Study on acute kidney injury

1. ACUTE KIDNEY INJURY
DR AJITE AB
MBChB, FMCPaed

2. OBJECTIVE
1.
2.
3.
4.
5.
STUDENTS SHOULD BE FAMILIAR WITH
DEFINITION OF AKI
CLASSIFICATION
CLINICAL FEATURES
MANAGEMENT
PREVENTION OF AKI

3. DEFINITION
1.
2.
3.
The KDIGO (Kidney Disease Improving Global
Outcome) Clinical Practice Guideline for AKI,
defines AKI as any of the following:
increase in serum creatinine by ≥0.3 mg/dl (≥26.5
μmol/L) within 48 hours; or
increase in serum creatinine to ≥1.5 times
baseline, which is known or presumed to have
occurred within the prior 7 days; or
urine volume <0.5 ml/kg/h for 6 hours
3/13/2022
3

4. The term AKI was introduced by the
International Consensus Conference
on Acute Dialysis Quality Initiative
(ADQI) workgroup [Critical Care 2004]
in place of the highly restrictive and
commonly used term; acute renal
failure (ARF).

5. PAEDIATRIC RIFLE CRITERIA (PRIFLE)
Class eCCL (Schwartz) Urine output
Risk Decrease by 25 % <0.5 ml/kg/hr X 8 hrs
Injury Decrease by 50 % <0.5 ml/kg/hr X 16 hrs
Failure Decrease by 75 %, or
< 35ml/min/1.73m²
<0.3 ml/kg/hr X 24hrs
or anuria >12hrs
Loss Failure > 4 weeks
ESRD Failure > 3 months
3/13/2022 5

6. CREATININE AS A MARKER OF AKI
Serum creatinine depends not only on urinary clearance
of creatinine, but also on the rate of production and
volume of distribution
Substantial rise does not occur until 48-72hrs after the
initial result

7. Serum creatinine does not accurately reflect GFR in
a non-steady state condition such as AKI
Correct interpretation of serum creatinine across
centres is hampered by variation in calibration of
different creatinine assay

8. NOVEL DIAGNOSTIC BIOMARKERS
Waiting for classic signs of kidney failure may lead
to unnecessary morbidity and mortality, early
biomarkers are critical to assess for AKI risk
Ideal markers of AKI should:
Identify the primary location of injury
Determine the duration of kidney failure
3/13/2022 8

9. Discern AKI subtypes
Identify AKI aetiologies
Differentiate AKI from other forms of acute kidney
diseases
E.g of new biomarkers include NGAL (neutrophil
gelatinase associated lipocalin, IL-18, KIM-1,
cystatin c)

10. KDIGO STAGING OF AKI SEVERITY
AKI stage Creatinine criteria Urine output criteria
AKI stage I Increase of serum creatinine by
≥ 0.3 mg/dl (≥ 26.4 μmol/L)
or
increase to ≥ 150% – 200% from baseline < 0.5 ml/kg/hour for > 6 hours
-------------------------------------------------------------------------------------------------------------------
AKI stage II Increase of serum creatinine to
> 200% – 300% from baseline < 0.5 ml/kg/hour for > 12 hours
-------------------------------------------------------------------------------------------------------------------
AKI stage III increase of serum creatinine to
> 300% from baseline < 0.3 ml/kg/hour for > 24 hours
or or
serum creatinine ≥ 4.0 mg/dl anuria for 12 hours
≥ 354 μmol/L) after a rise of at least 44 μmol/L
or
treatment with renal replacement therapy

11. EPIDEMIOLOGY
AKI formally called ARF is reported to have an
annual incidence of 11.3 million cases in the
developing world
1.7 million death has been attributed to AKI globally,
of which 1.4 million occur among the low and
middle socioeconomic class in developing
countries

12. CLASSIFICATION
I.
II.
III.
Classification of AKI can be based on aetiology
Pre-renal
Renal
Post renal
PRE RENAL AKI- This is AKI resulting from true
volume contraction or from decreased effective
blood volume. It is reversible with prompt recognition
and intervention before tubular necrosis occurs.

13. Causes of true volume depletion Causes of reduced effective blood
volume because of reduced CO
diarrhoea Congestive heart failure
haemorrage Cardiac tamponade
burns
Nephrotic syndrome
Capillary leak syndrome

14. I.
II.
RENAL –AKI resulting from intrinsic acute
damage to the renal parenchyma
Examples of renal causes of AKI include;
AGN
Acute interstitial nephritis AIN (Drugs that
have been implicated in AKI;
aminoglycoside, NSAID, ACEi, cisplastin,
amphotericinB, radiocontrast dye.
Exogenous toxins e.g heavy metals,
methanol, ethylene glycol. Endogenous
toxins e.g haemoglobin, myoglobin

15. POST RENAL – AKI usually from
obstruction , it is relatively less common
than the previously mentioned groups e.g
posterior urethra valve (PUV),
ureterovesical obstruction from kidney
stones, tumor

16. CLASSIFICATION BASED ON URINARY OUTPUT
1.
2.
3.
OLIGURIC (Urine output < 0.5mls/kg/hr in
children and < 1mls/kg/hr in infants
NON-OLIGURIC AKI; urine output >0.5ml/kg/hr
ANURIC; Urine output < 0.039ml/kg/hr in the
absence of obstruction

17. PATHOPHYSIOLOGY OF AKI
The primary event is tubular damage
Renal insult causes vasoconstriction,
desquamation of tubular cells which results in
intraluminal tubular obstruction and back leakage
of glomerular filtrate
There is an adaptive fall in GFR due to the renal
vasoconstriction
Neutrophils adhere to ischaemic endothelium and
release substances that promote inflammations.

18. CLINICAL FEATURES
Reduction in urine output
Facial puffiness which is worse on waking up from
sleep
Bipedal oedema
Vomiting
Convulsion
Impaired level of consciousness
There may be features of underlying cause e.g dark
coloured urine in haemoglobinuria

19. INVESTIGATIONS
Urinalysis
Urine microscopy, culture and sensitivity
FBC
Renal USS
Chest xray

20. E/U/Cr
Hyperkalaemia
Hyponatraemia
Hypocalcemia
Increased level of creatinine
Increased phosphate
Increased urea
Acidosis

21. TREATMENT
Establish your diagnosis
Determine the Fractional excretion of sodium (
(FeNa) ie urine/plasma Na ratio divided by urine/
plasma Cr ratio multiplied by 100)
FeNa= Urine Na/plasmaNa × Urine Cr/plasmaCr
value <1% describes pre renal azotemia that is
potentially reversible while a value >2% indicates
tubular dysfunction and acute tubular necrosis

22. TREATMENT OF PATIENT IN HYPOVOLAEMIC
STATE/SHOCK
Hydrate patient with 20-30ml/kg of normal saline
over 30mins for older children and over 1hr for
infant. Assess the blood pressure and urine output,
if there is no change in urine output, repeat iv fluid
and give with iv frusemide 1-2mg /kg.
If urine output remains inadequate manage as
intrinsic renal AKI

23. PHASES OF AKI DURING TREATMENT
1.
2.
3.
Oligo-anuric phase- patients present in this phase
with reduction in urine output
Diuretic phase- following appropriate treatment,
the glomerular filtration improves however tubular
reabsorption of fluid and electrolyte lags behind in
recovery and there is increase fluid and
electrolyte loss(K+) in urine
Recovery- resolution of signs and symptoms of
renal insufficiency

24. TREATMENT OF AKI
In oligo-anuric phase of AKI, fluid is restricted to
300-400mls/m2/day(insensible fluid loss) +the
previous day’s output
Restriction on salt ,low phosphorus and low
potassium diet and protein intake
Antibiotic in suspected infection ceftriazone 50mg/
kg/day

25. Strict monitoring of the total fluid input and output
Monitor E/U/Cr
Dialysis

26. When the oligo-anuric phase which may last for 10
days resolves, patient goes into the diuretic phase
where there is loss of electrolyte especially K in the
urine because of the delay in recovery of the tubular
cells relative to the glomerular filtration
IV fluid is changed to Ringer’s lactate +dextrose
Calorie requirement- 300-400kcal/m2/day

27. Avoid volume depletion due to polyuria, strict I/O
monitoring and replace deficit
Review daily with e/u/cr
Patient goes into the recovery phase and normal
diet is restored
Follow up

28. MANAGEMENT OF POST-RENAL AKI:

Prompt relief of urinary tract obstruction
e.g need to pass a urinary catheter or small sized NG
tube for patients with PUV
Management for UTI, Sepsis, fluid resuscitation as
necessary
Surgical consult to treat the underlying cause

29. HYPERKALAEMIA
AGENT DOSE ONSET MECHANISM
10% Ca gluconate 0.5-ml/kg
10mins
Immediate Cardioprotective
Couteracts effects of HyperK
8.4% NaHCO3 1-2ml/kg IV 20 minutes Drive K+ into cell
Salbutamol 5mg via
Nebulization
5 minutes Drive K+ into cell
50% glucose+regular
Insulin
0.5-1g/kg
0.1U/kg over 1-2hrs
30 minutes Drive K+ into cell
Ion exchange
Resin (Kayesalate)
1g/kg in 30%
sorbitol PR or in
70% sorbitol orally.
2 hrs oral
30 minutes PR
Remove K+
Dialysis Peritoneal dialysis/
haemodiaiysis
Gradual removal over
the duration of dialysis
Remove K+

30. METABOLIC ACIDOSIS




Severe acidosis
i.v sodium bicarbonate,
Dialysis therapy
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31. HYPONATRAEMIA




Usually dilutional
Fluid restriction,
If serum Na <120mEq/L correction to a level of
approximately 125 mEq/L with hypertonic saline (3%
saline) solution over several hours.
Dialysis

32. MGT OF HYPOCALCAEMIA &
HYPERPHOSPHATAEMIA



Severe hypocalcaemia/symptomatic
hypocalcaemia
i.v 10% calcium gluconate (dil. in 5% D/W; 1 in 4) 1ml/kg
up to a max.of 10 mls
Given slowly over 30 minutes under ECG monitoring or
auscultation for the heart rate
Oral Ca supplements
Hyperphosphataemia
Oral Calcium carbonate
Aluminium containing compounds should be avoided if
possible

33. HYPERTENSION
Diuretics
Oral long acting agents e.g Calcium channel
blockers p.o Nifedipine
ACE inhibitors should be used with caution and
watch out for hyperkalaemia.
Consider dialysis.

34. TREATMENT OF UNDERLYING ILLNESS


Malaria
Treat as for severe malaria
Septicaemia
Parenteral antibiotics e.g iv Cefuroxime or I.V
ceftriaxone

35. PRESCRIBING MEDICATIONS






Drugs metabolised or excreted in the kidneys
Adjust dose based on renal function.
Avoid nephrotoxic drugs
Monitor
drug levels
potential adverse effects

36. COMPLICATIONS OF AKI
Uraemic encephalopathy, pericarditis
Bleeding
Pulmonary oedema
CCF
Progression to CKD

37. PREVENTION OF AKI
Environmental sanitation to protect against
diarrhoea and malaria
Early presentation in the hospital
ORT
Early recognition and referral of AKI cases to
nephrologists
Avoidance of unsupervised and indiscriminate use
of drugs e.g analgesics , gentamicin

38. CONCLUSION
Prevention is the key to reduce the morbidity and
mortality associated with AKI

39. TOOLS OF PREVENTION
Clinical acumen

41. SPHYGMOMANOMETER

43. PROBLEM BASED LERNING SESSION
a)
b)
c)
a)
A 2year old boy was brought to the children
emergency with 3days history of vomiting
associated with diarhoea, one day history of
reduction in urine output and loss of consciousness
What is the likely diagnosis
What is the fluid of choice in rehydrating this
child
Mention two important investigations you want
to do and state their relevance
What are the complications to look out for in this
child