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Current Paediatrics (2004) 14, 547–555
www.elsevier.com/locate/cupe
The investigation of proteinuria
M.T. Christian, A.R. Watson
Children and Young People’s Kidney Unit, Nottingham City Hospital, Hucknall Road,
Nottingham NG5 1PB, UK
KEYWORDS
Proteinuria;
Orthostatic
proteinuria;
Nephrotic syndrome;
Glomerulonephritis;
Chronic renal
failure/chronic
kidney disease;
Urinalysis
Summary Proteinuria can be a major clue to underlying renal disease or a
transient finding in normal children. This article will deal with the evaluation of
a child with proteinuria, what basic investigations are needed and when to refer to a
paediatric nephrologist.
Urinalysis sticks for ward testing are quite sensitive for proteinuria. Suspected
proteinuria should always be sent for laboratory quantification, and the simplest
method is to measure with the protein:creatinine ratio on a spot sample.
Physiological proteinuria is not usually detected on urinalysis or dipstick testing.
Causes of non-physiological proteinuria include benign transient proteinuria,
orthostatic, renal and non-renal causes. Persistent proteinuria is more significant.
It is also likely to be more significant if associated with haematuria or hypertension.
Orthostatic proteinuria can only be diagnosed when the urinary protein from a
recumbent sample reduces to normal.
When there is persistent non-orthostatic proteinuria, baseline investigations
would normally include a renal ultrasound and a plasma chemistry profile. Plasma
albumin gives a good indication of the significance of proteinuria. If haematuria is
also present, a basic nephritis screen should also be carried out. Any child with
persistent non-orthostatic proteinuria should be referred to a paediatric nephrologist for consideration for renal biopsy.
r 2004 Elsevier Ltd. All rights reserved.
Practice points
All persistent proteinuria should be quantified in the laboratory and a urine protein:creatinine ratio is the simplest method
Corresponding author. Tel.: +44–115-969/1169x49680; fax:
+44-115-962-0564.
E-mail address: mchristi@ncht.trent.nhs.uk (M.T. Christian).
Many children with benign or orthostatic
proteinuria will require no more invasive
investigations beyond urinary protein quantification
The presence of haematuria and/or hypertension significantly increases the likelihood
of underlying renal disease
Any child with persistent non-orthostatic
proteinuria or any other sequelae of renal
0957-5839/$ - see front matter r 2004 Elsevier Ltd. All rights reserved.
doi:10.1016/j.cupe.2004.08.001
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548
M.T. Christian, A.R. Watson
disease should be referred to a paediatric
nephrologist for consideration for renal
biopsy
Typical nephrotic syndrome does not need
extensive investigations at the outset
Introduction
Proteinuria can be a major clue to underlying renal
disease or a transient finding in normal children. It
is likely to be much more significant if associated
with haematuria. The spectrum of referrals is
illustrated in Box 1.
Routine urinalysis is now part of the registration
process with general practitioners and hence the
first type of referral is not uncommon. Due to the
association between renal disease and proteinuria,
there is often considerable anxiety about the
finding of asymptomatic proteinuria on the part of
doctors and families. Nephrotic syndrome is a
particular scenario of heavy proteinuria in childhood that carries additional risks. It can cause
confusion in terms of the investigations required
and management.
This article will deal with the evaluation of a
child with proteinuria, what basic investigations
are needed and when to refer to a paediatric
nephrologist.
Physiology
The glomerular basement membrane provides both
a physical and electrical charge barrier to the
passage of most plasma proteins. A small number of
proteins do pass into the proximal tubule, depending on their size and plasma concentration.
Globulins are large molecules and as such are
effectively retained in the plasma. Albumin is a
smaller molecule. It is not known how much
albumin is filtered in healthy individuals, but there
appears to be a mechanism for resorption through
proximal tubular epithelial cells.
Smaller proteins such as N-acetyl-D-glucosaminidase, retinal-binding protein and b2-microglobulin
may be filtered at rates approaching the glomerular
filtration rate (GFR). Up to 98% of these are reabsorbed in the proximal tubule. One hallmark of
tubular disease is to see a marked increase of these
proteins in the urine. There is a further source of
protein secretion from the distal loop of Henle
(Tamm–Horsfall protein).
Definitions of proteinuria
Urinalysis sticks for ward testing are quite sensitive
for proteinuria. They are impregnated with bromocresol green that changes colour in the presence of
protein and is used as an indicator dye. They are
intended to correlate as follows: + with 0.3 g/l, ++
with 1 g/l, +++ with 3 g/l and ++++ with X20 g/l.
False-positive results may be obtained with concentrated or alkaline urine, and false-negative
results may be obtained with dilute or markedly
acidic urine.
Suspected proteinuria should always be sent for
laboratory quantification. The gold standard in
adults is a 24-h collection so that protein excretion
may be expressed per unit body surface area per
day (mg/m2/day). There is frequently confusion
about how to carry out a timed urine collection (see
Box 2). For an afebrile patient at rest, the urinary
protein excretion should not exceed 60 mg/m2/day.
Body surface area may be estimated from nomograms that are found in most paediatric formularies. It can also be estimated from the following
Box 1
Dear Consultant Paediatrician,
Re: Sally Smith
This 12-year-old girl has recently joined our practice. On her registration appointment, her urine
showed ++ protein. Does she need further investigation?
Dear On-call Paediatric SHO,
Re: Fred Brown
This 9-year-old boy has had puffy eyes on waking over the last 2 weeks which has not responded
to antihistamines. Today his urinalysis shows protein ++++ and blood ++. Please assess and
manage.
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Investigation of proteinuria
549
Box 2
Timed urine collections for proteinuria.
Set a start time, usually around 8 am.
The child should void into the toilet at 8 am.
From that time onwards, urine should be saved in a preservative-free container each time the child voids.
At the end of the collection period (usually 12 or 24 h), the child should void to complete the collection.
For a split 24-h collection, the second 12-h collection period begins immediately after the first 12-h period
has ended.
Samples may be stored in a home refrigerator until it is convenient to take them to the hospital
laboratory.
Parents should carefully label the container with start and finish times.
formula:
rﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃﬃ
heightðcmÞ weightðkgÞ
2
Body surface areaðm Þ ¼
:
3600
Table 1 Normal ranges for protein:creatinine
ratios in different age groups.
Timed urine collections may be carried out in
older children but are not always practical,
particularly in young children. The simplest means
of quantifying proteinuria is with a spot sample,
measuring the protein:creatinine ratio. The urinary
concentration of protein or albumin is referred to
urinary creatinine, and with the assumption that
urinary creatinine concentrations are proportional
to body surface area, there is no need to correct
these samples for body size. Normal values for
protein:creatinine ratios are shown in Table 1.
Some laboratories measure the albumin:creatinine ratio instead and this is more sensitive when
there is a need for accurate quantification of
albuminuria in the follow-up of glomerulopathies
or diabetic nephropathy.
0–6 months
6–24 months
42 years
Nephrotic range
Protein:creatinine ratio
*
Up to 50 mg/mmol*
Up to 50 mg/mmol
Up to 25 mg/mmol
4360 mg/mmol
May be even higher.
cause this form of proteinuria are rare in
children.
Benign proteinuria implies proteinuria that is
detected on urinalysis but which has no serious
underlying pathology. It includes proteinuria seen
in fever or after exercise, idiopathic transient
proteinuria, and orthostatic or postural proteinuria.
Causes of proteinuria are shown in Table 2.
Causes of proteinuria
The protein that is excreted in urine under
physiological conditions is not usually detected on
urinalysis or dipstick testing. Pathological proteinuria has been classified into four groups: glomerular, tubular, overflow and benign.1
Glomerular proteinuria occurs because of increased glomerular permeability to proteins.
Tubular proteinuria is due to decreased tubular
resorption of proteins contained in glomerular
filtrate and is seen in tubulo-interstitial diseases.
Overload proteinuria is secondary to increased
production, or release, of low-molecular-weight
proteins. The myeloproliferative conditions that
Benign proteinuria
Proteinuria may occur in febrile children or in the
context of disease states such as cardiac failure. It
may also occur after strenuous exercise. Proteinuria may prove to be transient. Before further
investigations are carried out, there must be
documented proteinuria on at least two occasions.
In some, there may be intermittent proteinuria.
This is generally believed to be associated with a
good prognosis. So long as there are no associated
sequelae of renal disease, these children do not
need a renal biopsy or long-term follow-up.
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M.T. Christian, A.R. Watson
Table 2
Causes of proteinuria.
Benign causes
Transient proteinuria (e.g. fever or post-exercise)
Intermittent proteinuria
Orthostatic proteinuria
Glomerular causes
Damage to glomerular basement membrane (chronic glomerulonephritides, e.g. MPGN, lupus, IgA nephropathy)
Diseases of deposition (e.g. amyloidosis, Fabry disease)
Loss of glomerular anionic charge (e.g. idiopathic or congenital nephrotic syndrome
Increased permeability of residual nephrons (chronic renal failure)
Tubular proteinuria
Tubulo-interstitial nephritis
Poisoning (vitamin D, heavy metals, non-steroidal analgesics)
Tubulopathies (e.g. Fanconi syndrome, Dent’s disease)
Overflow proteinuria
Myeloproliferative conditions
Rhabdomyolysis
Multiple transfusions or albumin infusions
MPGN, membranoproliferative (mesangiocapillary) glomerulonephritis.
Orthostatic proteinuria
Urine protein excretion increases with activity and
upright posture, and so the protein content of urine
passed late in the day will always be greater than
that passed first thing in the morning. This is not
usually detectable on dipstick testing but the
physiological increase is exaggerated occasionally.
The diagnosis is particularly common in adolescents and would need to be excluded in the first
case above. This is best done by carrying out a split
24-h urine collection (Box 2). If this is not possible,
a simpler method is to measure the protein:creatinine ratio in the first voided urine sample of the
morning and compare this with a urine sample
voided later in the afternoon or evening.
It should be remembered that proteinuria with a
pathological basis will also frequently have an
orthostatic component. Therefore, the diagnosis
of orthostatic proteinuria can only be made safely
when urinary protein during the recumbent period
returns to a normal value.
Orthostatic proteinuria is commonly transient
but may persist. The data on long-term follow-up of
these patients have been confusing. For some
studies showing minor glomerular abnormalities
on renal biopsy, it is apparent that not all patients
had true orthostatic proteinuria. What is clearer is
that the long-term follow-up of patients with pure
orthostatic proteinuria has shown an excellent
prognosis and it is no longer true to suggest that
these patients need long-term review.2 If orthostatic proteinuria is confirmed and there is no
significant proteinuria on a recumbent sample, the
child and family may be reassured and no follow-up
is necessary.
Renal causes
Plasma albumin gives a good indication of the
significance of proteinuria. For many hospital
biochemical departments, this is not part of a
routine chemistry profile and needs to be requested
separately. Hypoalbuminaemia in the context of
proteinuria suggests proteinuria to the extent that
hepatic synthesis of albumin is not able to keep up
with urinary losses.
The co-existence of haematuria is also important. The presence of haematuria with proteinuria
significantly increases the likelihood that there is
underlying renal pathology.
Chronic glomerulonephritis
A number of chronic glomerulopathies may present
with asymptomatic proteinuria. For many of these
conditions, one would expect to see further
evidence of renal disease such as co-existent
haematuria, hypertension or impaired renal function. However, conditions such as membranous
glomerulonephritis and focal and segmental glomerulonephritis might present without other sequelae of renal disease.
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Investigation of proteinuria
Many have specific serological markers. Low
complement is a feature of membranoproliferative
(mesangiocapillary) glomerulonephritis (MPGN) and
lupus nephritis, and there are usually raised antinuclear antibodies (ANA) or evidence of other autoantibodies such as double-stranded DNA, extracted
nuclear antibodies or lupus anticoagulant in lupus
nephritis. IgA may be raised in IgA nephropathy and
Henoch–Schönlein purpura nephritis but it is not a
very sensitive test. With other vasculitic illnesses
such as polyarteritis nodosa or Wegener’s granulomatosis, there may be associated systemic features
such as recurrent fevers, rashes or upper respiratory tract symptoms. Vasculitis is usually associated
with raised erythrocyte sedimentation rate (ESR) as
well as C-reactive protein (CRP), whereas in lupus
nephritis, there is typically only raised ESR in the
absence of infection. Antinuclear cytoplasmic antibodies (ANCA) may be present in vasculitides.
Hepatitis B or C can result in a secondary MPGN
or secondary membranous glomerulonephritis.
Streptococcal illnesses may precipitate a number
of glomerulonephritides. The hallmark of poststreptococcal glomerulonephritis is an initially
depressed complement that normalizes by 2–3
months. Proteinuria usually clears within several
months although it is common for haematuria to
persist for a year or longer. Asymptomatic proteinuria may present in the context of recovering
post-streptococcal glomerulonephritis when the
initial illness was not severe enough to come to
medical attention.
Chronic renal failure
Proteinuria frequently accompanies chronic renal
failure. Asymptomatic proteinuria is often the first
presentation of otherwise asymptomatic chronic
renal failure in children. It is important to have
some understanding of the range of normal values
for plasma creatinine in different age groups.
Calculation or measurement of GFR alleviates the
need to remember various reference ranges (that
can, in any case, have wide confidence limits).
551
indicative of proximal renal tubular pathology.
Frequently, this may be part of a more generalized
Fanconi syndrome and there may be abnormalities
in other functional markers such as acidosis,
hypokalaemia, reduced tubular re-absorption of
phosphate, glycosuria or aminoaciduria.
Clinical evaluation of a child with
persistent proteinuria
If evaluation proceeds in a stepwise manner
through a careful history taking, examination and
urinalysis, many children will not need invasive
investigations.
When taking a history, important areas to ask
about include episodes of illness, swelling (oedema), urinary tract infections, use of drugs such as
non-steroidal anti-inflammatory agents and family
history of renal disease. Renal disease may be
associated with a wide range of other conditions
and a careful systemic enquiry is important.
Examination must include blood pressure measured
with an appropriate-sized cuff, the presence
of oedema and parameters of growth. Clinical
assessment of the circulatory status is described
below.
Baseline investigations
These should be carried out sequentially in order of
increasing complexity and invasiveness as shown
below.
Tubular proteinuria
Low molecular proteinuria as described above is
not detected by dipstick testing, but laboratory
measurement of proteinuria is something to be
considered for a young child with faltering growth.
It occurs when there is failure of resorption of
proteins secreted by the proximal tubule, and is
Any concomitant haematuria?
Confirmation and laboratory quantification of
proteinuria (protein:creatinine ratio or timed
collection).
If significant proteinuria confirmed:
o renal imaging in the form of a renal tract
ultrasound scan (any renal scarring?).
o plasma chemistry profile (to include Na, K,
HCO3, urea, creatinine, Ca, PO4, alkaline
phosphatase and albumin).
If nephritic presentation (haematuria, hypertension or renal impairment):
o glomerulonephritis screen (complement levels,
ANA, ANCA, streptococcal serology (ASOT/
anti-DNAse B), hepatitis B and C serology, ESR
and CRP).
If the creatinine appears to be elevated for age,
the GFR may be estimated using the Schwartz
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M.T. Christian, A.R. Watson
formula:3
Predicted GFR ¼
40 heightðcmÞ
:
creatinineðmmol=lÞ
If the estimated GFR is 60 ml/min/1.73 m2 or
less, a formal clearance should be measured,
usually using the radionuclide 51Cr-EDTA. It can
also be measured using insulin clearance.
There is debate amongst paediatric nephrologists
about the need for renal biopsy in children with
isolated proteinuria where no other sequelae of
renal disease are present. In Japan, where routine
urinalysis is frequently carried out in children,
proteinuria has been found in 0.08% of primaryschool-aged children and 0.37% of secondaryschool-aged children in one study.4 In a separate
study, proteinuria was found on two occasions in
2.5% of a large cohort of children aged 8–15 years.5
Of the 28 children with isolated proteinuria who
underwent renal biopsy, mild non-specific changes
on renal biopsy were seen in 12 and mesangial
deposits in four. An argument for renal biopsy is
based on the data of two further Japanese studies.
In one,6 36 children with persistent asymptomatic
proteinuria were followed-up over an average of
2.9 years. On renal biopsy, 11 patients showed
moderate sclerosis and seven showed severe
sclerosis; in these patients, the proteinuria was
more likely to persist. However, in the relatively
short period of follow-up, only one patient developed deterioration in GFR. A second study from
Japan7 also demonstrated significant biopsy findings in 25 out of 53 children with persistent
asymptomatic proteinuria. There was deterioration
in GFR in seven of these children. Whether these
findings from a country with a high prevalence of
IgA nephropathy are applicable to the UK is
debatable. In the USA, with a racial mix more
similar to that in the UK, only 38% of paediatric
nephrologists would perform a renal biopsy in a
child with isolated proteinuria.8
Nephrotic syndrome
The classic triad of nephrotic syndrome is heavy
proteinuria leading to hypoalbuminaemia leading
to oedema. Nephrotic range proteinuria is defined as 43.5 mg/m2/day. This equates to a
protein:creatinine ratio of 4250 mg/mmol,
although it is usually much greater. On dipstick
testing, there is protein of +++ or greater. The
plasma albumin level is less than 25 g/l. Oedema is
rarely present with plasma albumin levels greater
than this.
Proteinuria occurs at the ultrastructural level
because of so-called ‘fusion’ of podocyte foot
processes resulting in disruption of the glomerular
basement membrane, leading to a large albumin
leak into Bowman’s capsule. The exact mechanisms
for this are not completely understood but the main
component is believed to be impairment of the
charge-specific barrier. The change in glomerular
permeability is also not well understood. It is
widely believed although not proven that there
is an immunological basis for the disease. It is
believed to be mediated via a circulating factor
such as a lymphokine. The presence of a circulating
factor is suggested by the appearance and rapid
resolution of nephrotic syndrome in neonates born
to mothers with the condition, but the factor has
not yet been identified.
Nephrotic syndrome has an incidence of 2–4 per
100 000 population but it is more common in Asian
children. It is more common in boys than girls (2:1)
and it has a peak incidence between the ages of 2
and 6 years. There is frequently an antecedent
upper respiratory infection, following which children typically present with peri-orbital oedema.
The diagnosis of allergy is frequently made before
the true nature of the condition becomes apparent
on urine testing.
The most common lesion causing nephrotic
syndrome in childhood is minimal change nephropathy (MCN); this accounts for around 85% of cases.
Under the age of 6 months, congenital nephrotic
syndromes predominate as a cause of nephrotic
syndrome, and from 6 years, other pathology
becomes progressively more common.
Investigation of the cause of nephrotic
syndrome
The initial investigations of a child with suspected
nephrotic syndrome are intended to exclude
atypical forms. When there is a nephritic element
to the nephrotic syndrome or when the child’s age
differs significantly from the typical age range,
they need further investigation. Children under the
age of 12 months and children over the age of 12
years need further investigation under the supervision of a paediatric nephrologist before commencement of high-dose steroids. Features that
suggest a nephritic element include frank haematuria, abnormal renal function and hypertension.
Haematuria up to ++ is not uncommon in MCN but
even haematuria of higher grades, whilst still
not visible to the naked eye, may be associated
with a greater incidence of steroid resistance.
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Investigation of proteinuria
Hypertension can only be diagnosed in a euvolaemic state. Both states of hypervolaemia and
hypovolaemia are common in nephrotic syndrome,
and both are frequently associated with hypertension due to a normal haemodynamic response.
Serum complement, ANA and hepatitis serology
need not be carried out in a child with typical
nephrotic syndrome prior to commencement
of high-dose steroids. However, the presence
of antibodies to varicella is worth documenting
to avoid unnecessary administration of varicella
zoster immunoglobulin for subsequent exposure
to chicken pox when the child is immunosuppressed.
Investigation of the consequences of
nephrotic syndrome
The nephrotic state causes concern because of the
risks imposed by hypoalbuminaemia. These include
the risk of hypovolaemia, thrombosis and infection.
These have justified the use of high-dose steroids
for long periods.
Hypovolaemia frequently accompanies the initial
presentation of nephrotic syndrome. It may present
with abdominal pain that is believed to be due to
underperfusion of the splanchnic circulation. Examination for hypovolaemia, whilst not easy, is
critical in a child with newly diagnosed nephrotic
syndrome. Isolated measurement of heart rate and
blood pressure are unhelpful. The best assessment
is in the temperature of the peripheries, usually
taken as the feet. In a warm room, these should be
warm to the touch (less than 21 below central body
temperature). In an older child, it is usually
possible to position them sitting up at an angle of
451 and assess the height of the jugular venous
pressure (JVP); this should be around 2 cm above
the sternal angle. Compression of the vein or
abdominal pressure may confirm that a JVP is
visible but considerably lower than this.
Confirmation of hypovolaemia may be obtained
by measurement of urinary sodium (UNa). Hypovolaemia results in sodium retention and UNao10 mmol/l is diagnostic whilst UNa420 mmol/l makes it
unlikely. These values are only valid when no
diuretic has been given in the preceding 6–12 h
and in the absence of renal impairment.
Investigation for suspected infection should
proceed as dictated clinically. Children with nephrotic syndrome should be given prophylactic
penicillin until they enter remission. In the
nephrotic state, there are urinary losses of antithrombotic proteins such as antithrombin III. There
553
are also increased plasma concentrations of clotting factors and these, together with the presence
of hypovolaemia, contribute to the prothrombotic
state. However, no investigations are traditionally
carried out. Children are not routinely anticoagulated for nephrotic syndrome unless there has been
a previous thrombotic event. In the presence of
severe hypovolaemia and apparent polycythaemia,
it would not be inappropriate to commence a lowmolecular-weight heparin until a state of euvolaemia is achieved and maintained.
Hyperlipidaemia is universal in nephrotic syndrome but does not form part of the diagnostic
criteria. It is not thought necessary to measure
the lipid profile in children with nephrotic syndrome due to the usually transient nature of the
nephrosis.
Initial treatment of nephrotic syndrome
The treatment for nephrotic syndrome is outside
the scope of this review. However, there is
currently no national or international consensus
regarding what should be the ideal steroid regimen
at disease presentation. The debate is between
longer, more-intensive steroid treatment at onset
and shorter courses (see Appendix).
Basic investigations in suspected
nephrotic syndrome
For a child who fulfils the triad criteria of the
nephrotic syndrome, the following basic investigations are suggested.
Quantification of proteinuria (usually by protein:creatinine ratio).
Plasma chemistry profile (to include Na, K, HCO3,
urea, creatinine, Ca, PO4, alkaline phosphatase
and albumin).
Varicella serology.
Table 3 Usual indications for renal biopsy in a
child with nephrotic syndrome.
Atypical features at onset
Macroscopic haematuria
Hypertension in a euvolaemic state
Impaired renal function
Age less than 12 months or greater than 12 years
Failure to respond to initial high-dose steroids
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M.T. Christian, A.R. Watson
Proteinuria on dipstick?
Confirmation samples
Reassure
Negative
Positive
Yes
Non-renal cause?
Referral to paediatric
nephrologist for biopsy
Take appropriate action
Yes
Other evidence of renal disease?
No
Document and quantify
further
Persistent
Non-orthostatic
Orthostatic
Intermittent
Referral to paediatric
nephrologist
Reassure
Discharge
Repeat urinalysis every 2-3 months at GPs
See in 1 year
Long-term follow-up
May biopsy
Figure 1 Schema for assessment of a child with proteinuria. Adapted from Postlethwaite RJ, Clinical Paediatric
Nephrology, 2nd edn, with permission.
Glomerulonephritis screen only if any atypical
features.
UNa if hypovolaemia is suspected.
The indications for a biopsy in a child with
nephrotic syndrome are shown in Table 3.
Summary
The key to assessment of a child with proteinuria is
the appreciation of benign forms of proteinuria and
clinical suspicion underlying renal pathology. A
suggested schema is shown in Fig. 1. A finding of
asymptomatic proteinuria is common. Since proteinuria has become increasingly recognized as a
marker of progressive renal injury, there should be
close liaison between general paediatricians and
paediatric nephrologists in cases of persistent
proteinuria.
Appendix
The British Association of Paediatric Nephrology is
sponsoring a national multicentre trial of prednisolone treatment in nephrotic syndrome that
would be adequately powered to address the
issue of the duration of steroid therapy for
the initial episode. Recruitment is about to
commence for a pilot study to provide data for a
power calculation, after which the definitive study
will commence. Since most nephrotic syndrome
presents to general paediatricians in the first
instance, it is hoped that general paediatricians
will actively recruit patients for the study. Further
information will be included with RCPCH mailings
and should be available from all paediatric
nephrologists who will act as local facilitators and
advisors.
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RJ editors. Clinical paediatric nephrology. 3rd ed. Oxford:
Oxford University Press; 2003. p. 1–27.
3. Schwartz GJ, Haycock GB, Edelmann CMJ, Spitzer A. A simple
estimate of glomerular filtration rate in children derived from
body length and plasma creatinine. Pediatrics 1976;58:
259–63.
4. Murakami M, Yamamoto H, Ueda Y, Murakami K, Yamauchi K.
Urinary screening of elementary and junior high-school
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Investigation of proteinuria
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children over a 13-year period in Tokyo. Pediatr Nephrol
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Vehaskari VM, Rapola J. Isolated proteinuria: analysis of a
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555
Further reading
1. Milford DV, Robson AM. The child with abnormal urinalysis,
haematuria and/or proteinuria. In: Webb NJA, Postlethwaite
RJ editors. Clinical Paediatric Nephrology. 3rd ed. Oxford:
Oxford University Press; 2003. p. 1–27.
2. Watson AR. Disorders of the urinary system. In: McIntosh N,
Helms PJ, Smyth RL editors. Forfar and Arneil’s textbook of
pediatrics. 6th ed. Edinburgh: Churchill Livingstone; 2003.
p. 631–7.
3. Haycock GB. The child with idiopathic nephrotic syndrome.
In: Webb NJA, Postlethwaite RJ editors. Clinical paediatric
nephrology. 3rd ed. Oxford: Oxford University Press; 2003.
p. 341–66.
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