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Hematuria

  • Author: Sanjeev Gulati, MD, MBBS, DNB(Peds), DM, DNB(Neph), FIPN(Australia), FICN, FRCPC(Canada); Chief Editor: Craig B Langman, MD  more...
 
Updated: Feb 07, 2016
 

Practice Essentials

Generally, hematuria is defined as the presence of 5 or more red blood cells (RBCs) per high-power field in 3 of 3 consecutive centrifuged specimens obtained at least 1 week apart. Hematuria can be either gross (ie, overtly bloody, smoky, or tea-colored urine) or microscopic. It may also be either symptomatic or asymptomatic, either transient or persistent, and either isolated or associated with proteinuria and other urinary abnormalities. See the image below.

Microscopy of urinary sediment. Typical appearance Microscopy of urinary sediment. Typical appearance in non-glomerular hematuria: RBCs are uniform in size and shape but show two populations of cells because a small number have lost their hemoglobin pigment.

Signs and symptoms

The first step in the evaluation of hematuria consists of a detailed history and a thorough physical examination. Efforts should be made to distinguish glomerular causes from extraglomerular ones, as follows:

  • Passage of clots in urine suggests an extraglomerular cause
  • Fever, abdominal pain, dysuria, frequency, and recent enuresis in older children may point to a urinary tract infection as the cause
  • Recent trauma to the abdomen may be indicative of hydronephrosis
  • Early-morning periorbital puffiness, weight gain, oliguria, dark-colored urine, and edema or hypertension suggest a glomerular cause
  • Hematuria due to glomerular causes is painless
  • Recent throat or skin infection may suggest postinfectious glomerulonephritis
  • Joint pains, skin rashes, and prolonged fever in adolescents suggest a collagen vascular disorder
  • Anemia cannot be accounted for by hematuria alone; in a patient with hematuria and pallor, other conditions should be considered
  • Skin rashes and arthritis can occur in Henoch-Schönlein purpura and systemic lupus erythematosus
  • Information regarding exercise, menstruation, recent bladder catheterization, intake of certain drugs or toxic substances, or passage of a calculus may also assist in the differential diagnosis
  • A family history that is suggestive of Alport syndrome, collagen vascular diseases, urolithiasis, or polycystic kidney disease is important

Physical examination should include the following:

  • Measurement of the blood pressure (with an appropriately sized cuff)
  • Evaluation for the presence of periorbital puffiness or peripheral edema
  • Detailed skin examination to look for purpura.
  • Abdominal examination to look for palpable kidneys
  • Careful examination of the genitalia
  • Detailed ophthalmologic evaluation (in familial hematuria)

The following findings help distinguish between glomerular and nonglomerular hematuria:

  • Glomerular hematuria: Brown-colored urine, RBC casts, and dysmorphic (small, deformed, misshapen, sometimes fragmented) RBCs and proteinuria
  • Nonglomerular hematuria: Reddish or pink urine, passage of blood clots, and eumorphic (normal-sized, biconcavely shaped) erythrocytes

See Clinical Presentation for more detail.

Diagnosis

The laboratory tests ordered for the evaluation of hematuria must be based on the clinical history and the physical examination. Tests that may be helpful include the following:

  • Urinalysis with careful microscopic review of the urine sample
  • Phase-contrast microscopy to help determine the source of the bleeding
  • Blood urea nitrogen (BUN) and serum creatinine levels
  • Hematologic and coagulation studies (eg, complete blood count [CBC] and, sometimes, platelet counts)
  • Urine calcium excretion
  • Serologic testing (eg, complement, antistreptolysin [ASO], anti-DNase B, antinuclear antibody [ANA], and double-stranded DNA [dsDNA])
  • Urine culture for suspected urinary tract infection (UTI)

The following imaging studies may be helpful:

  • Renal and bladder ultrasonography
  • Spiral CT
  • Voiding cystourethrography
  • Radionuclide studies

IV urography rarely contributes additional information in the evaluation of hematuria and may result in unnecessary exposure to ionizing radiation.

A kidney biopsy is rarely indicated in the evaluation of isolated asymptomatic hematuria. Relative indications for performing a kidney biopsy in patients with hematuria are as follows:

  • Significant proteinuria
  • Abnormal renal function
  • Recurrent persistent hematuria
  • Serologic abnormalities (abnormal complement, ANA, or dsDNA levels)
  • Recurrent gross hematuria
  • A family history of end-stage renal disease

In most patients, a renal biopsy either is normal or reveals minor changes, such as thin glomerular basement membranes, focal glomerulonephritis, or mild mesangial hypercellularity. In a minority of patients, histologic findings, together with historical or serologic data, may point to specific conditions.

Patients with hematuria may usefully be categorized into 1 of the following 4 groups:

  • Gross hematuria
  • Microscopic hematuria with clinical symptoms
  • Asymptomatic microscopic hematuria with proteinuria
  • Asymptomatic microscopic (isolated) hematuria

See Workup for more detail.

Management

General principles of treatment are as follows:

  • Hematuria is a sign and not itself a disease; thus, therapy should be directed at the process causing it
  • Asymptomatic (isolated) hematuria generally does not require treatment
  • In conditions associated with abnormal clinical, laboratory, or imaging studies, treatment may be necessary, as appropriate, with the primary diagnosis
  • Surgical intervention may be necessary with certain anatomic abnormalities (eg, ureteropelvic junction obstruction, tumor, or significant urolithiasis)
  • Dietary modification is usually not indicated, except for children who may tend to develop hypertension or edema as a result of the primary disease process (eg, nephritis)
  • Patients with persistent microscopic hematuria should be monitored every 6-12 months for the appearance of signs or symptoms indicative of progressive renal disease

See Treatment and Medication for more detail.

Guidelines on hematuria from the American College of Physicians (ACP) advises that clinicians should include gross hematuria in their routine review of systems and specifically ask all patients with microscopic hematuria about any history of gross hematuria.[1, 2]

The ACP also recommend that[1, 2] :

  • Clinicians should not use screening urinalysis for cancer detection in asymptomatic adults.
  • Clinicians should confirm heme-positive results of dipstick testing with microscopic urinalysis that demonstrates 3 or more erythrocytes per high-powered field before initiating further evaluation in all asymptomatic adults.
  • Clinicians should refer for further urologic evaluation in all adults with gross hematuria, even if self-limited.
  • Clinicians should consider urology referral for cystoscopy and imaging in adults with microscopically confirmed hematuria in the absence of some demonstrable benign cause.
  • Clinicians should pursue evaluation of hematuria even if the patient is receiving antiplatelet or anticoagulant therapy.
  • Clinicians should not obtain urinary cytology or other urine-based molecular markers for bladder cancer detection in the initial evaluation of hematuria.
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Background

Hematuria is one of the most common urinary findings that result in children presenting to pediatric nephrologists. Generally, hematuria is defined as the presence of 5 or more RBCs per high-power field in 3 of 3 consecutive centrifuged specimens obtained at least 1 week apart. In the office setting, a positive reaction on the urine dipstick test is usually the first indication of the presence of hematuria. Hematuria can be gross (ie, the urine is overtly bloody, smoky, or tea colored) or microscopic. It may be symptomatic or asymptomatic, transient or persistent, and either isolated or associated with proteinuria and other urinary abnormalities. The role of the primary care physician in the management of a child with hematuria includes the following:

  • Recognize and confirm the finding of hematuria.
  • Identify common etiologies.
  • Select patients who have significant urinary system disease that might require further expertise in either diagnosis or management and referral.
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Pathophysiology

The etiology and pathophysiology of hematuria vary. For instance, hematuria of glomerular origin may be the result of a structural disruption in the integrity of glomerular basement membrane caused by inflammatory or immunologic processes. Chemicals may cause toxic disruptions of the renal tubules, whereas calculi may cause mechanical erosion of mucosal surfaces in the genitourinary tract, resulting in hematuria.

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Frequency

United States

The prevalence of gross hematuria in children is estimated to be 0.13%. In more than half of the cases (56%) this is due to an easily identifiable cause. The most common cause appears to be cystitis (20-25%). Asymptomatic microscopic hematuria is, on the average, 10-fold as prevalent as gross hematuria (1.5%, range 0.4-4.1%, depending on the criteria used to define hematuria). With repeated evaluations, the prevalence of asymptomatic microscopic hematuria decreases to less than 0.5%, supporting the notion that most cases of hematuria in children are transient. The incidence of simultaneous hematuria and proteinuria is estimated to be only 0.06%, but their coexistence signals significant renal disease.

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Mortality/Morbidity

In general, children with isolated asymptomatic microscopic hematuria tend to do well, whereas those with associated findings (eg, hypertension, proteinuria, abnormal serum creatinine levels) are more likely to have serious problems. Because hematuria is the end result of various processes, the morbidity and mortality rates of the condition depend on the primary process that initiated it.

Race

The incidence of hematuria in specific racial groups is determined by the primary cause. For example, idiopathic hypercalciuria is infrequent in black and Asian children, but relatively common in whites. Conversely, hematuria caused by sickle cell disease is more common in blacks than in whites.

Sex

Sex may predispose a child to specific diseases that manifest as hematuria. For example, the sex-linked form of Alport syndrome has a male preponderance, whereas lupus nephritis is more common in adolescent girls.

Age

Prevalence of certain conditions varies with age.[3] For instance, Wilms tumors are more frequent in children of preschool age, whereas acute postinfectious glomerulonephritis is more frequent in the school-aged population. In adults, hematuria is often a sign of malignancy of the genitourinary tract (eg, renal cell carcinoma, bladder tumors, prostatic tumors). These conditions are rare in children.

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Contributor Information and Disclosures
Author

Sanjeev Gulati, MD, MBBS, DNB(Peds), DM, DNB(Neph), FIPN(Australia), FICN, FRCPC(Canada) Additional Professor, Department of Nephrology, Sanjay Gandhi Post Graduate Institute of Medical Sciences; Senior Consultant in Pediatric Nephrology and Additional Director, Department of Nephrology and Transplant Medicine, Fortis Institute of Renal Sciences Transplantation, India

Sanjeev Gulati, MD, MBBS, DNB(Peds), DM, DNB(Neph), FIPN(Australia), FICN, FRCPC(Canada) is a member of the following medical societies: American Society of Pediatric Nephrology, International Society of Nephrology, Royal College of Physicians and Surgeons of Canada, Indian Academy of Pediatrics

Disclosure: Nothing to disclose.

Coauthor(s)

Deogracias Pena, MD Medical Director of Dialysis, Medical Director of Pediatric Nephrology and Transplantation, Cook Children's Medical Center; Clinical Associate Professor, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Medical Director of Pediatric Nephrology, Florida Hospital for Children

Deogracias Pena, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Adrian Spitzer, MD Clinical Professor Emeritus, Department of Pediatrics, Albert Einstein College of Medicine

Adrian Spitzer, MD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Pediatric Society, American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Craig B Langman, MD The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, The Ann and Robert H Lurie Children's Hospital of Chicago

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, International Society of Nephrology

Disclosure: Received income in an amount equal to or greater than $250 from: Alexion Pharmaceuticals; Raptor Pharmaceuticals; Eli Lilly and Company; Dicerna<br/>Received grant/research funds from NIH for none; Received grant/research funds from Raptor Pharmaceuticals, Inc for none; Received grant/research funds from Alexion Pharmaceuticals, Inc. for none; Received consulting fee from DiCerna Pharmaceutical Inc. for none.

Additional Contributors

Richard Neiberger, MD, PhD Director of Pediatric Renal Stone Disease Clinic, Associate Professor, Department of Pediatrics, Division of Nephrology, University of Florida College of Medicine and Shands Hospital

Richard Neiberger, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Medical Association, American Society of Nephrology, American Society of Pediatric Nephrology, Christian Medical and Dental Associations, Florida Medical Association, International Society for Peritoneal Dialysis, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Shock Society, Sigma Xi, Southern Medical Association, Southern Society for Pediatric Research, Southwest Pediatric Nephrology Study Group

Disclosure: Nothing to disclose.

References
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Approach to hematuria.
Nonglomerular hematuria.
Microscopy of urinary sediment. Typical appearance in non-glomerular hematuria: RBCs are uniform in size and shape but show two populations of cells because a small number have lost their hemoglobin pigment.
Microscopy of urinary sediment. Typical appearance of RBCs in glomerular hematuria: RBCs are small and vary in size, shape, and hemoglobin content.
Microscopy of urinary sediment. A cast containing numerous erythrocytes, indicating glomerulonephritis.
Table. Histologic Findings
Condition Histology History Laboratory Data
Systemic lupus erythematosus Mild glomerulitis, proliferative changes, immune complex deposition, crescents, immunoglobulin deposition Hematuria, proteinuria, hypertension, joint pains, rashes Abnormal C3, C4, ANA, and dsDNA levels; anemia; thrombocytopenia
IgA nephropathy IgA deposition in the mesangium, glomerular sclerosis, proliferative changes, crescents in severe cases Gross, intermittent, painless hematuria No specific changes, although increased serum



IgA levels observed in some patients



Henoch-Schönlein purpura Same as IgA nephropathy Purpura, joint pains, abdominal pain, hematuria No specific laboratory data
Alport syndrome Some thinning of basement membranes, "basket weave" changes in the glomerular basement



membrane on electron microscopy



Sensorineural hearing loss, corneal abnormalities, hematuria, renal failure No specific changes
Thin basement membrane disease Average glomerular basement membranes reported to be 100-200 nm in children in this condition Persistent microscopic or gross hematuria, significant family history No specific changes
Mesangiocapillary glomerulonephritis Glomerular lobulations, thickening of the mesangial matrix and glomerular basement membranes, crescents Hematuria, proteinuria, hypertension C3 levels possibly abnormal
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