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Hematuria

Contents
  1. Read book excerpt
  2. Wegener's granulomatosis: Introduction
  3. Wegener's granulomatosis Misdiagnosis
  4. Wegener's granulomatosis Complications
  5. Wegener's granulomatosis Treatments
  6. Clinical trials
  7. Diagnosis of Wegener's granulomatosis
  8. Wegener's granulomatosis Overview
  9. More book excerpts for Wegener's granulomatosis

Hematuria: Excerpt from The Diagnostic Approach to Symptoms and Signs in Pediatrics

  • Hematuria—presenceof blood in urine—can be microscopic (urine is not discolored) orgross (urine has red or brown discoloration).
  • >5 red cells per high-powerfield in centrifuged urinary sediment is considered abnormal.
  • Hematuria can occur with or withoutproteinuria; however, presence of red cell casts indicates glomerularorigin for hematuria.

    • Principal Causes of Hematuria

    1. Hematuriawithout proteinuria
      1. Glomerular disorders
        1. Acute postinfectious glomerulonephritis
        2. Immunoglobulin A nephropathy
        3. Henoch-Schönlein nephritis
        4. Alport syndrome
        5. Membranoproliferative glomerulonephritis
        6. Systemic lupus erythematosus
        7. Familial benign hematuria (thin basementmembrane nephropathy)
        8. Nonfamilial benign hematuria
      2. Nonglomerular disorders
        1. Urinarytract infection
        2. Trauma
        3. Exercise
        4. Hydronephrosis
        5. Renal vein thrombosis
        6. Hemoglobinopathies
        7. Idiopathic hypercalciuria
        8. Urolithiasis
        9. Polycystic kidney disease
        10. Renal tuberculosis
        11. Vascular malformations
        12. Foreign body in the urethra or bladder
        13. Neoplasm
        14. Bleeding disorders
        15. Drugs
    2. Hematuria with proteinuria
      1. Glomerulardisorders
        1. Acutepostinfectious glomerulonephritis
        2. Immunoglobulin A nephropathy
        3. Henoch-Schönlein nephritis
        4. Alport syndrome
        5. Membranoproliferative glomerulonephritis
        6. Systemic lupus erythematosus
        7. Membranous nephropathy
        8. Glomerulonephritis of chronic infection
        9. Idiopathic rapidly progressive glomerulonephritis
        10. Hemolytic-uremic syndrome
        11. Polyarteritis nodosa
        12. Antiglomerular basement membrane disease(Goodpasture disease)
        13. Focal segmental glomerulosclerosis
        14. Wegener granulomatosis

    Clinical Features and Diagnosis

    Hematuria without Proteinuria

    Glomerular Disorders

    Acute Postinfectious Glomerulonephritis

  • Usuallypresents within 1–2 wks after streptococcal pharyngitisor skin infection.
  • Rare before 3 yrs of age.
  • Disease spectrum varies from asymptomaticmicroscopic hematuria with normal renal function to acute renalfailure.
  • Clinical manifestations include fever,abdominal or flank pain, edema, hypertension, and oliguria. Urinecolor is often reddish brown, and red cell casts are usually seen.Proteinuria may or may not occur. In almost all cases, C3 levelis decreased. Supporting evidence of preceding streptococcal infectioncan include positive throat culture, positive streptozyme, or elevatedantistreptolysin O titer.
  • C3 level should return to normal withinabout 8 wks after onset of illness. Proteinuria can last for 6 mosand microscopic hematuria for 1–2 yrs, but virtually allchildren recover.

    • Immunoglobulin A Nephropathy

  • Also knownas Berger disease.
  • Can occur at any age, but peak incidenceis in adolescence and young adulthood.
  • Usually presents with recurrent attacksof gross hematuria, which may be associated with upper respiratorytract infections.
  • Microscopic hematuria can occur betweenepisodes of gross hematuria. Mild proteinuria also may occur, particularlyearly in the course. Renal function tends to be normal. Hypertension,nephrotic syndrome, and rapidly progressive course are unusual findings.
  • Serum concentration of C3 is normal,and this helps to distinguish this disorder from acute postinfectiousglomerulonephritis. Immunoglobulin A is major immunoglobulin inmesangial deposits on renal biopsy.

    • Henoch-Schönlein Nephritis

  • Common causeof vasculitis in childhood.
  • Clinical features include abdominalpain, purpura on buttocks and lower legs, transient arthritis/arthralgiaof large joints, microscopic hematuria, and gastrointestinal bleeding.
  • Diagnosis is usually clinical.
  • Renal biopsy is indistinguishable fromimmunoglobulin A nephropathy.
  • Some children develop chronic nephropathywith progression to end-stage renal disease.

    • Alport Syndrome

  • Primaryfeature is recurrent gross hematuria or asymptomatic microscopichematuria. A number of affected children also have sensorineuralhearing loss. Later in life, individuals develop progressive renalinsufficiency.
  • Usual form of genetic transmissionis X-linked, although autosomal-dominant and autosomal-recessiveforms occur. X-linked phenotype is due to mutation in the gene foralpha-5 chain of basement membrane collagen.

    • Membranoproliferative Glomerulonephritis

  • Most commonin the second decade of life. 3 histologic types (I, II, III) havebeen described.
  • Presentation is variable: gross ormicroscopic hematuria with or without proteinuria or nephrotic syndrome.Hypertension is common, and renal function may be decreased.
  • Serum C3 level is usually low. C3 nephriticfactor may be present, especially in type II. Different types canonly be distinguished by renal biopsy.

    • Systemic Lupus Erythematosus

  • Chronicmultisystem autoimmune disease that is most common in adolescent girls.
  • Characteristic findings include fever,arthritis, weight loss, and nephritis. Hematuria and proteinuriaare common urinary findings. Antinuclear antibody is usually positiveand serum C3 is usually low.
  • Antibody to double-stranded DNA isdiagnostic. Renal biopsy usually shows proliferative glomerulonephritiswith immunoglobulin G and C3 deposits.

    • Familial Benign Hematuria (Thin Basement Membrane Nephropathy)

  • Autosomal-dominantdisorder in which hematuria is usually microscopic. Positive familyhistory of hematuria and absence of proteinuria suggest diagnosis.Electron microscopy shows thinning of glomerular capillary basementmembrane.
  • Although thought to be benign, reportby Dische et al. (1985) described thin basement membrane nephropathyin several individuals who developed progressive renal disease.Further study is required to determine whether this disorder isreally benign.

    • Nonfamilial Benign Hematuria

    In many children, diagnostic studies do notreveal the cause of hematuria. These children are categorized ashaving benign nonfamilial hematuria. After months or years, hematuriafrequently disappears. Although this disorder is often benign, somechildren may have slowly developing glomerulonephritis. As longas hematuria exists, these patients should be tested at 6-mo intervalsto determine whether proteinuria develops.

    Nonglomerular Disorders

    Urinary Tract Infection

  • Common symptomsare dysuria, frequency, urgency, fever, abdominal pain, flank pain,and vomiting. Microscopic or gross hematuria can occur along withpyuria and bacteriuria.
  • Positive urine culture confirms thediagnosis.
  • See Chap.15, Dysuria.

    • Trauma

  • Blunt orpenetrating injury to kidney or any portion of urinary tract cancause gross or microscopic hematuria.
  • With minor trauma and microscopic hematuriain asymptomatic individuals, renal U/S should be performedto search for anatomic abnormality (e.g., hydronephrosis or renalcyst) because minimal trauma rarely causes hematuria in normal kidneys.Otherwise, CT is radiologic study of choice.
  • Urethral trauma may occur followingcrush-type injury from fractured pelvis or direct injury, and urethrographymay be diagnostic.

    • Exercise

    Vigorous exercise can produce gross or microscopichematuria, which usually resolves within 1–2 days.

    Hydronephrosis

    In children with hydronephrosis, microscopicor gross hematuria may occur following mild flank or abdominal trauma.Renal U/S may be performed initially.

    Renal Vein Thrombosis

  • Predisposingfactors include perinatal asphyxia, dehydration, septicemia, shock,and coagulopathies (e.g., protein C deficiency).
  • Gross hematuria usually occurs alongwith palpable unilateral or bilateral flank masses.
  • Renal U/S with Doppler methodsis diagnostic.

    • Hemoglobinopathies

  • HemoglobinopathiesSA, SC, SS, CC, AC, and sickle beta-thalassemia can produce renalbleeding and microscopic or gross hematuria.
  • Hemoglobin electrophoresis is diagnosticand should be performed in any African-American child with hematuriaof unknown cause.

    • Idiopathic Hypercalciuria

  • Microscopicor gross hematuria may occur with increased urinary calcium excretion withoutevidence of urinary stone disease. However, hypercalciuria is riskfactor for development of urolithiasis.
  • Urine calcium:creatinine ratio (mg:mg)of greater than normal for age can screen for this disorder (Matoset al., 1997). If spot ratio is greater than normal, 24-hr urinecalcium excretion should be measured. Calcium excretion of >4mg/kg/day is indicative of hypercalciuria.

    • Urolithiasis

  • Causes inchildren include urinary tract infection, hypercalciuria, hyperuricosuria, cystinuria,and primary hyperoxaluria.
  • When urinary stone is being passed,abdominal or flank pain (renal colic) and microscopic or gross hematuriaare usual findings.
  • Diagnostic investigations should includeUA; urine culture; blood urea nitrogen; and serum measurements ofcalcium, phosphorus, uric acid, and creatinine.
  • CT is recommended to search for underlyingdisease and localize any obstruction.
  • When calculi are recovered from urine,their biochemical contents should be analyzed. If they are unrecoverablefrom urinary tract, determination of calcium:creatinine ratio inrandom urine specimen should be performed. Ratio greater than normalfor age can screen for hypercalciuria. More precise test is measurementof 24-hr urine calcium excretion.
  • If these tests are negative, 24-hrurinary excretion of cystine, oxalate, and uric acid should be performed.

    • Polycystic Kidney Disease

    Autosomal-Recessive

  • Gene hasbeen mapped to chromosome 6.
  • Common findings in neonates are grossor microscopic hematuria, bilateral flank masses, hypertension,and azotemia.
  • Renal U/S usually revealslarge echogenic kidneys. Cysts are microscopic and not seen by imaging.
  • Liver disease is congenital hepaticfibrosis.
  • Diagnosis is usually clinical and radiologic.

    • Autosomal-Dominant

  • Rarely encounteredin childhood.
  • At least 3 different genetic mutationshave been found.
  • Gross or microscopic hematuria, unilateralor bilateral abdominal masses, and hypertension are common findings.
  • Abdominal U/S shows enlargedpolycystic kidneys and hepatic cysts.
  • Diagnosis is usually based on clinicaland radiographic findings.

    • Renal Tuberculosis

  • Usuallydoes not occur until primary disease has been established over several years.
  • Usually associated with tuberculouscystitis, which can produce suprapubic pain and dysuria.
  • Gross or microscopic hematuria andpyuria are characteristic.
  • Mantoux test is usually positive.
  • Usual urine culture for bacteria isnegative, whereas urine culture positive for acid-fast organismsis diagnostic.

    • Vascular Malformations

  • Arteriovenousmalformations of kidney can present with gross hematuria.
  • Renal U/S and CT may locatemalformation. Renal angiography is definitive.

    • Foreign Body in Urethra or Bladder

  • Foreignbody in urethra or bladder usually produces urethral or suprapubicpain, dysuria, and hematuria.
  • Abdominal radiography may reveal radiopaqueforeign body. Cystoscopy can confirm diagnosis.
  • It is important to note that a foreignbody in the vagina can produce bleeding that may be mistaken forhematuria.

    • Neoplasm

  • A numberof genitourinary neoplasms occur in the pediatric population.
  • Wilms tumor, most common renal tumorin children, usually presents as abdominal or flank mass that doesnot cross midline unless it is very large. Gross hematuria occursin small number of cases. Renal U/S or CT shows renal massthat distorts collecting system.
  • Renal hemangioma is rare lesion thatcan present with recurrent gross hematuria. Diagnosis is confirmedby renal angiography.
  • Renal carcinoma is rare in pediatricpopulation, but renal U/S can demonstrate mass lesion.
  • Bladder tumors are exceedingly rarein children, but suprapubic mass is sometimes palpable. Most commonbladder tumor is rhabdomyosarcoma, which can present with hematuriaor acute urinary retention. Abdominal U/S, CT, and cystoscopyare useful in locating and defining extent of tumor.
  • In all cases of genitourinary tractneoplasms, histologic diagnosis is definitive.

    • Bleeding Disorders

    Although gross or microscopic hematuria mayoccur with bleeding disorders (hemophilias, thrombocytopenia, disseminatedintravascular coagulation), it is uncommon to have isolated hematuriaas only manifestation. See Chap.53, Recurrent Infection.

    Drugs

    A number of drugs (penicillins, sulfonamides,cephalosporins, rifampin, tetracycline, cisplatin, lithium) maycause gross or microscopic hematuria. Cyclophosphamide may causehemorrhagic cystitis.

    Hematuria with Proteinuria

  • Hematuriawith proteinuria may occur with several glomerular renal disordersas discussed previously:

  • Acute postinfectious glomerulonephritis
  • Immunoglobulin A nephropathy
  • Henoch-Schönlein nephritis
  • Alport syndrome
  • Membranoproliferative glomerulonephritis
  • Systemic lupus erythematosus
  • Other glomerular renal diseases thatusually present with hematuria and proteinuria are discussed inthis section.

    • Membranous Nephropathy

  • Most commonduring second decade of life and usually presents with nephroticsyndrome. Microscopic hematuria is more common than gross hematuria.
  • Renal biopsy confirms diagnosis.

    • Glomerulonephritis of Chronic Infection

  • Disordersassociated with glomerulonephritis of chronic infection includeendocarditis and ventriculoatrial shunt infections.
  • Clinical features are those of acuteglomerulonephritis, namely edema, hypertension, and renal insufficiency.Serum C3 is often decreased.

    • Idiopathic Rapidly Progressive Glomerulonephritis

  • Uncommondisease in children; often preceded by viral illness.
  • Affected children have acute onsetof hematuria, proteinuria, oliguria or anuria, and azotemia.
  • Serum C3 level is normal or mildlydecreased. Many children progress to end-stage renal disease withina few weeks or months without treatment.
  • Renal biopsy and clinical course arediagnostic.

    • Hemolytic-Uremic Syndrome

  • Typicalform follows prodromal illness consisting of fever, vomiting, abdominal pain,and, often, bloody diarrhea. This is followed in 5–10 daysby hemolytic anemia with fragmented red cells, thrombocytopenia,and acute renal injury with hematuria, proteinuria, and often oliguriaor anuria.
  • Most common pathogen is E. coli 0157:H7.

    • Polyarteritis Nodosa

  • Necrotizingvasculitis that affects small and medium-sized arteries. Althoughcause is unknown, it may follow viral URI, streptococcal infection,or chronic hepatitis B infection.
  • Characteristic findings include fever,abdominal pain, hematuria, hypertension, purpura, arthritis, andstroke.
  • Lab findings include increased sedimentationrate, anemia, leukocytosis, proteinuria, and hypergammaglobulinemia.In some cases, antineutrophil cytoplasmic antibody is found.
  • Biopsy demonstrating the vasculitisis diagnostic.

    • Antiglomerular Basement Membrane Disease (Goodpasture Disease)

  • Associationof pulmonary hemorrhage and glomerulonephritis in which antibodies againstlung and glomerular basement membrane can be demonstrated.
  • Characteristic findings are hematuria,proteinuria, hemoptysis, and progressive renal failure. Serum C3level is normal.
  • Renal biopsy shows linear stainingof immunoglobulin G along glomerular basement membrane.

    • Focal Segmental Glomerulosclerosis

  • Clinicallyindistinguishable from minimal change nephrotic syndrome but shouldbe suspected when there has been inadequate response to standardcorticosteroid therapy.
  • Microscopic hematuria and occasionallygross hematuria may occur.
  • Renal biopsy is diagnostic.

    • Wegener Granulomatosis

  • Disorderof unknown cause characterized by vasculitis that affects upperand lower respiratory tract and kidneys.
  • Fever, malaise, weight loss, hemoptysis,dyspnea, hematuria, and proteinuria are characteristic findings.
  • Antineutrophil circulating antibodiesthat bind to proteinase 3 are specific for this disorder. Sinus,airway, lung, or kidney biopsy that shows necrotizing granulomatouslesions and presence of specific antineutrophil circulating antibodiesthat bind to proteinase 3 confirm the diagnosis.

    • Diagnostic Approach

  • First stepin diagnosis is to determine whether there is blood in urine. Althoughblood may produce pink, red, or brownish color of the urine, othersubstances also may produce same type of urinary discoloration.
  • Urine dipstick detects hemoglobin containedin red cells as well as free Hgb. It can detect as few as 1 or 2red cells per high-power field in uncentrifuged specimen. Microscopydetermines whether red cells are in urine and thus the presenceof hematuria.
  • Urine sample that tests positive ondipstick but negative on microscopy indicates presence of hemoglobinor myoglobin. Serum is pink in color with hemoglobinuria and normalin color with myoglobinuria.
  • Best way to distinguish myoglobin fromHgb is immunochemically. Red, orange, or brownish urine that isdipstick negative for blood indicates that certain foods (blackberries,beets), food dyes, urate crystals, or drugs (pyridium, desferoximine)are coloring urine. Urine containing porphyrin initially has normalcolor but changes to red on standing; dipstick is negative, andno red cells are seen on microscopy.

    • Hematuria without Proteinuria

  • Microscopichematuria without proteinuria is most commonly due to urinary tractinfection, trauma, acute postinfectious glomerulonephritis, immunoglobulinA nephropathy, familial benign hematuria, or nonfamilial benignhematuria.
  • Following history and physical exam,these tests should be performed initially: UA of child and familymembers (to diagnose familial benign hematuria), urine culture,serum creatinine, blood urea nitrogen, C3, calcium:creatinine ratio,and renal U/S. If results of these tests are normal, andproteinuria is consistently absent, most causes of hematuria havebeen excluded and further diagnostic studies (e.g., cystoscopy andrenal biopsy) are usually unnecessary.
  • Children categorized as having nonfamilialbenign hematuria because they have normal evaluation and no recognizablerenal disease may prove to have transient hematuria, but as longas hematuria occurs, these children should be followed for possibleoccurrence of proteinuria. Those with familial benign hematuriaalso should be followed.
  • In addition to above tests, diagnosticevaluation of gross hematuria should include CBC, platelet count,antistreptolysin O or streptozyme titer, and Hgb electrophoresis(in African-American children). Renal angiography may be necessaryif vascular malformation is suspected. If proteinuria occurs whenhematuria subsides, renal biopsy may be indicated.

    • Hematuria with Proteinuria

  • Glomerulonephritisshould be suspected in every child with hematuria and proteinuria.
  • Presence of red cell casts indicatesglomerular bleeding.
  • Results of tests for urinary protein(urine dipstick, sulfosalicylic acid test) are usually positivewith gross hematuria. Although dipstick protein reading of 3+ to4+ may signify glomerular disease with gross hematuria,lower reading may have diagnostic significance. See Chap. 50, Proteinuria, forprotein concentrations corresponding to dipstick readings.
  • To more reliably detect proteinuriaassociated with glomerular disease, urine should be tested whengross hematuria subsides.
  • Renal biopsy is required for specificdiagnosis unless there is evidence of unequivocal acute postinfectiousglomerulonephritis or family history of Alport syndrome. Biopsymay be necessary with acute postinfectious glomerulonephritis ifserum C3 level does not become normal within 2 mos, if proteinuriapersists for >6 mos, or to distinguish it from idiopathicrapidly progressive glomerulonephritis if presentation is that ofacute renal failure.

    • References

    1. Barratt TM, et al., eds. Pediatric nephrology,4th ed. Baltimore: Lippincott Williams & Wilkins, 1999.
    2. Behrman RE, et al., eds. Nelson textbook of pediatrics,16th ed. Philadelphia: WB Saunders, 2000.
    3. Dische FE, et al. Abnormally thin glomerular basementmembranes associated with hematuria, proteinuria, or renal failurein adults. Am J Nephrol 1985;5:103–109.
    4. Lieu TA, et al. An approach to the evaluation and treatmentof microscopic hematuria. Pediatr Clin North Am 1991;38:579–592.
    5. Matos V, et al. Urinary phosphate/creatinine,calcium/creatinine, and magnesium/creatinine ratiosin a healthy pediatric population. J Pediatr 1997;131:252–257.
    6. Online Mendelian Inheritance in Man (OMIM). McKusick-NathansInstitute for Genetic Medicine, Johns Hopkins University (Baltimore,MD) and National Center for Biotechnology Information, NationalLibrary of Medicine (Bethesda, MD), 2000. World Wide Web URL: http://www.ncbi.nlm.nih.gov/omim.
    7. Ozen S, et al. Diagnostic criteria for polyarteritisnodosa in childhood. J Pediatr 1992;120:206–209.
    8. Rudolph AM, ed. Rudolph's pediatrics, 20thed. Norwalk, CT: Appleton & Lange, 1996.
    9. Spitzer A, Cruz CC. When you find protein or bloodin the urine. Contemp Pediatr 1998;15:89–109.
    10. Stapleton FB. Idiopathic hypercalciuria: associationwith isolated hematuria and risk for urolithiasis in children. AReport of the Southwest Pediatric Nephrology Study Group. KidneyInt 1990;37:807–811.
    11. Valentini RP, et al. Outcome of antineutrophil cytoplasmicautoantibodies–positive glomerulonephritis and vasculitisin children: a single-center experience. J Pediatr 1998;132:325–328.
    12. Welch TR. Current management of selected childhoodrenal diseases. Curr Prob Pediatr 1992;22:432–451.
    13. West CD. Asymptomatic hematuria and proteinuria inchildren: causes and appropriate diagnostic studies. J Pediatr 1976;89:173–182.

    Book Source Details

    • Book Title: The Diagnostic Approach to Symptoms and Signs in Pediatrics
    • Author(s): Paul S. Bellet
    • Year of Publication: 2006
    • Copyright Details: The Diagnostic Approach to Symptoms and Signs in Pediatrics, Copyright © 2006 Lippincott Williams & Wilkins.

    More About Wegener's granulomatosis

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    Medical Books Excerpts
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    • Hematuria
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    • "Signs & Symptoms: A 2-in-1 Reference for Nurses" (2007)
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    • "The Diagnostic Approach to Symptoms and Signs in Pediatrics" (2006)
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    • "Nursing: Interpreting Signs and Symptoms" (2007)
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    Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.



    More About This Book:
    Title: The Diagnostic Approach to Symptoms and Signs in Pediatrics
    Authors: Paul S. Bellet
    Publisher: Lippincott Williams & Wilkins
    Copyright: 2006
    ISBN: 0-78172-899-1

     » Next page: Respiratory Distress and Apnea (The Diagnostic Approach to Symptoms and Signs in Pediatrics)

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