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PROTEINURIA AND HEMATURIA

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PROTEINURIA AND HEMATURIA Powered By Docstoc
					PROTEINURIA AND
   HEMATURIA


CARMEN PRIET0-JIMENEZ, M.D.
Proteinuria and Nephrotic
        Syndrome
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 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 Syndrome
Nephrotic syndrome is characterized
by massive proteinuria,
hypoalbuminemia, edema, and
hyperlipidemia; the most common
presenting symptom is edema.
         Introduction
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.
           Definition
The diagnosis of NS is the presence
of urinary protein, with the albumin
disproportionately greater than
globulin.
Clinical 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
        Complications
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.
                 Prognosis
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
Glomerulonephitis
         Introduction
Recognition, definition, differential
diagnosis, and orderly evaluation of
hematuria in infants and children is
often an important issue in pediatric
practice
          Definition
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 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 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.
            Etiology
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.
-Neprholithiasis
-UTI
-Adenovirus
-Kidney tumor
-Polycystic kidney
-Urethral irritation
-Obstructive uropathy
-Post-traumatic kidney
-Onset of menarche
-Exposure to cyclophosphamide
-Thrombogenic condition
-Sickle cell trait
-Vascular bleeding
-”Nutcracker syndrome”
-Left renal vein entrapment
   (Also orthostatic proteinuria)
-Loin pain hematuria syndrome
-Urethrovesical bleeding
Renal Causes (Glomerular causes)
    Most patients also have proteinuria, red
cell casts, and/or renal insufficiency. The
clinical context is also suggestive.
-Postinfectious glomerulonephritis
-Henoch-Schonlein purpura
    (tetrad: rash, arthralgias, abdominal
pain and renal disease)
-IgA nephropathy                     persistent

-Alport Syndrome                     hematuria

-Thin base membrane disease
   (heterozygote carrier)
-Systemic diseases
   Lupus
   Shunt nephritis
   Hemolitic-uremic syndrome
Unexplained hematuria
  -Factitious hematuria
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.
            Treatment
General management
   Salt and water restriction.
Specific treatment
   Depends of the etiology or severity of
the disorder.

				
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posted:4/2/2008
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