Vascular Disorders
Pre-renal

7. 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).

8.  CXR : cardiomegaly, pulmonary congestion (fluid
overload) or pleural effusions.
 Renal USG :
Hydronephrosis /hydroureter,
Nephromegaly- s/o intrinsic renal disease.
Small kidney - Nephrosclerosis , CRF
 Renal biopsy : who do not have clearly defined
prerenal or postrenal ARF

12.  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)

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

16. Treatment of AKI
Aims of treatment:
1.Maintenance of Fluid and Electrolyte
Homeostasis
2.Preventing Life-threatening Complications
3.Avoiding Further Kidney Injury
4.Providing Appropriate Nutrition
5.RRT in most severe forms of AKI

17.  The treatment of AKI divided into:
 Nondialytic therapy
(supportive therapy and medical management)
 Dialytic therapy .

18. Management
 Catheterization - in newborn with suspected
posterior ureteral valves & nonambulatory
older children.

19. The nondialytic therapy:
to date the only effective nondialytic treatment of AKI entails:
1. Restoration of adequate renal blood flow
2. Avoidance of nephrotoxic medications or
those that interfere with renal compensatory
mechanisms
3. Assurance that renal perfusion has been
maximized before exposure to nephrotoxic
agents.

20. Creatinine clearance, GFR
 CrCl (ml/min/1.73m2)=
K * lengh(cm)/Pcr
K = 0.35 fr preterm/LBW till 1 yr
0.45 fr term ,<1yr
0.55 fr children & adolescent girls
0.70 fr adolescent boys

21. Est Creatinine clearnce
 (U. creatinine/ S.creatinine )Urine vol *
1.73/BSA
in Ml/min/m2

22. Assessment of the patient for fluid balance

 Weight, BP, heart rate, skin turgor and capillary
refill are each used to assess the intravascular
volume.
 1- in children who are intravascular volume
depleted, 10-20 ml / kg of normal saline can be
infused to re-establish intravascular volume
(dehydrated pt. generally void with in 2 hours) .

23. If U.O.P. does not increase and azotemia
does not improve after fluid resuscitation,
then catheterization of the blader and
central venous pressure monitoring may be
necessary to further guide fluid therapy.
the CVP normally between 2 and 12 cm H2O.
If clinical and laboratory evaluations show
that the patient is adequately hydrated, then
aggressive diuretic therapy may be
considered

24.  2- for fluid overload, fluid restriction or fluid
removal with dialysis or hemofiltration may be
instituted if the child does not respond to
diuretic therapy.
 When intravascular volume normalized,
euvoluemia can be maintained by providing
the child with fluid to replace normal water
losses from the skin, respiratory tract, and GIT
(insensible losses, 400 ml / m2
/ 24hr. + UOP)

25. Excess losses need to be accounted for as well and
replaced with the appropriate fluid.
In general, glucose containing solutions (10- 30%)
with out electrolytes are used as maintenance fluids
.
The composition of the fluid may be modified in
accordance with the state of electrolyte balance.
Daily weight measurements, BP, accurate fluid input
& output records, physical examination and
nutritional needs of the child guide on going fluid
therapy.

26. 7- Nutritional support
 . AKI is associated with marked catabolism &
malnutrition leading to delayed recovery from
AKI
 . if GIT is intact and functional, enteral feedings
with formula (similac PM 60/40 for Newborns &
infants) should be instituted .
 . Dilute formula should be given initially and then
feedings can be increase and concentrated to
achieve optimal calories intake.

27. . In older children a diet of high-
biologic-value protein, low-
phosphorus& low-potassium foods can
be used.
.Infants should receive maintenance
calories (120 Kcal/kg/day) and older
children appropriate maintenance
calories plus 20% extra calories due to
the catabolic state and malnutrition.

28. If enteral feeding are not possible, then
hyperalimentation, usually through a central
line, with high concentration of
dextrose (25%),
lipids (10-20%), and
protein (0.5-1.25g/kg/day) should be
instituted .
If the child is oliguric or anuric and sufficient
caloric intake cannot be achieved while
appropriate fluid balance is maintained,
dialysis should be initiated earlier than in the
usual case.

29. Therapy to Decrease injury and promote
Recovery
 Recovery of Renal function after ATN requires a
complex & not fully understood set of events that
leads to restoration of renal blood flow and
regeneration of renal tubular epithelial cells
 1- Post-ischemic infusion of growth factors including
 IGF-1, epidermal GF & hepatocyte GF → accelerate
recovery of renal impairment .

30. 2- Administration of melatonin-stimulating hormone,
thyroxine,
C5a receptor antagonist,
selective inhibitors of inducible nitric oxide synthase,
statins &
Novel inhibitor of the Na / H exchange subtype 3 as
well as inhibition of monocyte chemoattractant
protein 1 by gene therapy has been shown to
ameliorate AKI
3- Other studies demonstrate that anti-adhesion
molecule therapy markedly decrease ischemic
renal injury by preventing adhesion of activated
neutrophils to renal cells.

31.  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.

32.  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.

33. Table : Treatment of Hyperkalemia
Agent Mechanism Dose Onset of effect Complications
Sodium
bicarbonate
Shifts K+ into cells 0.5-1 mEq/kg IV
over 10-30 min.
15-30 min. Hypernatremia
Change in ionized
calcium level
Calcium gluconate
(10%)
Stabilizes membrane
potential
0.5-1 mL/kg over
5-15 min.
Immediate Bradycardia
Arrhythmias
Hypercalcemia
Glucose and
insulin
Stimulates cellular
uptake of K+
glucose50%
1ml/kg
insulin 0.1 U/kgIV
over 60min.
30-120 min. Hypoglycemia
β – Agonists
(albuterol)a
Stimulates cellular
uptake of K+
5-10 mg nebulizer
(adult dose)
30 min. Tachycardia
Hypertension
Sodium
polystyrene
sulfonate
(Kayexalate)
Exchanges Na+ for K+
across colonic mucosa
1g/kg PO or PR in
sorbitol
30-60 min. Hypernatremia
Constipation

34.  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

35. 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.

36.  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,

37.  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.

38.  GI bleeding
 because of uremic platelet dysfunction,
increased stress, and heparin exposure in
hemodialysis.
 Oral or intravenous H2 blocker-Ranitidine.

39.  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

40.  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.

41.  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.

42.  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

43.  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

44.  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

45. 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

46. Dialysis
Indications
 Volume overload with evidence of hypertension 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

47. Types of Dialysis
 Peritoneal dialysis
 Intermittent hemodialysis
 Continuous renal replacement therapy

48. Choice of procedure
depends on
 1. Age &size
 2. Cardiovascular status
 3. Availability of vascular acess
 4. Integrity of peritoneal membrane &
abdominal cavity
 5. Expertise available

55. Take Home Points
 Management of a patient with ARF involves:
 Treating potentially life-threatening complications
 Reversing pre-renal and post-renal causes
 Minimizing further hemodynamic and toxic insults to the
kidney stoppage of offending agent
 Admission and appropriate consultation in time
 Lack of evidence for converting oliguric to non-oliguric
ARF
 Features of the history and physical examination in
addition to relevant lab and radiologic investigations help
to determine the most likely cause(s) of ARF in a given
patient and appropriate Rx for the same

56. Referances
 Nelson Textbook of pediatrics 19 th edition
 Treatment Methods for Kidney Failure in
Children (National instt. of Diabetes &
Kidney disease)
 Bagga’s nephrology