Description of situations where acute renal failure encountered in childhood

1. • Dr.C.S.N.Vittal

2. • Abrupt loss of kidney function leading to a rapid decline in the
glomerular filtration rate (GFR), accumulation of waste products
such as blood urea nitrogen (BUN) and creatinine, and
dysregulation of extracellular volume and electrolyte homeostasis.
A reversible increase in the blood concentration of creatinine and nitrogenous waste products
and by the inability of the kidney to appropriately regulate fluid and electrolyte homeostasis.
• Susantitaphong P, Cruz DN, et al; World incidence of AKI: a meta-analysis; Clinical Journal of the American Society of
Nephrology. 2013 Sep 6;8(9):1482-93.

3. • The incidence of AKI varies from
2–5% of all hospitalizations to
> 25% in critically ill infants and
children.
• In neonates renal failure
accounts for 8 to 24% of all
admissions to NICUs

4. pRIFLE Classification 2004
Category Estimated Creatinine Clearance* (eCrCl) Urine Output
Risk (R) Decreased by 25% < 0.5 mL/kg/hr for 8 h
Injury (I) Decreased by 50% < 0.5 mL/kg/hr for 16 h
Failure (F) Decreased by 75% or
< 35 mL/min/1.73 m2
< 0.3 mL/kg/hr for 24 h OR anuric for 12
h
Loss (L) Loss of renal function > 4 weeks
End-Stage (E) End Stage Renal Disease (persistent failure >3 mo)
* Calculated bedside with:
• Schwartz equation:
eGFR = (0.41 x height in cm) ÷ serum Cr
• Counahan-Barratt Equation:
eGFR = (0.43 x height in cm) ÷ serum Cr

5. Stage Serum Creatinine Urine Output
1
• Increase of > 0.3 mg/dL within 48 hrs
OR
• Increase to 1.5 - 1.9 times baseline
• < 0.5 mL/kg/hr for 6 – 12 h
2 • Increase to 2-2.9 times baseline • < 0.5 mL/kg/hr for > 12 h
3
• Increase to 3.0 times baseline, OR
• S Cr ≥ 4.0 mg/dL, OR
• Initiation of renal replacement therapy,
OR
• eGFR < 35 mL/min per 1.73 m2 (< 18 yr)
• < 0.3 mL/kg/hr for > 24 h
OR
• anuric for > 12 h
• KDIGO: Kidney Disease Improving Global Outcomes

6. AKI
Pathogenesis

7. Etiopathogenesis - PRERENAL
Diminished effective circulating arterial volume, which leads to inadequate renal
perfusion and a decreased GFR.
• gastroenteritis;
• diabetes;
• burns;
• ileus;
• hemorrhage.
1.
Excess
Losses:
• congestive heart failure;
• pericardial tamponade;
• sepsis/shock
2.
Impaird Cardiac
Output

8. Etiopathogenesis – INTRINSIC RENAL
1
• Renal vein thrombosis
• Arterial occlusion
• Arteritis
• Hemolytic uremic syndrome.
Vascular
2
• Acute glomerulonephritis
• Postinfectious / poststreptococcal
• Systemic Lupus Erythematosus
• Henoch Schönlein Purpura
• Membranoproliferative
• Anti–GBM
Glomerular
3
• Nephrotoxins (tolune, heroin) / Drugs
(aminoglycosides, amphotericin B, radio contrasts)
• Myoglobinuria (trauma, burns)
• Crystal nephropathy (oxalates, multiple myeloma)
• Secondary to prerenal failure
Tubular

9. Etiopathogenesis - POSTRENAL
Disorders characterized by obstruction of the urinary tract

10. Acute Renal Failure - Clinical

11. Common Complications of AKI
Cardio
pulmonary
Metabolic Neurologic Gastro
intestinal Hematologic
• Metabolic acidosis
• Hyponatremia
• Hypocalcemia
• Hyperphosphatemia
• Hypermagenesemia
• Hyperuricemia
• Pulmonary edema
• Arrhythmias
• Pericarditis
• Hypertension
• Myocardial infarction
• Pulmonary embolism
• Neuromuscular
irritability
• Asterexis
• Seizures
• Mental status
changes
• Nausea
• Vomiting
• Malnutrition
• Hemorrhage
• Anemia
• Bleeding
manifestation

12. Four phases of AKI
• Decreased edema
• Normalization of
fluid & electrolytes
• Return of GFR to
70-80% normal
4
Recovery
Phase
• Renal tubular scarring
& edema
• Increase in GFR
• Daily urine output >
400 ml
• Possible electrolyte
depletion
• Osmotic effects of
high BUN
3
Diuretic
Phase
• Urine out put
< 400 ml/d or less
• Increase in Bun and
S.Creat
• Electrolyte
disturbances,
• Fluid overload and
acidosis
2
Oliguric
Phase
• Common triggering
events
• Renal Blood flow 25%
• Tissue oxygenation
25%
• Urine output < 0.5
ml/kg/hr
1
Onset
phase
Hours to days 8-14 days 8-14 days Months to years

13. Four phases of AKI

14. Acute Renal Failure - Evaluation

15. Acute Renal Failure - Investigations
01
02
03
04
05
Haematological indices
• blood film
• blood c/s
Imaging
• renal tract U/s
Biochemical indices
• renal function
• acid–base status
Urinalysis
• blood and protein, microscopy
and culture, urine electrolytes
Renal Biopsy
• in selected cases

16. Biochemical urine indices in renal failure
Parameter Prerenal Renal
Urine osmolality (mOsm/kg) > 500 < 350
Urine Na (mMol/L) < 20 > 40
U/P creatinine > 40 < 20
U/P urea > 15 < 5
FeNa = (U Na X P Cr) / (P Na X U Cr) < 1% > 3%

17. Newer Biomarkers of AKI
• Neutrophil gelatinase-associated lipocalin (NGAL)
• Interleukin-18 (IL-18)
• Kidney injury molecule 1 (KIM-1)
• Liver-type fatty acid–binding protein (L-FABP)
• Insulin like growth factor–binding protein 7
(IGFBP7)
• Calprotectin
• Urinary angiotensinogen
• Urinary microRNA
• Cystatin C

18. Conceptual model for AKI
• Clin J Am Soc Nephrol 2008; 3: 864–868

19. Assessment
RENAL
• Rule out sepsis
• Exclude obstruction
• Note urinalysis
• Assess fluid balance
• Look at drugs

20. AKI - Management Steps
A. Fluids and circulation
B. Electrolyte disturbances
– Hyperkalemia, Hyponatremia, Hypocalcemia, Hypomagnesemia
C. Acidosis
D. Nutrition
E. Hyperuricemia
F. Complications
– Anemia
– Hypertension
– Seizures
G. Renal replacement therapy

21. A. Fluid Repletion
• Dehydration is corrected by infusion of 20-30 ml/kg of NS or
R/L over 45-60 min.
• Blood transfusion s: if hemorrhage
• Potassium should not be administered until urine flow is
established
• Diuretics: if no diuresis occurs despite correction of dehydration
– frusemide (1-2 mg/kg IV)
Avoid overhydration

22. A. Fluid Restriction
• Daily fluid requirement: insensible water losses (300-!00 mL/ m2),
urine output and extrarenal fluid losses. Preferably given orally;
• Intake-output monitoring, daily weight, physical examination and
serum sodium guide fluid management.
• Patient should lose 0.5-1 % of weight every day and serum sodium
should stay within normal range.
• Indicators of fluid excess
– absence of weight loss and
– low serum sodium

23. B. Electrolyte Disturbances: Hyperkalemia
Treatment Onset of
action
Dose Duration of
action
Calcium gluconate /
carbonate (10%)
1-3 min 0.5 ml/kg over 5-10 min 50-60 min
Insulin (+/- dextrose) 15-30 min 0,5 g/kg/h with 0.1 u/kg/hr insulin 4-6 h
Salbutamol - Nebulization 30 min 4 mcg/kg in 10 ml of water over 10 min
(2.5 mg if < 25 kg or 5 mg if > 25 Kg
body wt)
2-4 h
Ion exchange resin
(Ca resonium)
2-3 h 1g/kg orally or rectally 4-6 h
8.4% Sodium bicarbonate 1-2 ml/kg IV (if acidosis +)
Hemodialysis immediate
Plasma potassium K+ > 6.5 mmol/l

24. B. Electrolyte Disturbances : Hyponatremia
• Hyponatremia : S. Na < 120 mMol/L
– Dilutional Hyponatremia: Fluid removal
– True Hyponatremia: Calculate Na loss
mMol Sodium deficit
= (140 – actual S. sodium X 0.6 X body wt in Kg)
Replace half of this deficit in first 24 hours and review

25. B. Electrolyte Disturbances : Other
• Hypocalcemia:
– Symptomatic patients - a bolus of 10% calcium gluconate 0.5 ml/kg
intravenously over 5–10 min.
– Slower correction may be achieved by an infusion of 10% calcium gluconate,
0.1 mmol/calcium/kg body weight/h.
– The dose should be adjusted by frequent blood monitoring at least 6-hourly.
– Reduction of high phosphate levels may also improve plasma calcium levels.
• Hypomagnesemia
– 50% magnesium sulfate 0.1 ml/kg intramuscularly.

26. C. Acidosis
• Isotonic (1.26%) Sodium bicarbonate IV
– Dose: 2 mMol/kg should be given intravenously as immediate treatment.
The total deficit may be calculated as follows:
(24 – the actual bicarbonate) X 0.6 X body wt in kg
• The acidosis be corrected partially by the IV route, by giving enough
bicarbonate to raise the arterial pH to 7.20 (~serum bicarbonate level of 12
mEq/L). The remainder of the correction may be accomplished by oral
administration of sodium bicarbonate after normalization of the serum calcium
and phosphorus levels.
Haemodialysis or haemofiltration will usually be required to treat severe acidosis in oligo/anuric patients.

27. D. Nutrition
• Dietary Protein
– 1.0-1.2 g/kg of in infants and
– 0.8-1.2 g/kg in older children
• Calories:
– Minimum of 60-80 Kcal/kg is recommended
• Vitamin and micronutrient supplements are provided
Once dialysis is initiated, dietary protein, fluid and electrolyte intake should
be increased.

28. E. Hyperuricemia
• No specific treatment is usually given.
• Allopurinol & an alkali therapy: in Tumor Lysis Syndrome
• Rasburicase:
– an agent that will oxidize uric acid to allantoin,
– reduces serum uric acid levels within 4 hours of IV administration.

29. F. Complications:
• Anemia
– Transfusion is only indicated if there are symptoms or the Hb
concentration is less than 6 g/dl or falling rapidly
• Hypertension
– May be due to fluid overload: Proper fluid therapy
– For sustained moderate hypertension: Beta blocker (propranolol) with or
without vasodialator (hydralazine) or Ca channel blocker (nefidipine)
• Seizures
– Anticonvulsants

30. F. Complications
• Pulmonary Edema
– Supplementary oxygen, non‐invasive ventilation, or intubation
and ventilation, depending on the state of the patient.
– Intravenous opioids
– Intravenous infusion of nitrate
– Larger doses of diuretics

31. Specific Therapy
Condition Therapy
Atypical Hemolytic Uremic Syndrome Plasmapheresis
Vasculitis with crescentic GN or SLE Immunosuppressants
Interstitial nephritis stop offending medication and
start prednisolone oral

32. • If a prolonged period of oliguria seems likely it is
better to dialyze earlier and be able to ensure
adequate nutrition as well as maintain metabolic
balance.

33. G. Renal Replacement Therapy
Indications:
• Severe hyperkalaemia, unresponsive to medical therapy
• Fluid overload with pulmonary oedema (in the context of
acute renal failure)
• Symptomatic uraemia (blood urea >30–50 mmol/l)
• Complications of severe uraemia: encephalopathy,
pericarditis, neuropathy/myopathy
• Severe acidosis (pH <7.1)
• Drug overdose with a dialysable toxin

34. • Modes
Hemofiltration
Peritoneal Dialysis
Hemodialysis

35. Peritoneal Dialysis
• A catheter is inserted in the peritoneal cavity.
• A glucose-rich fluid is drained in over a set period of time.
• The peritoneal lining acts as a membrane.
• The fluid remains inside the cavity for set period of time,
allowing osmosis, diffusion and convection to occur.
• The fluid is then drained out over a set period of time into a
collection bag.
• The fluid contains waste products and excess fluid.
• Twenty-minute rule.
• Water is dragged out of patient by the dextrose solution.

36. Peritoneal Dialysis
Advantages:
• No anticoagulation
required
• No direct blood access
needed
• No specialized staff
required
• Inexpensive
• Maintains
haemodynamic stability
• Gentle removal of fluid
and solutes
• Good fluid removal
Disadvantages:
• Time consuming
• Needs intact peritoneal
cavity
• Increased rate of infection
• Strict fluid balance required
• Daily weight
documentation
• Can compromise
respiratory status
• Requires specialized
glucose enriched dialysate
bags
• No control over fluid
removal volume

37. Haemodialysis
• Used in patients in whom there are technical difficulties encountered
in running peritoneal dialysis,
• Peritoneal dialysis is contraindicated
– children with intraabdominal sepsis,
– major intra-abdominal pathology or
– following recent abdominal surgery
• Treatment of choice for acute poisoning with nonprotein-bound drugs
or metabolic derangements such as hyperammonemia

39. Hemofiltration
• Provide controlled ultrafiltration and safe removal of fluid,
which is particularly useful in unstable critically ill patients.
• Disadvantages of continuous renal replacement therapies
is the need for anti-coagulation.

41. Haemodialysis vs Hemofiltration
Haemodialysis Hemofiltration
Diffusive therapy
• Movement of molecules down their concentration
gradient from one solution to another continues
until equilibrium is achieved in both the blood and
dialysate.
Convective therapy
• Hydrostatic pressure is applied across the
semipermeable membrane as a positive pressure
on the blood side of the membrane or a negative
pressure on the fluid collection side, or both
Removes mainly small solutes (less than 500
daltons) (e.g., K, Ca, Mg, PO4)
Removes larger molecules also as myoglobin
or cytokines
Lesser cost Costlier
Less prone for clotting More prone for clotting

42. RRT – Modes & Vascular Access
• Continuous Renal Replacement Therapy
(CRRT)
– Continuous hemodialysis (CHD)
• continuous arteriovenous hemodialysis
(CAVHD)
• continuous venovenous hemodialysis
(CVVHD)
– Continuous hemofiltration (CHF)
• continuous arteriovenous hemofiltration
(CAVH or CAVHF)
• continuous venovenous hemofiltration
(CVVH or CVVHF)
– Continuous hemodiafiltration (CHDF)
• continuous arteriovenous hemodiafiltration
(CAVHDF)
• continuous venovenous hemodiafiltration
(CVVHDF)
• Intermittent Renal Replacement Therapy
(IRRT)
– Intermittent hemodialysis (IHD)
• intermittent venovenous hemodialysis
(IVVHD)
– Intermittent hemofiltration (IHF)
• intermittent venovenous hemofiltration
(IVVH or IVVHF)
– Intermittent hemodiafiltration (IHDF)
• intermittent venovenous hemodiafiltration
(IVVHDF)

43. Novel Therapies
• Anti-endothelin antibodies
• Oxygen free radical scavengers
• Inhibitors of NO synthetases
• Infusion of Atrial Natriuretic Peptide (ANP) or synthetic
analogue Anaritide
• Lameire N, Van Biesen W, Vanholder R. Acute renal failure. Lancet 2005;365:417–30.

44. Indicators of Chronic Kidney Disease
i. Retarded physical growth
ii. Severe anemia
iii. Hypertensive retinopathy
iv. Hypocalcemia, hyperphosphatemia and high PTH
v. Features of mineral bone disease
vi. Small kidneys on imaging

45. Outcome
• AKI carries a mortality of 20-40%,
• Patients with septicaemia and HUS with prolonged anuria are associated
with poor prognosis.
• outlook is satisfactory in acute tubular necrosis without complicating factors.
• Poor outcome
– delayed referral,
– presence of complicating infections and
– cardiac, hepatic or respiratory failure.

46. Acute Renal Failure In Newborn
1. Perinatal hypoxemia, associated with birth asphyxia or respiratory distress
syndrome;
2. Hypovolemia sec to dehydration, IVH, heart disease and postoperatively
3. Sepsis with hypoperfusion
4. Increased insensible losses (phototherapy, radiant warmers, summer heat,
twin-twin transfusions, placental hemorrhage)
5. Nephrotoxic medications (aminoglycosides, ACE inhibitors
6. Renal vein thrombosis (IDMs, severe birth asphyxia, polycythaemia,
dehydration, umbilical vein catheterization)
7. Congenital anomalies of urinary tract

47. nRIFLE Classification
Category Urine Output
Risk (R) < 1.5 mL/kg/hr for 24 h
Injury (I) < 0.5 mL/kg/hr for 24 h
Failure (F) < 0.7 mL/kg/hr for 24 h OR anuric for 12 h
S. Creatinine – high at birth (1.2 mg/dL.
Returns to 0.5 mg/dL by 5-7 days of age

48. Acute Renal Failure In Newborn
Management
• Fluids: Insensible losses (30 ml/lg/d – full term or 50-100
ml/kg/d for preterm) + GI and renal losses
• Treatment of hypertension if systolic BP is > 95-100 mm Hg