Paediatric Nephrology

Nephritic, nephrotic syndrome and

AKI
Clinical case – Approach to haematuria
• M/8 yrs, presented with first attack of whole stream brown
colour urine for 2 days, now clearing
• No other urinary symptom
• Had URI symptoms within last 5 days, otherwise well
• P/E: - well, no pallor, no edema. BP 120/80. CVS,
abdomen, genitalia were all normal
• Urine multistix – large amount of blood and protein
• Urine microscopy - >100 RBC/uL
• Urine culture – no growth
• CBC, RFT were normal
• C3 normal
• Renal USS and plain AXR were normal
 Questions
Is acute post-infectious nephritis the most
likely diagnosis?
Are you concerned with the BP reading in this
case?
What further investigations are required?
Is renal biopsy indicated?

Houtman. Chapter 29. Tutorials in Paediatric Differential Diagnosis.

Glomerular Diseases
 Pathophysiology and clinical features

1. Glomerular leak of
Blood → haematuria 100% (macroscopic
30%)
Protein → proteinuria 85% (usually <
2g/m2/day)
 Pathophysiology and clinical features

2. Glomerular block i.e. a reduction in GFR

→ oliguria (50%) and uraemia
→ salt and water retention
→ volume expansion
→ edema (85%), hypertension (80%)
→ hypertensive encephalopathy, congestive heart
failure
 Pathophysiology and clinical features

3. Both leak and block

e.g. haematuria + volume expansion → anaemia

Nonspecific symptoms
– general malaise, weakness, anorexia 55%
– nausea, vomiting 15%
– dull lumbar pain 5%
Haematuria
 Causes of Haematuria
1. Trauma
2. Infection
• acute pyelonephritis
• Leptospirosis, syphilis, schistosomiasis, TB
• Bacterial endocarditis, infected ventriculoatrial
shunt
• Viral: infectious mononucleosis, acute
haemorrhagic cystitis (adenovirus)
3. Acute glomerulonephritis
4. Henoch-Schönlein (anaphylactoid) purpura
 Causes of Haematuria
5. Benign recurrent haematuria: fever, exercise, familial,
Berger’s disease
6. Chronic glomerulonephritis
7. Calculi
8. Haematological
• Bleeding: haemophilia, thrombocytopenia
• sickle cell anaemia
9. Tumour: nephroblastoma, rhabdomyosarcoma of bladder
10. Rare: haemoglobinuria, renal haemangioma, SLE,
Goodpasture’s syndrome, polyarteritis nodosa, familial
nephritis with deafness (Alport’s syndrome)
11. Polycystic kidney
Acute Nephritic Syndrome
Acute nephritic syndrome-definition
• acute onset of haematuria, proteinuria,
oliguria, hypertension and edema
Acute glomerulonephritis (or acute nephritis)
- acute inflammatory process of presumed
immunological origin affecting
predominantly or exclusively the
glomerulus. It can occur with few or even
no symptoms; acute nephritic syndrome is
only one of the clinical manifestations
 Etiology of Acute Nephritis
1. Infection
– Bacterial - Lancefield group A beta haemolytic
streptococcus, streptococcus viridans and
pneumoniae, staphylococcus species, Klebsiella
species, Brucellosis, Mycoplasma pneumoniae,
Treponema pallidum, Salmonella typhi, Leptospirosis,
meningococcus species
– Viral - Hepatitis B, Cytomegalovirus, Coxsackie B4,
Echo type 9, Influenza, mumps, measles, Epstein -
Barr virus
– Parasitic - Toxoplasmosis, Plasmodium malaria and
falciparum, Histoplasmosis, trichinosis,
schistosomiasis
– Rickettsial - scrub typhus
– Fungal - Coccidioides immitis
 Etiology
2. Acute on chronic glomerulonephritis
– membrano-proliferative glomerulonephritis
– mesangial proliferative glomerulonephritis
– IgA nephropathy
 Etiology
3. Systemic diseases associated with acute nephritic
syndrome
– Henoch - Schönlein purpura
– haemolytic uraemic syndrome
– SLE
– Polyarteritis
– Goodpasture’s syndrome
– Wegener’s granulomatosis
– essential cryoglobinaemia
 Etiology
4. Post-irradiation nephritis
5. Hypersensitivity interstitial nephritis
– Induced by drugs such as methicillin
(commonest), ampicillin, frusemide,
allopurinol, cephalothin, cephalexin, oxacillin,
phenothiazine derivatives, phenytoin,
rifampicin
6. Shunt nephritis
7. Hereditary nephritis
Acute poststreptococcal glomerulonephritis (APSGN)

• The prototypic form, account for 85% of all cases of

acute nephritic syndrome
• Age of presentation: 2-12 years (60%)
• Risk of developing nephritis after infection with
nephritogenic strain is about 15%
• Type & Site of streptococcal infection:
– pharyngitis - M type 12
– skin - M type 49, 55, 57
– middle ear
Very unusual to develop a second attack, hence no
need for prophylactic antibiotics
 Prognosis

– 90% complete recovery

– 0.5 - 2% die in acute stage from uraemia,
heart failure or encephalopathy
– < 10% develop chronic
glomerulonephritis
 Laboratory Investigation for acute nephritis

• urine examination
– microscopy of fresh urine for nephritic sediment
– haemastix, albustix
– culture
– 24 hour collection for protein and creatinine or
UPr/Cr
 Laboratory Investigation for acute nephritis
• blood
– CBP, platelet, smear, ESR
– electrolytes, urea, creatinine
– albumin, A/G ratio if proteinuria significant
– blood gases if oliguric
– C3 (almost always depressed in post-infectious
nephritis, recover in 6-8 weeks, failure to recover is a
poor prognostic sign indicating chronic GN)
– C4 is usually normal in post-infectious nephritis; if
depressed may indicate SLE, membranoproliferative
GN or endocarditis with renal involvement)
– bacteriologic and serological examination
• culture of throat and infected skin
• ASOT
• anti-DNase B, antihyaluronidase, streptozyme test if
available
• viral antibody titre
 Investigations
• others - ECG, CXR
• advanced investigation (if causes other than APSGN are
suspected)
– ANA, anti-double stranded DNA, anti-neutrophil
cytoplasmic antibodies (ANCA) indicating an
autoimmune process
– anti-glomerular basement membrane antibody
– cryoglobulins
– circulating immune complexes
– renal ultrasound to rule out obstruction
– renal biopsy
– Audiology if Alport’s syndrome suspected
 Management

Observation - ‘renal chart’

– serial BP
– daily urinalysis
– daily body weight
– accurate I & O chart
 Management
• oral penicillin x 10 days
• Bed rest indicated only in severe hypertension or
significant oedema
• Restrict salt and fluid to prevent their retention
• Restrict protein to 1g/kg/day only when azotaemia
and oliguria are present
• I.V. frusemide (1-4 mg/kg/day) to promote
diuresis and decrease BP
• Control moderate hypertension by imi hydralazine
0.15 - 0.5 mg/kg/dose
• Hypertensive encephalopathy or severe
hypertension is a medical emergency
• Treatment of acute renal failure including dialysis
when indicated
 Management

Follow up management
– clinic visit at 4-6 weeks interval in the first six
months for urinalysis and BP measurement
– control hypertension to prevent further renal
damage
– early recognition and treatment of chronic renal
failure to maximize skeletal growth and
physical activities
 Management
• Indication of renal biopsy
– rapidly deteriorating renal function
– atypical presentation (from APSGN)
No needa rmb details
• anuria
• nephrotic syndrome
• severe azotaemia
• lack of evidence of streptococcal etiology
• prior or family history of renal diseases
• abnormal growth suggestive of chronic glomerulonephritis
• significant systemic symptomatology such as SLE
– delay in rate of resolution
• oliguria and/or azotaemia persisting beyond 2 weeks
• hypertension or gross haematuria persisting beyond 3 weeks
• low C3 beyond 6 weeks
• persistent proteinuria with or without haematuria beyond 6
months
• persistent haematuria beyond 12 months
Clinical case – Approach to haematuria
• M/8 yrs, presented with first attack of whole stream brown
colour urine for 2 days, now clearing
• No other urinary symptom
• Had URI symptoms within last 5 days, otherwise well
• P/E: - well, no pallor, no edema. BP 120/80. CVS,
abdomen, genitalia were all normal
• Urine multistix – large amount of blood and protein
• Urine microscopy - >100 RBC/uL
• Urine culture – no growth
• CBC, RFT were normal
• C3 normal
• Renal USS and plain AXR were normal
 Questions
Is acute post-infectious nephritis the most
likely diagnosis?
Are you concerned with the BP reading in this
case?
What further investigations are required?
Is renal biopsy indicated?

Houtman. Chapter 29. Tutorials in Paediatric Differential Diagnosis.

Discussion on the clinical case with haematuria

Is acute post-infectious nephritis the most likely

diagnosis?
• URI not typical since it is just prior to onset of
haematuria
• Uncommon for C3 to remain normal in acute
phase of post-infectious nephritis
• Should consider other causes of
glomerulonephritis such as IgA nephropathy
Are you concerned with the BP reading in this case?

• 120/80 mmHg is on high side, both systolic

and diastolic pressure are about 95th – 99th
percentile (depending on the height)
• Although no treatment required at present,
need close monitoring
 Is renal biopsy indicated? Further Ix?

• Not now since the patient was quite stable

• But require further information or close
monitoring on
– BP
– C3, C4
– Renal function
– Amount of proteinuria (multistix is not enough)
– Bacteriological Ix
– Family history of haematuria and renal diseases
Henoch-Schonlein Purpura
 Henoch-Schonlein Purpura
• Incidence:
– 14 per 100,000 children aged 2-14 per year
– 75% of all cases were between 2-11 years old
• Etiology:
– unknown
– triggers - eg. microorganism
• Clinical manifestation:
– self-limited
– last 1-2 wks
– tendency to recur several times
• Skin
– palpable nonthrombocytopenic purpura
– prerequisite to diagnosis HSP
– presenting sign in 50%
• Joint
– arthritis or arthralgia - oligoarticular, pain out
of proportion to objective evidence of synovitis
– most frequently in knees and ankle in 60-84%
• Gastrointestinal
– in 85%
– colicky pain, nausea, vomiting, GIB
– in those with GI manifestation: 50% with occult
GI bleeding, 5% with major haemorrhage
– 2-3% has intussusception
• GU - scrotal swelling, orchitis
 Henoch-Schonlein Nephritis
– Renal involvement in 10-50% of HSP
– > 9 yr old children-higher incidence of developing
GN
– renal involvement and GI involvement - usually
occur together
– persistence of rash for 2-3 months ass. with
nephropathy
– no consistent relationship between severity of
nephritis and severity of extrarenal manifestation
• HSP associated nephritis
– haematuria in all
– haematuria and proteinuria: 15% develop
progressive renal insufficiency
– nephrotic syndrome and renal insufficiency:
50% with renal failure after 10 yrs
– ‘persistence of nephrotic-range proteinuria’:
most accurate predictor of eventual renal failure
Haemolytic uraemic syndrome (HUS)
• Triad of microangiopathic haemolytic anaemia,
thrombocytopaenia and renal injury
• Commonest type: D+HUS is associated with prodromal
diarrhoeal illness (usually bloody)
• Verotoxins esp. Shiga-like toxin from E coli O157:H7
binds to globoceramide receptor on endothelial cells
producing endothelial surface coagulation, microvascular
glomerular and interstitial vessel thrombosis
• Causes haemorrhagic enterocolitis & HUS; but any tissue
can become ischaemic
• outbreak of enterohaemorrhagic E.coli (EHEC) O104 strain
has been reported in May 2011 in Northern Germany, with
2.8% mortality
• D-HUS: no prodrome of diarrhoea
– If present with seizure – thrombocytopenia purpura (TTP)
 HUS
• Typically presents with gastroenteritis then oliguria
• May be dehydrated or volume overload with
hypertension
• May have seizure
• Diagnosis by microangiopathic haemolytic anaemia,
thrombocytopaenia and renal injury
• Treatment is mainly supportive, many require renal
replacement therapy
• Antibiotic has no significant effect on the duration of
GI symptoms and was shown to increase the risk of
HUS probably by inducing toxin release
• >95% survive the acute phase
Proteinuria
Causes of Transient Proteinuria in
Children

Fever Extreme cold

Orthostatic Epinephrine
Exercise Seizures
Stress Congestive heart failure
 Causes of persistent proteinuria in children
• Orthostatic
– U Pr/Cr >0.2 on a first morning specimen excludes
orthostatic proteinuria
• Benign (Sporadic or familial)
• Increased plasma concentration of protein
– Multiple myeloma, primary amyloidosis, lymphoma, chronic
lymphocytic leukemia
• Decreased tubular reabsorption of protein
– Hereditary: Fanconi’s syndrome associated with Wilson’s
disease, cystinosis, Lowe’s syndrome, polycystic kidney
– Acquired: drugs (aminoglycosides, phenacetin, lithium),
acute tubular necrosis, pyelonephritis, interstitial nephritis,
radiation nephritis
 Causes of persistent proteinuria in children

• Glomerular
– Primary:
• Minimal change disease
• focal segmental glomerulo-sclerosis
• membranous nephropathy
• membranoproliferative GN
– Secondary:
• Infectious; poststreptococcal GN, endocarditis, hepatitiis
• Immune/multisystem: SLE, Goodpasture’s syndrome, RA,
HSP, ulcerative colitis, polyarteritis
• Metabolic: diabetes mellitus
• Hereditary: Alport’s syndrome, Fabry’s disease
• Drugs: nonsteroidal anti-inflammatory agents
 Causes of persistent proteinuria in children

• Structural abnormalities of the urinary tract,

congenital or acquired:
– Polycystic kidney disease: autosomal recessive
or dominant
– Hydronephrosis: posterior urethral valves,
ureterovesical or ureteropelvic obstruction
– Hypoplastic-dysplastic disease
– Reflux nephropathy
 Persistent proteinuria

• is typically a sign of glomerular disease, although

also seen in renal tubular disease or increased
filtered load of protein
• The causative glomerular disease may be primary
or secondary to a systemic disease
• The clinical course, response to therapy, and
prognosis vary greatly depending on the
underlying cause.
Histologic classification of primary idiopathic
nephrotic syndrome in children (%)

Minimal change disease 78

Glomerular sclerosis 9
-Segmental (7)
-Global (2)
Mesangial proliferation 2
Membranoproliferative GN 7
Membranous glomerulopathy 3
Other 3
Nephrotic Syndrome
 Definition of Nephrotic syndrome
Definition of Nephrotic syndrome
nephrotic range of proteinuria (≥ 40 mg/m2/hr, albumin
to creatinine ratio >2mg/mg) and serum albumin level
≤ 2.5 gm/dL
Response:
Reduction in rate of urinary excretion of protein to < 4
mg/m2/hr (albustix 0 to trace) for 3 consecutive days
Relapse:
Reappearance of proteinuria ≥ 3 + on albustix or ≥ 4
mg/m2/hr for 3 consecutive days
 Definition
Frequent relapser: an early responder who had
• 2 relapses within 6 months of the initial response
• or 4 or more relapses within any 12-month period

Steroid dependency:
• relapse within 14 days after the end of a course of
steroid therapy or
• during the tapering regimen (eg. to an alternate-
day schedule)
 Classification
Primary (idiopathic)
Histopathological classification
• minimal change NS
• mesangial proliferative GN
• membranous nephropathy
• membranoproliferative GN
• focal segmental glomerulosclerosis
• focal and global glomerulosclerosis
• diffuse proliferative GN
Secondary:
• Systemic Lupus Erythematosus
• Anaphylactoid Purpura
• PSAGN
• Infections - malaria, varicella, hepatitis
• Toxins
• Drugs eg penicillamine, trimethadone, Hg, gold
• Renal vein thromobosis
 Treatment of complications
• Hypovolaemia & severe edema:
– IV albumin (salt poor) followed by furosemide
• Infection- low Ig & complement
– Appropriate antibiotics
– Diuretics if oedema severe
• For peritonitis
– parenteral penicillin for pneumococcal infection
– parenteral aminoglycosides for g -ve organisms
• Arterial and venous thrombosis
– uncommon in Chinese
– due to hypercoagulable state
– ? Anticoagulant therapy
 Protocol for treatment
1. Initial attacks (ISKDC)
nOW MANY CENTER PREDER TAPERING ALT DOSE FORA ANOTHER 4 WKS -> TOTAL STEROID DOSE IS FOR 3M
– Prednisone 60 mg/m2/day in 3 divided doses x 4/52
then 40 mg/m2 single morning dose on alternate day x 4/52
– UK-60 mg/m2 /day until remission then alternate day dose
– APN (German) 6 weeks + 6 weeks. Less relapse in 1 yr.
R/O contradiction eg active fHUS
TB

2. Relapses
Prednisone 60 mg/m2/day till protein free for 5 out of 7 days
then 35 mg/m2 single morning dose alternate day x 4/52
 Protocol for treatment
3. Frequent relapsers
• Prednisone as for relapse
• Cyclophosphamide for 8 weeks or 12 weeks for more severe
cases together with steroid
• Cyclosporin A for 6 months
– Need renal monitoring
– Indicated in steroid dependence with toxicity after 1 course
of CYP or before CYP in pre-pubertal boys
– Dose related, no sustained effect
• Levamisole on alternate day for 6 months to 1 year
– ↓ relapse by 55% & ↓ steroid dosage
– Cx: Leucopaemic (rare), rash
– Not very effective but as adjunct
 OUTCOME
1. Minimal change:
• Most eventually go into remission and relapses decrease
with time
• Nearly 80% experience relapse
• About half still relapse after 5 years, and 20% after 10
years
• rarely recurs when free of disease for 4 years and has
reached adolescence, those who do relapse are steroid
responsive
• only 3% initially steroid sensitive, become resistant
• less than 1% goes to renal insufficiency

2. Poorer prognosis with Mesangial proliferative GN,

Membranous nephropathy and Membranoproliferative
GN
 Treatment of ARF
(Price’s Textbook of Medicine 1941)

Potassium citrate 15 grains

Liq. Ammon. Acetatis 60 minims
Sp. Aetheris nitrosi (ether) 15 minims
Aq. Chloroform 1/2 oz - in water, q.d.s.
Senna or liquorice
Urea 30-60 g three times daily
Venesection
5 minims tincture of digitalis
 ARF, ATN or AKI?

It is now acute kidney injury

Editorial. Anaesth Intensive Care 2007;35:843

(still not universally accepted to replace acute renal failure)

 Acute Kidney Injury
• Introduced by the Acute Kidney Injury Network
(AKIN) (in adults)
Definition:
• Rapid time course (less than 48 hours)
• Reduction of kidney function [absolute increase
in serum Cr either > 26.4 umol/L or a % increase
of > 50% (1.5 fold from baseline)] or
• Reduction in urine output, defined as <0.5
ml/kg/hr for more than 6 hours
 AKI
• Previously called acute renal failure
• Characterized by
– usually reversible increase in Cr and
nitrogenous waste
– inability to regulate fluid and electrolyte
homeostasis
• (definition in children is not universally
accepted)
 The pRIFLE classification
Estimated creatinine clearance Urine output
(eCCI) by Schwartz formula
Risk Decreases by 25% <0.5 ml/kg/hour x 8hrs

Injury Decreases by 50% <0.5 ml/kg/hour x 16 hrs

Failure Decreases by 75% or eCCL < <0.5 ml/kg/hour x 24 hrs or

35ml/min/1.73m2 anuric x 12hrs
Loss Persistent failure >4 weeks

End-stage ESRF (Persistent failure > 3 months)

=> AKIN criteria (diff timeframe)

 Oliguria
Urine output:
• <400 ml/1.73m2/24 hr in adolescents and adults
• <0.8 ml/100 kcal/hr or <200 ml/m2/24 hr in children
• <1.0 ml/kg/hr in infants
• <0.5 ml/kg/hr in newborn
These are the minimum amount of urine to excrete the
nitrogenous waste of a normal diet
Example:normal solute load: 10-40 mosm/100 kcal/day
osmolarity of concentrated urine:1000 mosm/L
minimum amount of urine:25 ml/100 kcal/day
ie. 1 ml/kg/hr
 Non-oliguric AKI
(a) Concept:
G F R = 100 m l/m in G F R =10 m l/m in
Proxim al tubule fluid: 144 L/day 14 L/day
R eabsorbed: 142 L/day 12 L/day
U rine: 2 L/day 2 L/day

(b) Better prognosis

• less severe renal injury
• better fluid/electrolyte balance
(c) Conversion of oliguric to nonoliguric AKI by diuretics
• obviates the need for fluid restriction and simplifies nutrition
• however has not been shown to alter the course of renal failure
may even cause poorer prognosis except in neonate
 Etiology of AKI

• Vary according to age

• Simple classification:
(I) Pre-renal failure
(II) Renal/Intrinsic/Renal parenchymal
(III) Postrenal
• Several mechanisms may occur simultaneously
• May superimpose on pre-existitng CKD
 Causes of AKI in children
(ESPED Germany 1993)

Age Renal HUS GN Others

ischaemia
Newborns 13 0 0 0
Infants 10 5 1 0
1-5 years 3 (6% ) 45 (86% ) 2 (4% ) 2 (4% )
5-16 years 16 (33% ) 15 (31% ) 17 (35% ) 1 (4% )
Total 42 (32% ) 65 (50% ) 20 (15% ) 3 (3% )
Prophylaxis and conservative treatment of AKI

(1) Recognition of the patient at risk

• Chronic disease states
• anaesthesia
• surgery and/or trauma
• sepsis and toxaemia
• hypotension and hypovolaemia
• hypoxia and acidosis
• nephrotoxic agents
Prophylaxis and conservative treatment of AKI
(2) Assessment of the adequacy of the volume status
(3) Preventing or antagonizing the various
pathophysiological processes leading to AKI
• optimize circulation, BP, haematocrit and oxygen
delivery
• restore renal to systemic vascular resistance ratio
(a) Inotropic agents
Dopamine - increases renal perfusion
- natriuresis
- increase water excretion
Prophylaxis and conservative treatment of AKI

(b) Furosemide
• synergistic actions with dopamine
• facilitate fluid management by maintaining
a non-oliguric state but has no impact on the
course of AKI
• may even enhance renal injury if given
together with nephrotoxic drugs particularly
in presence of volume depletion
Prophylaxis and conservative treatment of AKI

(c) Calcium-channel-blocker
• nephroprotective effect in AKI secondary to
ischaemia and in nephrotoxic AKI
(aminoglycosides)
• limited use because of systemic effect
Mx:Hypertension
Drug Dose Onset Comments

Nifedipine 0.25-0.5 20-30 Sublingual

mg/kg/SL min administration
Labetolol 1-3 mg/kg/hr IV 1-5 min Contraindications:
Congestive heart
failure
Heart block
Asthma
Sodium 0.5 - 8.0 1-5 min Intensive care
nitroprusside µgm/kg/min monitoring
Cyanide toxicity
Diazoxide 1-2 mg/kg IV 3-30 min Unpredictable
BP control, long
duration of effect
 Mx:Hyperkalaemia
Mx:
Result of catabolism, haemolysis, acidosis and transfusion of
blood products
Treatment of hyperkalaemia:

D rug Effect O nset D uration

Calcium Stabilizes Im m ediate M inutes
m yocardium
N aH CO 3 Shifts K + into 30-60 m in H ours
cells
G lucose and Shifts K + into 30 m in H ours
insulin cells
Sodium Exchanges N a + 1h H ours
polystyrene for K + and
sulfonate rem oves K +
 Mx: Metabolic acidosis

• Maximal respiratory compensation requires 12-36 hours

pCO2 should reach a value of 1.5x serum bicarbonate +
8mm Hg
• Caution with iv bicarbonate
 Dialysis: Indications
1. Fluid overload unresponsive to conservative management
– congestive heart failure
– pulmonary edema
– intractable hypertension, hypertensive encephalopathy
2. Life-threatening or uncontrollable metabolic disturbance
– hyperkalaemia
– intractable acidosis
– hyperuricaemia
– hyperphosphataemia
3. Symptomatic azotaemia leading to lethargy, neurological changes
or seizures
4. Posioning due to dialyzable
paedi onco*
or haemofilterable compounds
5. Tumour-lysis syndrome, hyperammonaemia, organic acidaemia
6. When oliguria is prolonged and nutritional support is a problem
 Trend in management of AKI
• progressive shift towards continuous
therapies
– essentially complete in Australia
– very strong in Europe
– less in USA
• earlier start of renal replacement therapy
• tighter control of blood urea concentration
• provision of more aggressive, nitrogen rich,
nutritional support
Questions: Epidemiology studies of AKI in
children has shown that
Which of the followings is/are true:
A. the incidence of AKI is decreasing.
B. genetic factors may play a role in the
susceptibility to AKI.
C. hypoxic/ischemic AKI is a rare cause of AKI
in children.
D. nonsteroidal anti-inflammatory therapy is a
risk factor for AKI in newborns.
Andreoli SP. Pediatr Nephrol (2009) 24:253-263
F T F T
Question: Diagnosis and etiology of AKI in children
Which of the followings is/are true:
A. definition of AKI in children is well established.

B. serum creatinine is a sensitive marker of AKI.

C. in utero exposure to ACE inhibitors is associated with

AKI in neonates.

D. AKI in hospitalized children may be the result of

multiple etiologies.

E. urinary sodium concentration is a reliable indicator of

pre-renal versus hypoxic/ischemic AKI in premature
newborns.
Andreoli SP. Pediatr Nephrol (2009) 24:253-263 F F T T F
 Question: Hypoxic/ischemic AKI
Which of the followings is/are true:
A. alterations in blood flow are not thought to play a role
in hypoxic/ischemic AKI.

A. reactive oxygen molecules generated by activated

PMNs may play a role in hypoxic/ischemic ATN.

C. ATP depletion is an early response to

hypoxic/ischemic AKI.

D. hypoxic/ischemic AKI is always reversible and has

no long-term consequences.
Andreoli SP. Pediatr Nephrol (2009) 24:253-263 F T T F
Question: Management of AKI in children

Which of the followings is/are true:

A. diuretic therapy in AKI shortens hospital stay,
decreases the need for dialysis therapy and decreases
mortality rates.

B. ‘renal-dose’ (<5 ug/kg/min) dopamine therapy has

not been shown to be effective in adult patients

C. prevention of AKI is important on a global scale in

lowering the number of deaths from AKI.

Andreoli SP. Pediatr Nephrol (2009) 24:253-263 F T T

 Question: Prognosis of AKI

Which of the followings is/are true:

A. neonates, infants, children and adolescents
who have recovered from AKI do not need
long-term follow up.

B. AKI that occurs before completion of

nephrogenesis may lead to later chronic
kidney diseases
Andreoli SP. Pediatr Nephrol (2009) 24:253-263 F T
Thank you