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Mar 12, 2025
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About This Presentation
Kidney
Size: 1.76 MB
Language: en
Added: Mar 12, 2025
Slides: 73 pages
Slide Content
PROTEINURIA AND PROTEINURIA AND
HEMATURIAHEMATURIA
ASHIK HAYAT M.D.
Proteinuria and Nephrotic Proteinuria and Nephrotic
SyndromeSyndrome
Occurrence of proteinuria in a single
urine is relatively common.
Will present in 5% to 15% of normal
children in a random urine specimen.
-Proteinuria is a marker of renal
disease.
-The dilemma for the PCP is to
differentiate the child with transient
or any other benign forms of
proteinuria from children with renal
disease.
PATOPHYSIOLOGY AND CLASSIFICATION
Normal protein excretion
normal child <100 mg/m2/day or 150mg/day
neonates is higher up to 300 mg/m2
(reduced reabsorption of filtered protein)
The normally low rate of urinary protein excretion
is:
-Restriction of the filtration
-Reabsorption of freely filtered low
molecular weight protein
Abnormal protein excretion
Urinary protein excretion in excess of 100
mg/m2/day or 4mg/m2/hr
Nephrotic range proteinuria is defined as
>1000 mg/m2/day or 40mg/m2/hr
Three main mechanism:
Glomerular (increase filtration)
Tubular (increase excretion-
decrease reabsorption)
Overflow (marked overproduction of
a particular protein)
Measurement of urinary protein
Urine dipstick
negative
trace between 15-30mg/dl
1+ 30-100 mg/dl
2+ 100-300mg/dl
3+ 300-1000mg/dl
4+ >1000mg/dl
Quantitative assessment
Measurement of 24-hour protein
excretion or total protein/creatinine
ratio
in a spot urine in the morning
normal in children:
<0.2mg protein/mg creatinine (+2 years)
<0.5mg protein/mg creatinine (6-24-
month)
Qualitative assessment
May be necessary to differentiate
glomerular from tubular protein
Approach to the child with proteinuria
Transient or Intermittent
Orthostatic
Persistent
History and physical
Thorough history and physical
change in urine volume or color
edema
increase BP
recent strep infection
family history for renal disease and
hearing loss (Alport
disease)
The Need for Renal BiopsyThe Need for Renal Biopsy
The key indication for biopsy in any
renal disorder are the need to make
specific diagnosis for therapeutic
reasons or to provide a prognosis.
Neprotic SyndromeNeprotic Syndrome
Nephrotic syndrome is characterized
by massive proteinuria,
hypoalbuminemia, edema, and
hyperlipidemia; the most common
presenting symptom is edema.
IntroductionIntroduction
The annual incidence of Nephrotic
syndrome in healthy children is 2 to
7 new case per 100,000 children
younger than 18 years of age.
The peak age lf onset is at 2 to 3
years.
DefinitionDefinition
The diagnosis of NS is the presence
of urinary protein, with the albumin
disproportionately greater than
globulin.
Clinical Diagnostic CriteriaClinical Diagnostic Criteria
1- Generalized edema
2- Hypoproteinemia <2 g/dL
(disproportionately low albumin in
relation to globulin)
3-Urine protein to urine creatinine
ratio in excess of 2 (first A.M. void)
or a 24- hour urine that exceeds
50mg/Kg body weight
4-Hypercholesterolemia (>200 mg/dL)
The mechanisms for edema include:
-Transudation of fluid from the
intravascular space into the
intestitium secondary to decreased
albumin and
- Increased renal tubular
reabsorption of sodium and water
The hyperlipidemia is secondary to:
-Increase in lipoprotein
synthesis by the liver and
-Decrease in lipid catabolism
resulting from reduced activity of
the enzyme lipoprotein lipase and
lecithin cholesterol
acetyltransferase.
INCIDENCE FOR UNDERLYING
PATHOLOGY
TREATMENT
ComplicationsComplications
One true complication of NS is the
tendency to developed infections.
IgG antibody is lost in the urine,
and complement activation is impaired
by concomitant loss of factor B.
Marked intravascular depletion
causes diminished splachnic blood
flow and hypoxia, and a marked
tendency to thrombosis cause
microinfarction, lowering resistance
of the bowel wall to bacteria passage.
Peritonitis is a major contributor to
the 1% to 2% mortality in NS
The second major contributor is
Thromboembolism, however
anticoagulant therapy is not justified
during remission.
Growth is often impaired in NS
There may be losses of IGF-binding
protein, which could account for the
depressed serum concentration of
IGF-I and IGF-II.
PrognosisPrognosis
Mortality in minimal-change NS is
approximately 2%
Of the remaining 98%, most are steroid-
responsive
about 2/3 experience 1/3 possible
single relapse developing
protracted series of
relapses
Hematuria and Hematuria and
GlomerulonephitisGlomerulonephitis
IntroductionIntroduction
Recognition, definition, differential
diagnosis, and orderly evaluation of
hematuria in infants and children is
often an important issue in pediatric
practice
DefinitionDefinition
Hematuria is defined by the presence
of an abnormal quantity of red blood
cells in the urine
Macroscopic: grossly visible
Microscopic: only upon urinalysis
>5-10 RBC’s per high power field
A large number of benign and serious
conditions can cause hematuria in
children.
Gross hematuria
UTI
Irritation of the meatus or perineum
Trauma
Nephrolithiasis
Sickle cell disease/trait
Post infectious glomerulonephritis
IgA nephropathy
Microscopic hematuria
Glomerulopathies
Hypercalciuria
Microlithiasis
UTI
Children with hematuria may present
in one of three way
1-Onset of gross hematuria
2-Onset of urinary or other
symptoms with incidental finding
3-Incidental finding during a
health evaluation
Historical clues
The color of the urine
Glomerulonephritis may be brown
and/or frothy urine,
while bleeding is suggested by the
presence of blood clots, or pink or
clearly red urine
The timing of the hematuria
Initial (urethral bleeding)
Terminal (bladder)
Throughout (no localizing value)
Circumstances associated
History of trauma, pain,
micturating symptoms, systemic signs
including fever and skin and
nasopharyngeal infection
Age of onset
Periodicity
Blood on diapers of underwear
Exposure to medications
Relation with exercise
Flank pain (loin pain hematuria
syndrome)
Physical examinationPhysical examination
Should Include
Blood Pressure measurement
Assessment for edema or weight gain
Close skin examination
Direct visualization of the genitals
Abdominal mass or discomfort
Laboratory evaluationLaboratory evaluation
-Urinalysis, urine culture, and urinary
excretion studies
-Glomerular bleeding evaluation
(24-hour urinary protein
excretion/creatinine ratio,
excretion of casts, protein
excretion, blood clots)
Imaging studies
USD of the kidney and bladder.
Cytoscopy
Is rarely indicated. May be
useful to determine if the bleeding
comes from bladder or one or both
ureters.
EtiologyEtiology
The causes of gross and microscopic
hematuria are extensive.
Anatomical abnormalities
Bladder and kidney infection
Coagulation/hematology
Drugs
Exercise
Familial hematuria
Glomerulonephritis
Hypercalciuria-hyperuricosuria-urolithiasis
Interstitial nephritis
Trauma and tumors
Extrarrenal causes
Usually gross hematuria, no
proteinuria, and RBC’s that are suggestive
of nonglomerular origin.
Renal Causes (Glomerular causes)
Most patients also have proteinuria,
red cell casts, and/or renal insufficiency.
The clinical context is also suggestive.
Poststreptococcal glomerulonephritis
The most common type in children
results through immunologic process, from
A Beta-hemolytic streptococcus.
Immunoglobulin A nephropathy
The most common variety of primary
glomerulonephritis. Usually negative
family history.
Mesangial IgA deposition is the most
prominent finding on renal biopsy.
Alport Syndrome
Its classically X-linked form,
suggested by hematuria in a male.
Positive family history of hematuria,
deafness, and renal failure.
Abnormal collagen IV composition.
Thin base membrane disease
Also called benign familial hematuria,
transmitted in a dominant fashion but, in
most cases a heterozygous form of
autosomal recessive Alport syndrome.
TreatmentTreatment
General management
Salt and water restriction.
Specific treatment
Depends of the etiology or severity
of the disorder.