Acute Kidney Injury (AKI)

By
Prof Grace Irimu
Consultant Pediatrician and
Nephrologist
 Outline
• Definition of AKI
• Causes of AKI
• Types of kidney injury, diagnosis and
treatment
– Prerenal failure
– Intrinsic kidney failure
– Post-renal
• Treatment of complications of AKI
 Acute Kidney Injury(AKI)
ARF is a clinical syndrome in which sudden
deterioration in renal function results in the
inability to maintain fluid and electrolyte
homeostasis
• Occurs in 2-3% of children admitted in
tertiary care centers
• Occurs in 8% of infants in NICU
 Paediatric Modified pRIFLE
criteria
Estimated Creatinine Urine output
clearance (eCCl)
Risk eCCl decrease by 25% <0.5ml/kg/hr for 8hrs
Injury eCCl decrease by 50% <0.5ml/kg/hr for 16hrs
Failure eCCl decrease by 75% <0.3ml/kg/hr for 24hrs
OR anuric for 12hrs
loss Persistent failure >4 weeks
End stage Persistent failure >3 months
 Cause of AKI
3 large groups of causes are recognized.
• Pre-renal
• Intrinsic
• Post renal (obstructive)
 Common causes of AKI
Pre-renal Intrinsic renal – renal
parenchymal damage
Dehydration Glomerulonephritis
-Post infectious eg post-
Haemorrhage
streptococcal
-Lupus erythematosus
Sepsis -HSP
Hypoalbuminemia -Membrano-proliferative
-Anti GBM
Cardiac failure Haemolytic uremic syndrome
Acute tubular necrosis
Renal vein thrombosis
Rhabdomyolysis
Tumour infiltration
Tumour lysis syndrome
Acute interstitial nephritis
Post renal
Post urethral valves
Uretero- pelvic
junction obstruction
ureterocele
Uretero- vesicular
junction obstruction
Tumour
urolithiasis
Neurogenic bladder
In patient with 2
kidneys obstruction
have to be bilateral
 Pre-renal
There is an inadequate perfusion of the kidney or due to
hypoxia.
If the decreased perfusion is reversed promptly, kidney
function improves.
• Decreased true intravascular volume
-Gastrointestinal losses
-Salt wasting renal or adrenal cause
-Burns
-Dehydration from other causes
-Third space losses (sepsis, Nephrotic syndrome)
• Decreased effective intravascular volume as in CCF
• Hypoxia -Pneumonia, Respiratory distress syndrome
 Prerenal failure
• The kidneys are intrinsically normal, with
restoration of renal perfusion the renal
function becomes normal
• Decreased GFR – amount of filtrate decreases.
Urea is reabsorbed in the DT but not
creatinine thus BUN/CR ratio >20
 Compensatory mechanisms of renal
hypoperfusion:
• Perfusion is maintained by vasodilatation of
renal microvasculature mediated by
prostaglandins eg prostacyclin. Administration
of NSAIDS- aspirin, ibuprofen can inhibit
this ppt ARF
• When the renal perfusion pressure is low the
GFR is preserved by increasing efferent
arteriolar resistance mediated by angiotensin
II. Use of ACEI can ppt ARF
Very intense vascular constriction leads to
hypoxic ischemic injury /acute tubular necrosis
 Prerenal failure vs ATN
• If no proper mnx prerenal failure evolves to acute
tubular necrosis (intrinsic kidney damage)
• In prerenal failure the tubules are working
appropriately conserves water &solutes
-urine of high osmolarity, low urinary sodium
• In ATN the tubules have irreversible damage
Urine:plasma diagnostic indices
acute pre-renal acute intrinsic
failure failure
urine osm >500 <350
UNa <20 >40
FeNa <1% (<2.5% in neonates) >3%
Fe(Na) = (UNa/PNa) / ( UCr/P Cr) X 100
 Effects of ARF
The kidneys are unable to perform their major
functions of:-
• Fluid and electrolyte balance
• Blood pressure control
• Regulation of acid-base balance
• Hormonal control
• Excretion of toxic products of metabolism
 Treatment of prerenal failure
• Restore circulation:
• Dehydration due to loss of fluid – Normal
saline 20ml/kg over 30min-1hr .
• If urine output does not improve catheterize
patient and fix CVP line to guide fluid
management
• If urine output improves manage dehydration
as per WHO guidelines
• If after volume restoration patient does not
void in 2 hrs suspect intrinsic kidney
damage.
Ct/ Treatment of prerenal failure
• CCF, pneumonia  specific Rx , dopamine
• Nephrotic syndrome  use albumin infusion
• Hemorrhage  Volume expanders e.g. normal
saline , blood as soon as available
• USE DIURETICS IF NEEDED ONLY AFTER
RESTORATION OF VOLUME OR CVP IS
NORMAL.
• STOP NSAIDS, ACEI, AND NEPHROTOXIC
DRUGS
 Causes of intrinsic failure
• Acute tubular necrosis ATN – may evolve from prerenal failure
• Drug nephrotoxicity may be due to acute tubular necrosis
Aminoglycosides
IV contrast peak rise of Cr 3-5 days latter
NSAIDS, acetaminophen, cisplatin,
• Acute cortical necrosis
Ischemic/hypoxic insults more common in the neonates– may
have hematuria( gross or microscopic), HTN, thrombocytopenia,
Oliguria and azotemia
• Endogenous toxins
Hemoglobinuria myoglobinuria blood positive on dipstick
UA but no RBCs on microscopy
 Ct/ Causes of intrinsic failure
• Glomerulonephritis
-Poststreptococcal
-Lupus erythematosus
-Membranoproliferative
-Idiopathic rapidly progressing GN
• Vascular
-Hemolytic uremic syndrome
(azotemia, thrombocytopenia, anaemia-
MAHA) commonest cause of ARF in toddlers.
Follows E.coli GE.
-Renal vein thrombosis esp in neonates
 Ct/ Causes of intrinsic failure
• Interstitial Nephritis
-Drugs
(Pencillins,Rifampicin,NSAIDs,sulfonamides
(Rash,fever,eosinophilia, +/-eosinophiluria)
• Tumors
-Renal parenchymal infiltration
-Uric acid nephropathy (esp.ALL,B-cell
lymphomas)
 Acute kidney injury.
Proposed mechanism of renal injury:
• Intrarenal heamodynamics
 -Insult to renal tubular epithelium leads to release of vasoactive
substance eg endothelin that lead to vasoconstriction of the
afferent and efferent arterioles(lowers GFR)  oliguria
 The decrease in GFR is an adaptive response and prevents
severe depletion of ECF
 Vasomotor nephropathy may be a more appropriate term for
ARF.
• Activation of the coagulation system within the kidney  small
vein thrombosis.
 Intrinsic renal failure.
Proposed mechanism of renal injury(nephronal
factors)
• Tubular obstruction due to sloughing of the brush
boarder.
• Vascular endothelial injury causes upregulation of
adhesion molecules (enhances impaction of cells to
the nephron)
• Passive backflow of the glomerular filtrate across
injured tubular cells into the peritubular capillaries
Post-renal Causes
• Obstruction of the urinary tract
-Post urethra valves
-Tumor
-Bilateral ureteral obstruction
-Neurogenic bladder
 Signs and symptoms
S/S of the precipitating illness
• Diarrohea,vomiting,bleeding.
• URTI PSAGN
• SLE  skin rash, joint pains, fever
• Henonch Schonlein purpura  skin rash
• Drug ingestion (previous 44 days)
• RVT in neonates
• Recent UTI - obstructive uropathy
• Pain +/-heamaturia
 S/S Related to renal failure
1.Oliguria or anuria
2.Pallor
3.Oedema
4.Hypertension
5.Uremic encephalopathy – Vomiting,
lethargy, behavioral changes
S/S related to complications of
ARF
-Fluid overload - CCF, pulmonary odema
-seizures
-coma
-gastrointestinal bleeding 2 to stress ulcers
 Investigations
• Blood urea nitrogen and creatinine
• Electrolytes (Na, K, Ca,PO,) –
• Blood gasses if serum HCO3 is less than 20 mEq/l.
• Uric acid
• Serum C3 levels (decreased in post strept. GN,
Lupus and membrano-proliferative)
• ASOT
• HIV, Hep B surface antigen, Heb C antibody
• ANA if positive ds DNA
 Ct/ Investigations
• Urine electrolytes (Na, creatitine) to differentiate
prerenal from ITN
• Urinalysis & microscopy C/S
-Protenuria rbc’s wbc’s casts suggest
intrinsic renal failure
-Eosinophils – drug induced tubule-interstitial
nephritis
• FBC & PBF + platelet count and ESR
• Blood sugar- may be due to poor feeding
• Blood slide for malaria parasite
• Renal biopsy depending on the cause
 Imaging
• Renal ultrasound should be done urgently
for every patient to rule out obstruction.
 Treatment
• Proper hydration of dehydrated patients
• Avoidance of nephrotoxic drugs as much as
possible
• Avoid use of prostaglandin synthetase inhibitor
and ACEI in patients with volume depletion and
renal hypoperfusion
• Proper hydration when toxic insults are
anticipated eg proper hydration in child receiving
chemotherapy, intravascular contrast(1.5 times
normal daily fluid requirement)
• Treatment depends on underlying causes.
 Treatment
If hypovolemic:
Normal saline 20mls/kg-to run in 30 min
-1hour
If no urine output within 2 hours. Reassess
patient and catheterize patient
 If well hydrated use diuretic
• Frusemide 2-4mg/kg as a single dose
• IV mannitol 0.5g/kg over 30 min (do not repeat
dose)
• Low dose dopamine 0.5-5 microgm/kg/min
These interventions may improve the urine flow.
It makes dietary & fluid mnx easier but does not
alter the course of renal failure
 Treatment of Intrinsic kidney
Failure
• Treat depending on the cause. Use relevant
guidelines
• Guidelines for management of AGN, HUS

• Give supportive treatment

• Treat any complications as for above
Restrict fluid input to a minimum if patient oliguric
insensible + previous = intake
loss days output
insensible loss 400ml/m2/day
IVF 10-30% dextrose
May decrease the fluid intake than shown above if patient
already has fluid overload.
Best guide is weight. Should be taken daily.
BP should be monitered carefully.
During recovery - diuretic phase adjust fluid requirement
accordingly. Stop the diuretics
 Nutritional support
Prompt and proper nutrition improves
outcome of ARF
• Protein 1-2g/kg (high biological value)
• low potassium avoid citrus fruits, most
fruits, bananas
• low phosphate,
• low soduim .
 Treat Complications
1. Hyperkalemia
Stop any medication, IVF and foods which can cause
hyperkalemia
-exchange resin 1gm/kg PO 2hourly or PR in sorbital
If >7mEq/l or ECG changes
• Above treatment
• 10% calcium gluconate 0.5ml/kg over 10 min (max 10ml)
• NaHCO3 1mEq/kg over 30 min if there is acidosis
• Glucose and insulin (glucose-1ml/kg of 50% dextrose ie
0.5g/kg of glucose + Insulin 0.1 unit/kg over 1hr)
Monitor blood sugar and K may need to repeat infusion
6 hourly until dialysis
• Beta agonists
 Treat Complications
2. Severe acidosis

0.5-1 mEq/kg of NaHCO3Give in 30mins.

If the child’s CNS is intact respiratory compensation

will provide partial compensation of acidosis. If
obtunded acidosis may be severe.
The remainder to be corrected orally after knowing
serum Ca.
Intact respiratory system is necessary
 Hypertension

• More than ≥95th

percentile for age,
gender and height
• Appropriate size
of the cuff
– Too small cuff –
overestimate
 Hypertension
Mild-Moderate HTN
Salt and water restriction and diuretic
Amlodipine 0.1-0.6mg/kg/24hrs (OD or BD)
Severe HTN / hypertensive encephalopathy
-Continuous IV medication
-IV sodium nitroprusside
-IV labetolol
Hypocalcemia
• Low phosphate diet and phosphate binders (eg Tums
tablets-Calcium carbonate, selemer (Renagel)
• If severe or bicarbonate therapy is necessary
give 10% calcium gluconate 0.5-1 ml/kg (max.
10ml) over 15min
• Hyperphosphatemia : Dietary restriction and
phosphate binders.
Oral calcium carbonate and other calcium
compounds bind phosphorous and prevent its
absorption. Should be taken just before meals.
It also provides calcium
calcium carbonate 30-50mg/kg/dose 6 hourly
 Stress ulcers
GIT bleeding - anti acids
Rantidine 1mg/kg /dose TDS (max
50mg/dose).
• Adjust Other medication required for the degree of
renal failure
Management of post-renal failure
Diagnosis is made from:
• History
• Clinical examination and insertion of
urethra catheter ( or vescicostomy in
selected cases)
• Renal/bladder ultrasound
Management of post-renal failure
Management is surgical ( NO DIURETICS!!!)
• An indwelling urethra catheter should be inserted
immediately using sterile procedure
• If the obstruction is relieved investigate the patient
to determine the level of obstruction. –
Renal/bladder ultrasound, MCU, DTPA
• In most cases surgical intervention is required
• if urine is obtained on catheterization surgical
intervention is required immediately.
• Anticipate post-obstructive diuresis and manage
accordingly. May need IVF.
 Estimation of GFR from
Plasma creatinine
(if children with normal habitus)
Estimated GRF(ml/min/1.73m2)=kL/PCr
K is a constant derived from body surface area
L is by length in cm
PCr is Plasma creatinine in micromol/l

K values
Low birth weight during first year of life =29
Term AGA in first of life =40
Children and adolescent girls =48
Adolescent boys =62
 Indications For Renal Replacement
Therapy
Haemodialysis, Peritoneal dialysis, hemofiltration)
• Severe acidosis not responding to treatment
• Hyperkalemia not responding to Rx
• Volume overload with CCF not responding to Rx
• Uremic toxicity
• To facilitate nutritional support and fluids for
medicine
 Outcome
Mortality in high. 42%
Poor prognosis in HUS and in those with
neurological complications.
Infections are the important cause of death.