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Proteinuria & Hematuria
 

Proteinuria & Hematuria

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    Proteinuria & Hematuria Proteinuria & Hematuria Presentation Transcript

    • 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.
      • A natomical abnormalities
      • B ladder and kidney infection
      • C oagulation/hematology
      • D rugs
      • E xercise
      • F amilial hematuria
      • G lomerulonephritis
      • H ypercalciuria-hyperuricosuria-urolithiasis
      • I nterstitial nephritis
      • T rauma 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.
    •